ST-elevation Myocardial Infarction: Straight To The Point of Care

ST-elevation
myocardial infarction
Straight to the point of care
Last updated: Apr 22, 2021

Table of Contents
Overview 3
Summary 3
Definition 3
Theory 4
Epidemiology 4
Risk factors 4
Aetiology 6
Pathophysiology 6
Classification 7
Case history 8
Diagnosis 9
Recommendations 9
History and exam 47
Investigations 53
Differentials 65
Criteria 68
Screening 68
Management 69
Recommendations 69
Treatment algorithm overview 121
Treatment algorithm 124
Emerging 164
Primary prevention 164
Secondary prevention 165
Patient discussions 165
Follow up 167
Monitoring 167
Complications 168
Prognosis 171
Guidelines 172
Diagnostic guidelines 172
Treatment guidelines 173
Online resources 176
References 177
Images 194
Disclaimer 236
ST-elevation myocardial infarction Overview
Summary
ST-elevation myocardial infarction (STEMI) presents with central chest pain that is classically heavy in nature,
like a sensation of pressure or squeezing. Examination is variable, and findings range from normal to a
OVERVIEW
critically unwell patient in cardiogenic shock.
Give a loading dose of aspirin as soon as possible to any patient with suspected acute coronary syndrome.
Make a clinical diagnosis of STEMI and start immediate treatment when a patient presents with symptoms
suggestive of myocardial ischaemia and has persistent ST-segment elevation in at least 2 anatomically
contiguous ECG leads.
A rise in cardiac-specific troponins confirms the diagnosis but do not wait for laboratory results before
starting treatment.
Immediate and prompt reperfusion can prevent or minimise myocardial damage and improve the chances of
survival and recovery. Primary percutaneous coronary intervention (PCI) is the best management option for
most patients, with fibrinolysis reserved for those without access to timely primary PCI.
Survivors of acute MI should receive cardiac rehabilitation and be closely followed up to ensure adequate
modification of risk factors and optimisation of (and adherence to) pharmacotherapy for secondary
prevention, and to monitor for the development of post MI complications and/or residual angina symptoms.
Definition
Acute myocardial infarction is myocardial cell death that occurs because of a prolonged mismatch
between perfusion and demand. In the case of ST-elevation myocardial infarction (STEMI) this is caused
predominantly by complete atherothrombotic occlusion of a coronary artery.
In the appropriate clinical context, a STEMI is diagnosed clinically when there is new (or increased) and
persistent ST-segment elevation in at least two contiguous leads of ≥1 mm in all leads other than
leads V2-V3 where the following cut-off points apply :[1]
• ≥2.5 mm in men <40 years old

• ≥2 mm in men >40 years old
• ≥1.5 mm in women regardless of age
• 1 mm = 1 small square (at a standard ECG calibration of 10 mm/mV).
Contiguous ECG leads lie next to each other anatomically and indicate a specific myocardial territory.
This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2021.
BMJ Best Practice topics are regularly updated and the most recent version
3
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2021. All rights reserved.
ST-elevation myocardial infarction Theory
Epidemiology
Ischaemic heart disease (IHD) is the most common cause of death globally but in Europe mortality has been
falling over the past 30 years.[4] IHD now accounts for almost 1.8 million deaths per year across Europe,
THEORY
around 20% of all deaths, but rates vary significantly between countries.[4]
In Sweden, which keeps the most comprehensive European STEMI registry, the annual incidence of STEMI
in 2015 was 58 per 100,000.[4] Across Europe, incidence estimates range from 43 to 144 per 100,000 per
year.[4]
The incidence of STEMI has been steadily declining over the past 20 years. In England, Wales, and Northern
Ireland, there were around 87,000 cases of myocardial infarction (MI) between April 2018 and March 2019;
36% were STEMI. There was a 2.4% decrease in MI cases compared with the previous year.[5] In the US,
38% of patients with acute coronary syndrome have STEMI.[3]
STEMI patients are often younger than non-STEMI (NSTEMI) patients, with a median age of 65 years for
STEMI and 71 years for NSTEMI.[5] STEMI is more common in men than in women.[4]
MI tends to occur at a younger age in men than in women, with a median age difference of 8 years for all
heart attacks (66 years vs. 74 years) and 9 years for STEMI (63 years vs. 72 years).[5] The incidence in
women increases after the menopause. Women under 60 have higher 30-day mortality rates from STEMI
than men under 60, even after adjusting for medications, primary percutaneous coronary intervention, and
other co-existing comorbidities.[6]
Risk factors
Strong
smoking
Single most important modifiable risk factor.
People who smoke 20 or more cigarettes a day have a 2- to 3-fold increased risk of dying from
coronary heart disease compared with non-smokers or those who have quit for >10 years. Even mild
and passive smoking is associated with increased risk.[3]
hypertension
Only 2 out of 3 patients with hypertension are diagnosed and only 1 in 3 are adequately controlled on
treatment.
Systolic blood pressure (SBP) and diastolic blood pressure (DBP) both contribute to development of
coronary artery disease.
Even pre-hypertension (untreated SBP 120-139 mmHg and untreated DBP 80-89 mmHg, or both)
increases risk 2-fold compared with normal levels.[3]
diabetes
Patients with diabetes have impaired endothelial and smooth muscle function with increased leukocyte
adhesion, promoting atherosclerosis.
4 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Apr 22, 2021.
They have a 4-fold increased risk of cardiovascular disease compared with people who do not have
diabetes.[8]
An HbA1c of <53 mmol/mol (<7%) is the goal of treatment for patients with diabetes.[3] [9] However,
THEORY
for patients with coronary heart disease, this goal may be less stringent (i.e., <64 mmol/mol [<8%]).[9]
obesity
Increased risk in patients with a body mass index >25.[3]
metabolic syndrome
May be present in men with a waist circumference >100 cm (>39 inches) and women with a waist
circumference >90 cm (>35 inches).[10]
Characterised by glucose intolerance, hyperinsulinaemia, elevated triglycerides, low HDL-cholesterol,

and central obesity and is a marker for increased risk of coronary artery disease, even in patients
without diabetes.[3] [11]
physical inactivity
Physical inactivity is responsible for 12.2% of the global burden of MI after accounting for other
cardiovascular disease risk factors such as cigarette smoking, diabetes mellitus, hypertension,
abdominal obesity, lipid profile, alcohol intake, and psychosocial factors.[3]
dyslipidaemia
Elevated LDL-cholesterol, elevated triglycerides, decreased HDL, and elevated ratio of LDL to HDL are
all independently associated with increased risk of atherosclerosis.
Early studies on cholesterol showed that a reduction in serum cholesterol by diet and medications
reduces non-fatal MI by 25% and fatal MI by 14%.[10]
Current guidelines recommend high-dose statin therapy in patients with known coronary artery
disease (CAD) or CAD equivalent, irrespective of LDL levels.[12] Other lipid-lowering treatments can
be considered in patients who are contraindicated or intolerant of statins.
renal insufficiency
Renal dysfunction is a marker of vascular damage.[13]
Excess cardiovascular disease in patients with chronic kidney disease is caused, at least in part, by
higher prevalence of traditional risk factors in this group.[3]
established coronary artery disease

18% of coronary events are in patients with preceding long-standing angina pectoris.[3]
family history of premature coronary artery disease

Onset affecting first-degree male family member aged <55 years or female family member <65
years.[3]
cocaine use
Regular use of cocaine predisposes young people (aged 18-45 years) to MI.
5
The risk is increased by 24 times over baseline 1 hour following cocaine use, and chronic exposure
appears to accelerate atherosclerosis.[14]
male sex
THEORY
STEMI is more common in men than in women.[4]
age >50 years

STEMI most commonly occurs in people aged 50 to 79 years. STEMI patients are often younger than
non-STEMI (NSTEMI) patients, with a median age of 65 years old for STEMI and 71 years old for
NSTEMI.[5]
MI tends to occur at a younger age in men than in women, with a median age difference of 8 years for
all heart attacks (66 years vs. 74 years) and 9 years for STEMI (63 years vs. 72 years).[5]
Aetiology
MI is usually a consequence of coronary artery disease. Atherosclerosis with plaque fissuring or rupture and
thrombus formation is the underlying aetiology for STEMI in most patients. A small proportion of patients
present with STEMI caused by coronary spasm reducing myocardial perfusion, coronary embolism, or
following chest trauma or spontaneous coronary or aortic dissection.
Pathophysiology
Atherosclerotic plaques form gradually over years.[7] They begin with the accumulation of low-density
lipoprotein cholesterol and saturated fat in the intima (the inner layer) of blood vessels. This is followed by the
adhesion of macrophages to endothelium, then diapedesis and entry into the intima, where they accumulate
lipids and become foam cells. Foam cells are a rich source of proinflammatory mediators. The lesion up to
this point is referred to as a fatty streak, and may be reversible to a certain extent.
Subsequent evolution involves migration of smooth muscle cells from the media, and their proliferation and
deposition of extracellular matrix, including proteoglycans, interstitial collagen, and elastin fibres.[7] Some of
the smooth muscle cells in advanced plaques exhibit apoptosis. Plaques often develop areas of calcification
as they evolve. The plaque initially evolves with the artery remodelling outwards, followed by encroachment
on the arterial lumen. Eventually the stenosis can limit flow under conditions of increased demand, causing
angina.
STEMI typically occurs after abrupt and catastrophic disruption of a cholesterol-laden plaque. This results
in exposure of substances that promote platelet activation and aggregation, thrombin generation, and
thrombus formation, causing interruption of blood flow. If the occlusion is severe and persistent, myocardial
cell necrosis follows.
On interruption of blood flow in the coronary artery, the zone of myocardium supplied by that vessel
immediately loses its ability to shorten and perform contractile work. Early hyperkinesis of the non-infarcted
zones occurs, probably as a result of acute compensatory mechanisms including increased sympathetic
activity and Frank-Starling mechanism. As necrotic myocytes slip past each other, the infarction zone thins
and elongates, especially in anterior infarction, leading to infarction expansion.
If a sufficient quantity of myocardium undergoes ischaemic injury, left ventricular (LV) systolic function
becomes depressed; cardiac output, stroke volume, blood pressure, and compliance are reduced; and end
systolic volume increases. Clinical heart failure occurs if 25% of myocardium has abnormal contraction, and
cardiogenic shock occurs on loss of >40% of LV myocardium. Decreased compliance and increased LV end
diastolic pressure give rise to diastolic dysfunction.
THEORY
Classification
Acute coronary syndrome (ACS)
Historically ACS has been divided into three clinical categories according to the presence or absence of ST-
segment elevation on a presenting ECG and on elevations of cardiac troponin T or I.[2] [3]
1. ST-elevation myocardial infarction (STEMI): ECG shows persistent ST-segment elevation in at least two
anatomically contiguous leads.
2. Non-STEMI (NSTEMI): ECG does not show ST-segment elevation, but cardiac biomarkers are elevated.
The ECG may show ischaemic changes such as ST-segment depression, T-wave inversion, or biphasic T
waves.
3. Unstable angina pectoris: non-specific ischaemic ECG changes, but cardiac biomarkers are within the
normal range.
Fourth Universal Definition of Myocardial Infarction[1]

In the contemporary setting MI can also be classified according to variations in pathological, clinical, and
prognostic factors, alongside the different management strategies recommended for each type.[1]
• Acute myocardial infarction (types 1, 2, and 3 MI)
• Defined as acute myocardial injury with clinical evidence of acute myocardial ischaemia and
with detection of a rise and/or fall of cardiac troponin values with at least one value >99th
percentile of the upper reference limit (URL)
• A type 1 MI is characterised by identification of a coronary thrombus by angiography (or
autopsy)
• Includes STEMI and NSTEMI

• In type 2 MI there is evidence of an imbalance between myocardial oxygen supply and demand
that is not associated with an acute atherothrombotic event
• Includes vasospasm, coronary microvascular dysfunction, and non-atherosclerotic

coronary dissection
• A type 3 MI is cardiac death in a patient with symptoms of myocardial ischaemia and new
ischaemic ECG changes prior to a cardiac troponin level becoming abnormal or available
• Coronary procedure-related MI (types 4 and 5 MI)
• Type 4a MI – related to percutaneous coronary intervention

• Type 4b MI – related to stent thrombosis
• Type 4c MI – related to stent restenosis
7
• Type 5 MI – related to coronary artery bypass graft surgery
Case history
THEORY
Case history #1
A 54-year-old man with a medical history of hypertension, diabetes, dyslipidaemia, smoking, and family
history of premature coronary artery disease presents with retrosternal crushing chest pain (10/10 in
intensity), radiating down the left arm and left side of the neck. He feels nauseated and light-headed and
is short of breath. Examination reveals hypotension, diaphoresis, and considerable discomfort with diffuse
bilateral crackles on chest auscultation. ECG reveals convex ST-segment elevation in leads V1 to V6.
Case history #2
A 70-year-old woman is 2 days post-operative for knee replacement surgery. Her past medical history
includes type 2 diabetes and a 40 pack-year history of smoking. She reports feeling suddenly unwell with
dizziness, nausea, and vomiting. She denies any chest pain. On examination she is hypotensive and
diaphoretic. ECG shows convex ST-segment elevation in leads II, III, and aVF with reciprocal ST segment
depression and T-wave inversion in leads I and aVL.
Other presentations
Patients with STEMI may also be asymptomatic or present with atypical chest pain or epigastric pain.
ST-elevation myocardial infarction Diagnosis
Recommendations
Urgent
Assessment and diagnosis of STEMI is a time-critical process . The shortest possible delay from
symptom onset to coronary reperfusion maximises the patient’s chances of survival and recovery.[1]
[4] [10] [20] [21] [22] [23]
Obtain an ECG immediately and certainly no more than 10 minutes from the point of first
medical contact .[4] [24] [25]
Establish the patient’s haemodynamic status and specifically look for any signs of cardiogenic
shock .
• Cardiogenic shock complicates 6% to 10% of STEMI admissions . Look for persistent

hypotension ( systolic blood pressure <90 mmHg ) and/or any signs of end-organ
hypoperfusion or fulminant heart failure.[4] [26] [27]
Give all patients with suspected acute coronary syndrome a single loading dose of aspirin as soon
as possible , unless they have aspirin hypersensitivity.[23]
• Check your local protocol or discuss the patient with a senior colleague if they have hypersensitivity
to aspirin.
Make a clinical diagnosis of STEMI based on a combination of ST-segment elevation in at
least two contiguous ECG leads together with presenting symptoms suggestive of myocardial
ischaemia (e.g., chest pain).[4]
As soon as a clinical diagnosis of STEMI is made, make an immediate assessment of

eligibility for coronary reperfusion therapy (irrespective of age, ethnicity, sex, or level of
consciousness) and seek input from the interventional cardiology team . Primary percutaneous
coronary intervention is the preferred reperfusion strategy for any eligible patient who presents within
12 hours of symptom onset provided it can be delivered within 120 minutes of the time when fibrinolysis
could have been given.[23] [28]
DIAGNOSIS
Key Recommendations
Presentation
Patients typically present with central chest pain that is heavy in nature, like a sensation of pressure
or squeezing . It may radiate to the left arm, neck, or jaw and can be associated with nausea,
vomiting, dyspnoea, lightheadedness, palpitations, or syncope .[1] [4] [29]
• Beware atypical symptoms , particularly in older patients, women, and patients with
diabetes.[29]
Focus your history on:[4] [10] [22]
• Characteristics of symptoms of myocardial ischaemia (including time since symptom onset

, which will inform the most appropriate reperfusion strategy)
• Previous cardiac history
• Evidence of cardiac risk factors.
Examination is variable, and findings range from normal to a critically unwell patient in
cardiogenic shock. Your priorities from examination and history-taking are to:[4] [10] [23] [29]
9
• Confirm a STEMI diagnosis

• Rule out alternative diagnoses/causes of ST-segment elevation
• Establish the patient’s haemodynamic status
• Look for complications of acute MI.
Always consider right ventricular involvement when there is a triad of hypotension, elevated
jugular venous pressure, and clear lung fields .[4] [30]
Clinical diagnosis
In a patient who has chest pain or other ischaemic symptoms, make a clinical diagnosis of
STEMI when there is new (or increased) and persistent ST-segment elevation in at least two
contiguous leads of ≥1 mm in all leads other than leads V2-V3 where the following cut-off
points apply :[1]

• ≥1.5 mm in women regardless of age
• 1 mm = 1 small square (at a standard ECG calibration of 10 mm/mV)

• Contiguous ECG leads lie next to each other anatomically and indicate a specific myocardial
territory.
Think posterior STEMI when there is deep ST-segment depression in leads V1-V3.[1] [4]
Consider complete left main coronary artery obstruction if the following are both present,
especially if the patient has haemodynamic compromise:[4] [31]
• ST depression ≥1 mm in ≥6 surface leads (i.e., inferolateral ST depression)

• ST elevation in aVR or lead V1.
ECG diagnosis of STEMI is problematic in the presence of left bundle branch block (LBBB).
• One of the best indicators is concordant ST-segment elevation (i.e., in leads with positive QRS
deflections).[4] [32] The Sgarbossa criteria can also be helpful.[1] [33]
• New LBBB does not on its own indicate a STEMI.[4] [34]
DIAGNOSIS
• If there is old LBBB but with a high index of suspicion for ongoing myocardial ischaemia, manage
the patient as per the standard STEMI protocol.[4]
Cardiac biomarkers
Although STEMI can usually be diagnosed by ECG alone, a rise in cardiac-specific troponins
definitively confirms the diagnosis.[1] [4] [29] [35] [36] [37]
• However, do not delay coronary reperfusion to wait for cardiac biomarker laboratory
results (or any other blood results).
• Start treatment and assess eligibility for coronary reperfusion immediately a clinical diagnosis has
been made based on ECG changes in a patient with symptoms/signs of myocardial ischaemia.
Full Recommendations
Diagnostic criteria
Practical diagnosis of STEMI

Assessment, diagnosis, and management of acute STEMI is a time-critical process. [4] [1] [10]
[22] [23]
• Always remember the guiding principle that 'time is muscle' – the shortest possible delay from
symptom onset to coronary reperfusion is vital to protect the myocardium from ischaemic
damage and maximise the patient’s chances of survival.[20] [21]
• For a patient diagnosed with STEMI, nearly half of potentially salvageable myocardium is lost within
1 hour of the coronary artery occlusion and two-thirds is lost within 3 hours.[38]
Make a clinical diagnosis of STEMI and start immediate treatment if the patient meets BOTH
of the following criteria: [4]
1. ST-segment elevation in at least two contiguous leads on a 12-lead ECG of ≥1 mm in all

leads other than leads V2-V3 where the following cut-off points apply :[1]

• ≥1.5 mm in women regardless of age.
2. Persistent typical central chest pain or other symptoms consistent with myocardial
ischaemia.
As soon as a clinical diagnosis is made, immediately assess eligibility for coronary
reperfusion therapy. [4] [23]
• Do not wait for a definitive diagnosis from cardiac troponin levels as coronary reperfusion is a
time-critical intervention.[1] [4]
• Primary percutaneous coronary intervention (PCI) is the preferred reperfusion strategy
for any eligible patient who presents within 12 hours of symptom onset provided it can be
delivered within 120 minutes of the time when fibrinolysis could have been given .[23]
[28] Start medical treatment and refer immediately to the interventional cardiology team.[4] [20] [21]
[23]
• Give fibrinolysis (unless contraindicated) if primary PCI cannot be delivered within 120
minutes of the time when fibrinolysis could be started. [23] [28]
DIAGNOSIS
• Fibrinolysis can be administered as part of the pre-hospital management of STEMI.[20]
[21]
Formal diagnostic criteria for STEMI

A definitive diagnosis of STEMI requires evidence of a rise in cardiac troponin levels – but
do not wait for this to be confirmed before starting treatment. [1]
• Evidence of myocardial injury (via acutely elevated cardiac troponin levels) is required for a
definitive confirmation of the diagnosis of STEMI.[1] [4] [29]
• However, do not wait for troponin results before proceeding to coronary reperfusion ,
which is a time-critical intervention that must be started as soon as a clinical diagnosis is made.[4]
[23]
STEMI is classified as a type 1 MI under the Fourth Universal Definition of Myocardial
Infarction. [1]
• Type 1 MIs are caused by ischaemia due to rupture or erosion of an atherosclerotic plaque
leading to partial, or in the case of STEMI total, intraluminal occlusion of the coronary artery
.[1] [29]
11
Under the Fourth Universal Definition, an acute type 1 MI is definitively diagnosed based on a
rise and/or fall of cardiac troponin levels, with at least one value above the 99th percentile of
the upper reference limit in a patient who also has at least one of the following :[1] [29]
• Symptoms of acute myocardial ischaemia

• ECG changes indicative of new ischaemia
• Development of pathological Q waves in the ECG
• A new regional left ventricular wall motion abnormality consistent with a coronary artery territory
(e.g., on transthoracic echocardiography)
• New loss of viable myocardium (e.g., on cardiac magnetic resonance imaging)
• Presence of intracoronary thrombus found on coronary angiography.
The presenting ECG is central to determining whether a type 1 MI is a STEMI or a non-ST-
elevation MI (NSTEMI). [1]
Clinical presentation
Patients typically present with central chest pain: [1] [4] [29]
• Classically retrosternal, crushing, heavy, severe, and diffuse in nature

• Might be described by the patient as 'pressing or squeezing'
• May occur at rest or on activity
• May be constant or intermittent, or wax and wane in intensity
• Sometimes radiating to the left arm, neck, or jaw .
The chest pain may be associated with nausea, vomiting, dyspnoea, diaphoresis,
lightheadedness, palpitations, or syncope. [4] [29]
• Dyspnoea is a common feature secondary to pulmonary congestion from left ventricular

systolic dysfunction. It can also occur due to other mechanical and electrical complications
of acute MI, which occur less commonly in the context of contemporary rapid revascularisation, for
example:
• Left ventricular aneurysm

• Ventricular septal rupture
DIAGNOSIS
• Left ventricular free wall rupture

• Acute mitral regurgitation – papillary muscle rupture/functional (ischaemic) mitral
regurgitation
• Pericardial effusion
• Cardiac tamponade
• Supraventricular tachyarrhythmias
• Ventricular tachyarrhythmias
• Bradycardia and atrioventricular block.
• Nausea and vomiting are common features.
• These are non-specific symptoms but are commonly associated with inferior-wall STEMI due
to increased vagal tone.
• May be the only indicator of inferior-wall STEMI.
• Patients sometimes report anxiety and/or an impending sense of doom .
• Some patients present with palpitations. [4]
• Tachycardia
• Supraventricular tachyarrhythmias such as atrial fibrillation

• Ventricular tachyarrhythmias such as ventricular tachycardia
• Bradycardia
• Sinus bradycardia
• Atrioventricular block secondary to inferior STEMI
• Atrioventricular block secondary to anterior STEMI
• Irregular heart beat

• Ventricular extrasystoles
Be aware of patient groups who are more likely to present atypically. [29]
• Women, older patients, and patients with diabetes are more likely to present with atypical
features.[4] [10] [22] [39]
• Atypical chest pain might be described by the patient as burning, throbbing, tight, or a
feeling like trapped wind .
• The patient may describe indigestion rather than chest pain.

• In the absence of chest pain, there may be epigastric pain, back (interscapular) pain, neck
or jaw pain, or arm pain (typically left-sided).
• Patients may present with breathlessness, sweating, palpitations, dizziness, nausea, or
vomiting but no chest pain .
• Clinical suspicion is key to making the diagnosis. It is, therefore, vital to make a full assessment
based on the history, examination, and serial ECGs.[1] [36] [37]
Practical tip
Do not rely on a positive patient response to glyceryl trinitrate as a reliable diagnostic

indicator of ischaemic chest pain. [4] [29] [40]
• Response to nitrates can be misleading. Patients who get symptom relief still need confirmatory
ECG testing to inform the diagnosis.
DIAGNOSIS
• Complete normalisation of ST-segment elevation along with resolution of chest pain after buccal
or sublingual nitrates suggests coronary vasospasm (with or without associated MI).[4]
Patients with STEMI may be asymptomatic – this is known as a silent STEMI. [1]
• STEMI is rarely truly asymptomatic but some patients have only mild, non-specific symptoms
that can lead to a delay in presenting or to the STEMI going undiagnosed.
• In practice, a patient who has a 'silent' STEMI may present to their primary care doctor a few days
after the episode of non-specific symptoms, at which point evidence of ST-segment elevation might
still be present on the ECG. Seek advice from the cardiology team for such patients.
History
Your history should cover the following. [41] [42] [43]
• Characteristics of symptoms ; in particular, chest pain:[29]
• “Have you ever had this type of pain before?”
13
• Nature, severity, and duration of pain

• Radiation
• Associated symptoms
• “Do you normally have chest pain when you exert yourself? If so, is it similar in quality to the
chest pain experienced when you don’t?”
• Time since symptom onset – this is crucial to inform the appropriate reperfusion strategy.[4] [22]
[23]
• If symptoms are intermittent, it is important to ask when the last episode of pain occurred.[29]
• Any history of cardiovascular disease ; in particular, ischaemic heart disease .[29]
• Also check for any previous episodes of investigation or treatment for chest pain.
• Cardiovascular risk factor profile: [29]
• Smoking status
• Hypertension
• Diabetes mellitus
• Hypercholesterolaemia
• Family history of premature coronary artery disease (<60 years)
• Established coronary artery disease
• Advanced age
• Obesity
• Metabolic syndrome
• Physical inactivity
• Chronic kidney disease
• Cocaine use
• Male sex (although there is a similar risk in post-menopausal women and men of the same
age group)
• Existing peripheral vascular disease or cerebrovascular disease.
DIAGNOSIS
• Medication history:
• Will help to consolidate the risk factor profile assessment, especially if the history given by
the patient is limited or vague
• Record any use of chronic oral anticoagulation – this will influence what type of
arterial access can be used if the patient proceeds to coronary angiography or primary
percutaneous coronary intervention (PCI).
Practical tip
The choice of coronary reperfusion strategy depends on time since symptom onset –
but obtaining an exact time for this can be difficult.
• Patients can often give only an approximate idea of when their symptoms began.
• Patients sometimes ignore chest pain (or associated symptoms) until they can no longer tolerate
it.
• The reliability of the assessment of time since symptom onset is determined by a combination of
the patient’s ability to give an accurate history and the experience and skill of the clinician taking
the history.
• If you question the patient carefully, they may describe warning signs, or less severe or less
long-lasting symptom episodes preceding the more severe episode that has prompted them to
seek medical help.
The time between symptom onset and first medical contact is referred to as the 'patient delay'
component of the 'total ischaemic time'.#
• The total ischaemic time continues until coronary reperfusion with either primary PCI or fibrinolysis.
• If the patient contacts medical services in the community, then the total ischaemic time = Patient
Delay + Emergency Medical Services Delay + System Delay.
• If the patient presents directly to a hospital (PCI-capable or non-PCI-capable), then the total
ischaemic time = Patient Delay + System Delay.
Physical examination
The clinical picture of acute MI varies from asymptomatic through to fulminant acute heart
failure and cardiogenic shock.
• Your priorities are to establish the following as quickly as possible :[29]
• Confirm the STEMI diagnosis

• Rule out alternative diagnoses/causes of ST-segment elevation (see Important
differentials to consider below)
• Establish the patient’s haemodynamic status – seek immediate senior support and
specialist input if there are any signs of cardiogenic shock (see Cardiogenic shock below)
• Look for complications of acute MI (see Acute MI complications sections below).
• Your examination should check :[29]
• Blood pressure, heart rate, and heart rhythm

• Consciousness level (e.g., Glasgow Coma Scale, AVPU [alert, verbal, pain, unresponsive]
scale)
• However, do not use the level of consciousness after cardiac arrest caused by
DIAGNOSIS
suspected acute STEMI to determine whether the patient is eligible for coronary
angiography ± primary percutaneous coronary intervention (PCI)[23]
• Airway patency
• Ox ygen saturations
• For radio-radial and radio-femoral delay
• Jugular venous pressure (JVP) – a raised JVP could indicate:
• Congestive cardiac failure

• Right ventricular involvement after an inferior or extensive anterior STEMI
• Underlying (chronic) lung disease
• Large pericardial effusion or cardiac tamponade
• Pulmonary embolism (which can also give rise to ST-segment elevation).
Look for pallor, cool/clammy to touch skin, and any signs of peripheral shutdown.
• These are common presenting features due to high sympathetic output resulting in peripheral
vasoconstriction.
Auscultate the heart and lungs.
15
• Muffled heart sounds could suggest a pericardial effusion or even cardiac tamponade.
• Is there a third (S3) or fourth (S4) heart sound ?
• These added heart sounds could suggest severe heart failure.

• A murmur might suggest:
• Acute ventricular septal defect

• Acute mitral regurgitation
• Underlying chronic valvular heart disease.
• Crackles/crepitations or cardiac wheeze would suggest congestive cardiac failure ±
pulmonary oedema.
• Is the patient coughing up pink frothy sputum ?
• This would suggest congestive cardiac failure ± pulmonary oedema.
Check for peripheral oedema and hepatomegaly.
Document the Killip class. This classifies degree of heart failure after acute MI and predicts
30-day mortality: [43]
• Killip class I = no signs of heart failure/pulmonary congestion

• Killip class II = S3 and basal crackles/crepitations
• Killip class III = acute pulmonary oedema
• Killip class IV = cardiogenic shock.
Evidence: Killip class and prognosis
Risk of death is strongly correlated to Killip class.
• The original paper on the impact of Killip class on prognosis dates from 1967 , when it was
reported that the associated in-hospital mortality rates were 6% for class I, 17% for class II,
38% for class III, and 81% for class IV.[44]
• With advances in treatment, particularly the introduction of coronary reperfusion therapy,
mortality rates have fallen by 30% to 50% in each Killip class . In the GUSTO
international trial of 41,021 patients, after adjustment for all other factors, the OR associated
DIAGNOSIS
with Killip class III versus I for an average-age patient was 4.37 (95% CI, 3.34 to 5.71), whereas
the OR for Killip class IV versus I was 7.86 (95% CI, 5.88 to 10.49).[43]
Cardiogenic shock
Cardiogenic shock complicates 6% to 10% of STEMI admissions. [4] [45]
• In-hospital mortality remains high (≥50%.)

• There is a bimodal presentation: the majority occur within 24 hours; the remainder occur within the
first week.[46]
Seek immediate senior support and specialist input if your clinical assessment suggests
cardiogenic shock.
See our topic Shock .
Patients present with signs of hypoperfusion and/or fulminant heart failure, such as :
• Altered mental status/reduced consciousness

• Tachypnoea
• Severe dyspnoea
• Tachycardia
• Orthopnoea
• Cool peripheries
• Grey, ashen, pale appearance.
Cardiogenic shock is defined as persistent hypotension (systolic blood pressure [SBP] <90
mmHg) together with signs of end-organ hypoperfusion. [4] [26] [27]
• Clinical criteria:[26]
• SBP <90 mmHg despite adequate volume replacement, or if inotropes and/or mechanical
circulatory support are needed to maintain SBP ≥90 mmHg
• Urine output <30 mL/hour
• Cool extremities.
• Haemodynamic criteria:[26]
• 2
Cardiac index ≤2.2 L/minute/m
• Wedge pressure ≥15 mmHg.
• Cardiogenic shock results from extensive left ventricular infarction and/or mechanical
complications such as :
• Papillary muscle rupture

• Left ventricular free wall rupture leading to pericardial tamponade
• Right ventricular infarction.
Important differentials to consider

Always consider alternative diagnoses that might explain the presenting symptoms and/or
ST elevation on ECG, including :[29]
• Aortic dissection (ST elevation can be present on the ECG)
DIAGNOSIS
• Pulmonary embolism (ST elevation or ST depression can be present on the ECG)
• Pericarditis (ST elevation can be present on the ECG)
• Myocarditis (ST elevation can be present on the ECG)
• Pneumothorax
• Pneumonia
• Intracranial pathology (e.g., subarachnoid haemorrhage)
• Gastro-oesophageal reflux disease
• Oesophageal spasm
• Costochondritis
• Anxiety or panic.
Be aware of spontaneous coronary artery dissection (SCAD), especially in younger women
presenting with ST-segment elevation and chest pain.
• SCAD is defined as an epicardial coronary artery dissection that is not associated with
atherosclerosis or trauma and is not iatrogenic.[47]
• The left anterior descending artery is the most commonly affected artery.[47] [48] [49] [50]
[51] [52] [53]
17
• It can lead to coronary artery obstruction secondary to intramural haematoma or intimal
disruption (in contrast to the atherosclerotic plaque rupture or intraluminal thrombus seen
with STEMI).
• Patients almost always present with an acute coronary syndrome causing chest pain and
elevation in cardiac enzymes .[47]
• A minority can present in cardiogenic shock (2% to 5%).[48] [49]

• Consider the possibility of SCAD in any young patient (especially female) who
presents with an acute MI and who has no history of or risk factors for cardiovascular
disease. [47]
• SCAD occurs predominantly in women (average age 45-53 years) and may account for
up to 35% of MI presentations seen in women ≤50 years old [47] [49] [53] [54] and up
to 43% of pregnancy-associated MIs.[47] [55]
• Patients tend to have few or no conventional cardiac risk factors .[47]
• SCAD is an important cause of ST-segment deviation on the ECG , with different patient
series reporting that:[47] [48] [49] [50] [51] [52]
• 26% to 87% of patients with SCAD present with STEMI

• 13% to 69% present with NSTEMI .
• If SCAD is suspected, coronary angiography should be performed as soon as possible to
confirm the diagnosis.[47]
• There is a paucity of evidence available to guide management decisions once SCAD is confirmed
on angiography. The most appropriate approach depends on individual patient characteristics.
• Conservative management with close ongoing monitoring is preferred for most

patients who are clinically stable , as observational data suggest the SCAD lesion will
usually heal.[47]
• Urgent intervention with PCI or coronary artery bypass grafting should be considered
for high-risk patients (e.g., ongoing ischaemia, haemodynamic instability, left main artery
dissection).
Practical tip
DIAGNOSIS
Takotsubo cardiomyopathy syndrome can mimic MI and has similar mortality to STEMI/
NSTEMI. [1]
• It is triggered by a wide spectrum of physical and emotional triggers and is also referred
to in the literature as broken heart syndrome, apical ballooning cardiomyopathy, or stress
cardiomyopathy.[56] [57] [58]
• 'Takotsubo' comes from the Japanese word for octopus trap.

• Takotsubo cardiomyopathy is characterised by a temporary left ventricular wall motion
abnormality associated with signs and symptoms of acute coronary syndrome, [57]
[58] for example:
• Chest pain
• ST-segment deviation on ECG
• Raised cardiac biomarkers such as troponin (although the peak value is often modest).[1]
• In-hospital mortality is similar to STEMI and NSTEMI.[1]
• It is estimated to represent 1% to 3% of all patients and 5% to 6% of female patients who
present with suspected STEMI .[57] Over 90% of affected patients are post-menopausal
women.[1]
Patients may present with ST-segment elevation on their ECG. [57] [58]
• ST-segment elevation is present in over 40% of patients but the extent of the elevation is usually
widespread across the lateral and precordial leads , beyond that of a single coronary
artery distribution.[1]
Suspect takotsubo cardiomyopathy if the clinical manifestations and ECG
abnormalities are out of proportion to the degree of elevation of cardiac biomarkers; [1]
echocardiography findings may include hyperdynamic basal segments with apical ballooning.
• Manage the patient as for STEMI in the first instance if there are signs and symptoms
consistent with myocardial ischaemia.
• Refer for urgent coronary angiography and left ventriculography to confirm or exclude
takotsubo cardiomyopathy.
• If there are coronary culprit lesions on angiography that correspond to the regional wall
motion abnormalities, the patient is treated the same as for an acute coronary syndrome.
• If there are no coronary culprit lesions that correspond to the regional wall motion
abnormalities and acute infectious myocarditis can be ruled out, the patient is treated as a
takotsubo cardiomyopathy.
Co-existing coronary artery disease does not exclude the diagnosis.

• It is present in 10% to 29% of patients with takotsubo cardiomyopathy.[57] [58] [59] [60] [61]
Investigations
ECG interpretation for STEMI

Perform a 12-lead ECG within 10 minutes of first medical contact in any patient who presents
with chest pain and/or other signs of possible STEMI. [1] [4]
• If the patient presents in the community, obtain a pre-hospital ECG and send it digitally to the
receiving hospital as quickly as possible.[4] [29]
• If the ECG is equivocal despite a high clinical suspicion of acute MI, perform serial ECGs in the
appropriate hospital setting and compare these with historical ECGs, if available.[1] [4] [29]
In the appropriate clinical context (chest pain or other symptoms of ischaemia), make
DIAGNOSIS
a clinical diagnosis of STEMI if there is new (or increased) and persistent ST-segment
elevation in two or more contiguous leads of ≥1 mm in all leads other than leads V2-V3 where
the following cut points apply: [1]

• 1 mm = 1 small square (at a standard ECG calibration of 10 mm/mV).
Make the diagnosis when these criteria are met in the absence of left ventricular hypertrophy, left
bundle branch block (LBBB), or a paced rhythm on the ECG .
• Severe cases of left ventricular hypertrophy can appear identical to LBBB.

• A paced rhythm can appear identical to LBBB.
• Note that the presence of left ventricular hypertrophy, LBBB, or a paced rhythm does
not preclude a diagnosis of STEMI if the patient presents with typical symptoms of myocardial
ischaemia.
• See Less common ECG presentations below for more on diagnosis of STEMI in the presence of
LBBB.
Consult a cardiology specialist immediately if the ECG changes are equivocal.
19
• An urgent transthoracic echocardiogram to look for regional wall motion abnormalities is indicated.
Practical tip
Measure ST-segment elevation from the J point. [1] [4]
Identifying the J point on the ECG

Created by the BMJ Knowledge Centre
Practical tip
Contiguous leads lie next to each other anatomically and indicate a specific myocardial
territory.
DIAGNOSIS
12-lead ECG placement

Created by Npatchett (own work) [CC BY-SA 4.0], via Wikimedia Commons
DIAGNOSIS
Coronary anatomy and ECG leads

21
Coronary anatomy and ECG leads table

Less common ECG presentations
Posterior STEMI [1] [4]

• Consider this when there is ST-segment depression in leads V1-V3 along with characteristic
signs and symptoms of myocardial ischaemia.
• Confirm with posterior lead ECG : ST-segment elevation ≥0.5 mm in V7-V9.
Right ventricular infarction [1] [4] [30]

DIAGNOSIS
• Can complicate an inferior STEMI.

• Check right precordial leads (V3R and V4R).
• Look for ST elevation ≥1 mm in aVR and V1 .
• Confirmation will have an impact on choice of therapeutic intervention.
Left main coronary obstruction [4] [31]

• Consider complete left main coronary artery obstruction if the following are both present,
especially if the patient has haemodynamic compromise:
• ST depression ≥1 mm in ≥6 surface leads (i.e., inferolateral ST depression)

STEMI in the presence of LBBB [33] [62]

ECG diagnosis of STEMI is problematic in the presence of LBBB. [4]
• It is often possible to make the diagnosis if marked ST-segment abnormalities are present.[4]
• The presence of concordant ST-segment elevation (i.e., in leads with positive QRS
deflections) is one of the best indicators of total coronary occlusion and ongoing MI in the
context of a patient with concomitant LBBB.[32]
• Manage any patient with LBBB and clinical suspicion of ongoing myocardial
ischaemia in a similar way to STEMI , regardless of whether or not the LBBB was previously
known.[4]
• Presumed new LBBB alone does not indicate the presence of a STEMI.[34]
• If in doubt, seek immediate input from the cardiology team .
More info: Sgarbossa criteria for diagnosis of MI in the presence of LBBB
Consider using the Sgarbossa criteria to improve the diagnostic accuracy for STEMI in patients who
have LBBB at presentation.
Original criteria [1] [33]
• ST elevation of ≥1 mm, concordant with the QRS complex: 5 points .

• ST depression ≥1 mm in leads V1, V2, or V3: 3 points .
• This has a sensitivity of 19% and a specificity of 81% to diagnose acute MI.[63]
• ST elevation ≥5 mm, discordant with the QRS complex: 2 points .
• This has a sensitivity of 10% and a specificity of 99% to diagnose acute MI.[63]
• An aggregated score of 3+ is 90% specific for MI but only 36% sensitive.
Components of the Sgarbossa criteria have high specificity but low sensitivity so are
useful to confirm acute MI but less useful to rule it out. [64]
• The low sensitivity means you must maintain a high index of suspicion if the
presentation is consistent with MI regardless of the criteria score .
• 'Weighted' Sgarbossa criteria rely on the points system; however, only two of the criteria carry a
score ≥3 to make the diagnosis of acute MI.[65]
• 'Unweighted' Sgarbossa criteria are applied without the points system – this is more sensitive
but less specific.[65]
• The criteria were originally based on the outcome of acute MI as measured by creatine kinase-
MB rather than angiographic evidence of acute coronary occlusion – further reducing sensitivity
DIAGNOSIS
because the criteria encompass both STEMI and NSTEMI.[65]
23
Sgarbossa criteria for MI in the presence of LBBB

The modified Sgarbossa criteria have bet ter sensitivity but worse specificity for STEMI.
[65] [66]
• The original rule for >5 mm discordance is replaced with a proportionately excessive
discordance: ST-elevation/S-wave amplitude ≤-0.25.
DIAGNOSIS
• The modified criteria were found to be more sensitive versus the 'weighted' (80% vs. 49%; P
<0.001) and 'unweighted' (80% vs. 56%; P <0.001) Sgarbossa criteria.[65]
• Modified criteria specificity is not significantly different from the 'weighted' criteria.[65]
• Modified criteria specificity is significantly greater than the 'unweighted' original
criteria.[65]
ST/S ratio under the modified Sgarbossa criteria

Previous silent/unrecognised STEMI

Be aware of the possibility that abnormal ECG features might be due to a previous silent/
DIAGNOSIS
unrecognised STEMI. [1]
• Residual ST elevation on the ECG from an old STEMI may be detected either incidentally in
an asymptomatic patient who is having an ECG for another reason, or occasionally in a patient
with symptoms of ischaemia who is experiencing a non-ST-elevation MI (NSTEMI) against the
background of a previous history of STEMI.
• In such cases, there may be ST-segment elevation on the current ECG that was already
present on old ECGs (e.g., in the case of left ventricular aneurysm formation). It is important to
distinguish this from new ST elevation as management will differ.
• The historical STEMI may have been 'silent' and gone unrecognised at the time. The
resulting old ECG features will usually be fixed .
• It is helpful to take a thorough history, together with diligent ECG interpretation and comparison with
old ECGs (plus medical records) if available.
• Seek specialist input from the cardiology team.
The following criteria for previous (or silent/unrecognised) MI can be helpful. There may be
:[1]
• Pathological Q waves with or without symptoms, in the absence of non-ischaemic causes[1]
25
• Loss of viable myocardium in a pat tern consistent with a coronary artery territory
(regional wall abnormality) seen on cardiac imaging :
• Echocardiography
• Myocardial perfusion scintigraphy (MPS)
• Positron emission tomography (PET)
• Cardiac magnetic resonance imaging
• Pathological findings of a healed or healing MI on cardiac imaging.
Practical tip
A Q wave is defined as any negative deflection preceding an R wave in the QRS complex.
• A Q wave represents the normal left-to-right depolarisation across the interventricular septum.
• Small Q waves tend to be normal in most leads (e.g., left-sided leads such as I, aVL, V5, and
V6).
• More pronounced Q waves (>2 mm deep) may be seen in lead III or aVR as a normal variant.
• Q waves are not usually seen in the right-sided leads (V1-V3).
• Pathological Q waves can be a sign of previous MI. The precise definition of pathological Q
waves has been debated. The 2018 Fourth Universal Definition of MI defines them as follows:[1]
• Any Q wave in leads V2-V3 >20 milliseconds (0.02 seconds) or any QS complex in leads
V2 and V3
• Q wave ≥30 milliseconds (0.03 seconds) and ≥1 mm deep or QS complex in leads I, II,
aVL, aVF, or V4-V6 in any two leads of a contiguous lead grouping (I, aVL; V1-V6; II, III,
aVF)
• R wave >40 milliseconds (0.04 seconds) in V1-V2 and R/S >1 with a concordant positive
T wave in the absence of a conduction defect.
ECG examples
Anterior STEMI
DIAGNOSIS
Anterior STEMI
From the personal collection of Dr Aung Myat (used with permission)
Key learning points
• Tombstone’ ST elevation in anterior chest leads V1-V6 = anterior STEMI (red arrows)
• Reciprocal inferior ST-segment depression in II, III, and aVF (blue arrows)
• This is a high-risk ECG
Anterolateral STEMI example I
Anterolateral STEMI example I

Key learning points
• ‘Tombstone’ ST elevation in leads V2-V6, I, and aVL = anterolateral STEMI (red arrows)
High lateral STEMI
High lateral STEMI
DIAGNOSIS
Key learning points
• ST-segment elevation in high lateral chest leads I and aVL = high lateral STEMI (red arrows)
• Reciprocal inferior ST-segment depression in leads III and aVF (blue arrows)
• There is also saddle-shaped ST-segment elevation in lead II (green arrow) – difficult to state the
significance of this
27
Inferoposterior STEMI example II
Inferoposterior STEMI example II
Key learning points
• Note the deep ST-segment depression and R:S wave ratio of >1 in V1-V3 = posterior STEMI (blue
arrows)
• ST-segment elevation in leads II, III, and aVF = inferior STEMI (red arrows)
• Reciprocal ST-segment depression in the lateral leads I and aVL (yellow arrows)
• Consider performing a posterior lead ECG (leads V7-V9) for further confirmation of a posterior
STEMI
Inferoposterolateral STEMI example III

DIAGNOSIS
Inferoposterolateral STEMI example III

Key learning points
• Note the deep ST-segment depression and R:S wave ratio of >1 in V1-V2 = posterior STEMI (blue
arrows)
• ST-segment elevation in leads V3-V6 = lateral STEMI (green arrows)
• Reciprocal deep ST-segment depression in leads I and aVL (yellow arrows)
• The patient has marked sinus bradycardia – there can be several reasons for this but with this
degree of ischaemia on the ECG it suggests current or impending haemodynamic instability
More info: Library of ECGs with learning points
Anterolateral STEMI example II
Anterolateral STEMI example II

Key learning points
• ST elevation in leads V2-V5, I, and aVL = anterolateral STEMI (red arrows)

• Note there are no pathological Q waves in the anterior chest leads (V2-V6) – contrast with
Anterolateral STEMI example I)
Anteroseptal STEMI example I
DIAGNOSIS
Anteroseptal STEMI example I
Key learning points
• ST-segment elevation in leads V2-V5 = anteroseptal STEMI (red arrows)

• There are, however, no reciprocal ischaemic changes on the ECG
• Reciprocal ST-segment depression represents either true distant ischaemia as a by-product of a
collateral circulation or an electrical phenomenon arising from a mirror reflection of ST-segment
elevation elsewhere
• Take a careful history and examination with this ECG – the anteroseptal ST-segment elevation
may represent ‘high take-off’(or early benign repolarisation) rather than true myocardial
ischaemia
• If there are signs and symptoms of ongoing myocardial ischaemia then treat as a STEMI
Anteroseptal STEMI example II
29
Anteroseptal STEMI example II

Key learning points
• ST-segment elevation in leads V2-V5 = anteroseptal STEMI (red arrows)

• Reciprocal ST-segment depression in the inferior leads II, III, and aVF
• Compared with Anteroseptal STEMI example I: here the ST-segment elevation is less
pronounced but the reciprocal ST-segment depression inferiorly make this ECG more
compelling for an acute MI
• Again, take a careful history and examination looking for signs and symptoms of ongoing
myocardial ischaemia
Left bundle branch block example I
DIAGNOSIS
Left bundle branch block example I

Key learning points
• Left bundle branch block (LBBB) ECG criteria :
• QRS duration >120 milliseconds (i.e., greater than 3 small squares on the ECG)
• Monomorphic R wave in leads I, V5, and V6 – look for the characteristic ‘M-pattern’ shape
(notched R wave) to the QRS complex in leads V5 and V6
• Deep and broad S wave in leads V1-V2
• ST-segment depression and T-wave inversion in left-sided leads (V5, V6, I, and aVL)
• ST-segment elevation and positive T waves in V1-V3 (ST-segment elevation rarely
exceeds >5 mm – refer to Sgarbossa versus modified Sgarbossa criteria)
Left bundle branch block example II
Left bundle branch block example II

Key learning points
• LBBB ECG criteria:
(notched R wave) to the QRS complex in leads V5 and V6
• Deep and broad S wave in leads V1-V2 – more pronounced when compared with
example I
Left bundle branch block example III
Left bundle branch block example III DIAGNOSIS

Key learning points
• LBBB ECG criteria:
(notched R wave) to the QRS complex in leads V5 and V6, which are very pronounced
here
• Deep and broad S wave in leads V1-V2 – just as pronounced when compared with
example II
31
Inferoposterior STEMI example I
Inferoposterior STEMI example I

Key learning points
• Note the deep ST-segment depression and R:S wave ratio of >1 in V1-V4 = posterior STEMI
(blue arrows)
STEMI
Inferoposterolateral STEMI example I
DIAGNOSIS
Inferoposterolateral STEMI example I

Key learning points
(blue arrows)
• Also note the ST-segment elevation in leads V4-V6 (green arrows) – this could suggest lateral
involvement of the STEMI and/or represent occlusion of a very large dominant right coronary
artery with a posterior descending branch artery wrapping around the left ventricular apex
STEMI
Inferoposterolateral STEMI example II
Inferoposterolateral STEMI example II

Key learning points
(blue arrows)
• ST-segment elevation in leads V3-V6 = lateral STEMI (green arrows)
• Reciprocal deep ST-segment depression in leads I and aVL (yellow arrows)
• The patient has marked sinus bradycardia – there can be several reasons for this but with this
degree of ischaemia on the ECG it suggests current or impending haemodynamic instability
‘Possible’ inferolateral STEMI
DIAGNOSIS
Possible’ inferolateral STEMI
33
Possible’ inferolateral STEMI: ST-segment shift

Key learning points
• ST-segment elevation in the inferior leads II, III, and aVF and the lateral leads V5-V6 (red
arrows)
• The ST-segment shift, however, is more saddle-shaped (concave) rather than convex – see
second figure above
• A convex ST-segment elevation morphology is more likely to be associated with an acute
DIAGNOSIS
• There are no reciprocal ischaemic changes elsewhere on the ECG either
• Take a thorough history and examination looking for the signs of myocardial ischaemia and also
seek a specialist cardiology consult when managing a patient who presents with this ECG – it
can still be a STEMI
• Also consider acute pericarditis as a differential
Inferior STEMI example I
Inferior STEMI example I

Key learning points
• Subtle reciprocal ST-segment depression in the lateral leads I and aVL (blue arrows)
Inferior STEMI example II
Inferior STEMI example II

Key learning points
• Subtle ST-segment elevation in leads II, III, and aVF = inferior STEMI (red arrows)
• Deep reciprocal ST-segment depression in the lateral leads I and aVL (blue arrows)
• Take a thorough history and examination for signs and symptoms of myocardial ischaemia
Inferior STEMI example III
DIAGNOSIS
Inferior STEMI example III
Key learning points
• Pathological Q waves in leads II, III, and aVF (yellow arrows)
• Note the lack of reciprocal ST-segment changes in other leads
• These changes suggest a late-presentation inferior STEMI
• Consult the cardiology team to discuss management options once you have performed a
thorough history and examination
Paced rhythm example I
35
Paced rhythm example I

Key learning points
• There is a right bundle branch pattern here due to cardiac pacing
• Note the QRS is negative in lead I and positive in V1

• There is atrial pacing here with the pacing spike preceding the P wave
• There is ventricular pacing here also with the pacing spike preceding the QRS complex
• Right ventricular pacing = QRS morphology similar to left bundle branch block
• Left epicardial pacing = QRS morphology similar to right bundle branch block pattern
• We cannot diagnose a STEMI from a paced rhythm ECG but this does not mean an acute
MI can be excluded if a patient presents with the signs and symptoms of ongoing myocardial
ischaemia
Paced rhythm example II
DIAGNOSIS
Paced rhythm example II

Key learning points
• There is atrial pacing here with the pacing spike preceding the P wave
• There is ventricular pacing here with the pacing spike preceding the QRS complex
ischaemia
Paced rhythm example III
Paced rhythm example III

Key learning points
• There is a bundle branch pattern here due to cardiac pacing

• There is only ventricular pacing here with the pacing spike preceding the QRS complex
• Right ventricular pacing = QRS morphology similar to left bundle branch block – this is the case
on this ECG
ischaemia
Left ventricular hypertrophy example I
DIAGNOSIS
Left ventricular hypertrophy example I
Key learning points
• A STEMI cannot be diagnosed from the ECG on a background of left ventricular hypertrophy
(LVH)
• Numerous criteria for diagnosing LVH
• Sokolov-Lyon voltage criteria: S wave depth in V1 + tallest R wave height in V5 or V6 >35 mm
• Non-voltage criteria: ST-segment depression and T-wave inversion in left-sided leads I, aVL, V4-
V6 (blue arrows) – this is often referred to as a left heart strain pat tern
• Voltage and non-voltage criteria must be present to confirm an ECG diagnosis of LVH
Left ventricular hypertrophy example II
37
Left ventricular hypertrophy example II

Key learning points
• A STEMI cannot be diagnosed from the ECG on a background of left ventricular hypertrophy
(LVH)
• Sokolov-Lyon voltage criteria: S wave depth in V1 + tallest R wave height in V5 or V6 >35 mm
• Non-voltage criteria: ST-segment depression and T-wave inversion in left-sided leads I, aVL, V4-
V6 (blue arrows) – this is often referred to as a left heart strain pat tern
• Voltage and non-voltage criteria must be present to confirm an ECG diagnosis of LVH
• Also note this type of ECG may be a normal variant in athletes and people of African-Caribbean
heritage
DIAGNOSIS
Acute pericarditis
Acute pericarditis
Key learning points
• Global saddle-shaped (concave) ST-segment elevation (red arrows)

• Reciprocal ST depression (blue arrow) and PR depression (yellow arrow) in leads II and aVF
• Sinus tachycardia can also feature due to the increased sympathetic drive from pain and/or
to maintain cardiac output if there is a large pericardial effusion associated with the inflamed
pericardium
• This ECG appearance does not exclude STEMI – ensure a thorough history and examination
and if any doubt seek specialist help
Coronary angiography
DIAGNOSIS
After making a clinical diagnosis of STEMI, offer coronary angiography, with follow-on primary
percutaneous coronary intervention (PCI) if indicated, as the preferred coronary reperfusion strategy,
if:[23]
• The patient presents within 12 hours of onset of symptoms, and

• Primary PCI can be delivered within 120 minutes of the time when fibrinolysis could have been
given.
Seek immediate specialist advice from cardiology to discuss management options for any STEMI
patient who presents >12 hours after symptom onset . Coronary angiography ± primary PCI should
be considered if there is:
• Evidence of continuing myocardial ischaemia or cardiogenic shock[23]

• ECG evidence of continuing ischaemia and/or dynamic ECG changes, ongoing symptoms of
myocardial ischaemia, symptoms and/or signs of heart failure, shock, or malignant arrhythmias.[4]
If a patient with acute STEMI has had fibrinolysis , offer angiography:[23]
• Immediately if an ECG 60-90 minutes after fibrinolysis shows residual ST-segment elevation
• After seeking specialist cardiology advice if the patient has recurrent myocardial ischaemia after
fibrinolysis
39
• During the same hospital admission if the patient is stable after successful fibrinolysis.
Radial arterial access is preferred to femoral access in all patients undergoing coronary angiography.[23]
Laboratory work-up
Do not delay coronary reperfusion treatment to wait for blood results. [4]
• Start management as soon as a STEMI has been clinically diagnosed based on ECG findings
together with signs and symptoms consistent with ongoing myocardial ischaemia .[29]
• Immediately assess the patient’s eligibility for coronary reperfusion therapy

(irrespective of age, ethnicity, sex, or level of consciousness).[23]
• Alert the interventional cardiology team using the agreed local protocol.
Cardiac biomarkers
Request a baseline high-sensitivity cardiac troponin (cTn) along with your set of routine
blood work whenever a patient presents with a possible acute MI – but do not delay coronary
reperfusion if the patient has a clinical diagnosis of STEMI. [1] [29]
• Troponin I and T are the preferred biomarkers for definitive confirmation of an MI, with high-
sensitivity assays preferred to standard ones.[1] [29]
• Cardiac troponins are biological markers of cardiac muscle death (cardiomyocyte necrosis)
that are released into the circulation when damage to cardiac muscle has occurred.[1] [35] [36]
• Creatine kinase-MB fraction is less sensitive and less specific and is now rarely used or
measured.[1]
A pathological rise in troponin level followed by a later fall provides definitive confirmation
of an acute MI in a patient who has clinical/ECG evidence of ongoing myocardial ischaemia.
[1] However, STEMI can usually be diagnosed by ECG alone.[35]
• Acute MI is definitively confirmed by a rise and/or fall in cardiac troponin (with at least one value
>99th percentile of the upper reference limit ) in a patient who has symptoms or signs of
ischaemia.[1] [29]
Troponin level deviations and normal cut-offs are assay-specific so check local protocols.
DIAGNOSIS
• Note there is significant variability in :[1]
• The time to peak value – levels usually begin to rise around 2-3 hours after onset of
myocardial ischaemia but this varies according to the underlying mechanism
• The time when a normal value may become greater than the 99th percentile of the upper
range limit (URL)[67]
• The 99th percentile threshold is designated as the decision level for the presence of
myocardial injury
• It varies between men and women and is established separately for each specific
assay[1] [29]
• The time window to observe a fluctuating pattern of values.
• Because assays are not standardised, values from one assay cannot be compared with
those from a different assay .[1]
Always interpret troponin values in the context of :[29]
• Current and previous ECGs

• Signs and symptoms reported by the patient (in particular, the time since symptom onset )
• The possibility of an alternative cause for an elevated troponin . This may be cardiac (e.g.,
myocarditis, aortic dissection, severe heart failure) or non-cardiac (e.g., pulmonary embolism,
impaired renal function, underlying sepsis)[29]
• The demonstration of a rising and/or falling pat tern is important to distinguish acute
myocardial injury from a chronically elevated cTn
• Historical troponin levels recorded for the individual patient (e.g., measured during previous
admissions)
• Some patients may have a higher baseline compared with the general population.[29]
Cardiac troponin kinetics after acute myocardial injury including acute MI [1]
DIAGNOSIS
Cardiac troponin kinetics after acute myocardial injury including acute MI
Other blood tests at presentation

Your routine blood panel should also include the following.
• Full blood count
• Look for anaemia , which may influence the duration of dual antiplatelet therapy prescribed.
• Raised inflammatory markers may be a direct result of the acute-phase response to
acute MI or may point to a concomitant infection.
• Urea and electrolytes and estimated glomerular filtration rate (eGFR)
• Potassium, calcium, and magnesium homeostasis is crucially important to prevent both

bradyarrhythmias and tachyarrhythmias during the peri-infarct interval.
• Baseline renal function at the time of hospital admission will provide a benchmark to
allow for subsequent up-titration of medications and allow for the identification of contrast-
induced nephropathy after primary angioplasty (if the patient is eligible for coronary
reperfusion therapy).
41
• Note patients on potentially nephrotoxic drugs on admission, especially if they are

eligible for primary angioplasty.
• Aim to record an eGFR as early as possible to help guide contrast load and specific
contrast agent used during primary PCI.[4]
• Plasma glucose [4]
• Look for uncontrolled hyperglycaemia in all patients (not just those with diabetes).
Hyperglycaemia is common in the setting of acute MI, with or without a history of diabetes.
• Also look for hypoglycaemia in critically ill patients.
• Serum lipids
• Not useful in the acute period of STEMI management but will inform assessment of the
patient's risk factor profile for recurrent cardiovascular events.
• C-reactive protein (CRP)
• May be raised as a direct result of the acute-phase response to acute MI but may also point
to a concomitant infection .
• Not useful in the acute period of STEMI management but an elevated level may inform
assessment of the patient’s continued risk for recurrent cardiovascular events.[68]
• In a secondary analysis of the VISTA-16 trial, elevated levels of high-sensitivity CRP during
the index admission and the subsequent 16 weeks after an acute coronary syndrome were
associated with a higher risk of the combined end point of cardiovascular death, myocardial
infarction, non-fatal stroke, unstable angina, and all-cause death.[20]
Check arterial blood gas only if there is severe dyspnoea, hypoxia, and/or clinical evidence of
pulmonary oedema or cardiogenic shock, and in survivors of cardiac arrest.
• Patients may require airway stabilisation and aggressive ox ygen supplementation before
proceeding to primary percutaneous coronary intervention.
• This should not be performed routinely and must not delay coronary reperfusion
therapy if there is no current or impending objective respiratory compromise.
• Taking an arterial blood gas may cause trauma to the radial artery, which is typically
DIAGNOSIS
the access point for coronary angiography.
• Survivors of cardiac arrest may have :
• Low PaO 2
• High PaCO 2
• PaCO 2 is an independent predictor of achieving sustained return of spontaneous

circulation after cardiac arrest[69]
• Raised lactate
• Severe metabolic acidosis.
• Cardiogenic shock
• Elevated serum lactate (>2 mmol/L [18.2 mg/dL]) is an indicator of shock.[27]

• Rising lactate levels during resuscitation indicate an extremely poor prognosis.[27]
• Metabolic acidosis can be an indicator of shock.
• Base deficit increase correlates with the occurrence and severity of shock.
• Signs of acute pulmonary oedema:
• Respiratory acidosis
• Respiratory alkalosis (in the early stages)
• Metabolic acidosis
• Reduced PaO 2
• Reduced oxygen saturations
• Acidosis is a significant predictor of mortality in acute heart failure patients.[70]
Imaging
Do not delay coronary reperfusion treatment to undertake imaging investigations.
• Start treatment and assess the patient’s eligibility for coronary reperfusion therapy immediately
after a clinical diagnosis of STEMI has been made.
Chest radiographs
Use a chest x-ray to exclude alternative causes and to aid indirect assessment of cardiac
function. [29]
• Widened mediastinum may indicate acute aortic dissection.

• Pulmonary oedema suggests impaired left ventricular systolic function.
• A large globular cardiac contour or significantly increased cardiothoracic ratio may suggest
pericardial effusion.
Echocardiogram
Use a point-of care transthoracic echocardiogram to :o[4]
• Look for regional wall motion abnormalities of the left ventricle in patients with an
atypical presentation or equivocal ECG
• Assess the patient’s eligibility for coronary reperfusion therapy in the event of a delayed
DIAGNOSIS
presentation
• In practice, however, the patient's clinical status and the presence of pathological Q waves
in the ECG are usually enough to assess their eligibility for coronary reperfusion therapy if
presentation is delayed
• Look for mechanical complications of acute MI (see Acute MI complications – mechanical
below):
• Left ventricular function

• Right ventricular function
• Cardiac tamponade.
An echocardiogram can also be used to :
43
• Exclude STEMI in patients who present with global saddle-shaped ST-segment elevation (as
seen with acute pericarditis)
• Confirm the diagnosis of takotsubo cardiomyopathy (usually after normal coronary arteries are
found on a STEMI angiogram).[1]
A pre-discharge echocardiogram is indicated for all patients post-acute MI to assess left
ventricular function after coronary reperfusion therapy. [10] [23]
Emerging investigations
Cardiac myosin-binding protein C (cMyC)
CMyC may perform bet ter than cardiac troponin T or I in patients who present early after
symptom onset. [71]
• CMyC is a cardiac-restricted protein that is released more rapidly than cardiac troponin after acute
MI.
• CMyC is also more abundant than cardiac troponins.
• It may become the gold standard test for the early diagnosis of acute MI.
Early risk stratification

Risk stratification scores for STEMI are of limited use in the emergency department set ting.
• This is largely because the emphasis should be on rapid triage and assessment of eligibility for
immediate coronary reperfusion therapy.
• Nonetheless, risk scores can :
• Provide evidence-based prognostic information

• Be used to support decisions on the optimum reperfusion strategy.
The European Society of Cardiology recommends the GRACE risk score. [4] [72] [73]
• This calculates the overall risk of death while in hospital and from hospital discharge to 6 months.
DIAGNOSIS
• The Thrombolysis In Myocardial Infarction (TIMI) Risk Score for STEMI is an alternative.[74] [75]
Acute MI complications – mechanical

Left ventricular dysfunction [4] [10]
• Severity depends on the duration of ischaemia, premorbid functional state, and presence of
concomitant mechanical complications of acute MI.
• Can be transient (myocardial stunning) or persistent.
• May be clinically silent or lead to symptoms and signs of heart failure.
Left ventricular aneurysm [4] [10]
• Affects <5% of those with large transmural MIs (especially anterior STEMI)
• May present with signs of heart failure, ventricular arrhythmias, or clinical sequelae of
thromboembolism.
• ECG changes can support clinical suspicion.
• Will require imaging to confirm the diagnosis.[76]
Left ventricular thrombus [4] [10]
• Relatively frequent complication of large anterior STEMI.[77]

• No specific clinical signs.
• May present with signs of heart failure or sequelae of systemic thromboembolism.
• (Contrast) echocardiography required to confirm diagnosis.
Right ventricular infarction [4] [10]
• May present with the triad of hypotension, elevated jugular venous pressure (JVP), and
clear lung fields .[4] [30]
• Can complicate up to one third of inferior STEMIs.
• Check for ST elevation in aVR, V1, and right precordial leads.
• Confirm the diagnosis with echocardiography.
Ventricular septal rupture [4] [10]
• Presents with acute heart failure or cardiogenic shock.

• Look for a loud systolic murmur.
• Rupture after anterior STEMI = apical ventricular septal defect (VSD).
• Rupture after inferior STEMI = basal VSD (worse prognosis).
• Resulting left-to-right shunt may give rise to signs of acute right heart failure.
• The diagnosis is confirmed by echocardiography and Doppler (to quantify the degree of shunting).
Left ventricular free wall rupture [4] [10]
• Presents with sudden-onset chest pain and/or haemodynamic collapse.

• Rupture leads to haemopericardium and ultimately tamponade.
• Followed by electromechanical dissociation and typically death.
• Mortality rates range from 20% to 75%.[78]
• More common after first MI, anterior STEMI, lack of reperfusion, or late fibrinolysis, and in elderly
patients and women.
• The diagnosis is confirmed by echocardiography.
Acute mitral regurgitation (MR) [4] [10]
DIAGNOSIS
• Secondary to:
• Papillary muscle rupture or

• ‘Functional/ischaemic’ MR
• Post-infarction left ventricular remodelling characterised by: papillary muscle

displacement, leaflet tethering, and annular dilatation
• Look for signs of severe dyspnoea, acute pulmonary oedema, and/or cardiogenic shock.
• Classical pansystolic murmur of mitral regurgitation may not always be audible due to
the severity of the regurgitation.
• Inferior STEMI can cause rupture of the posteromedial papillary muscle.
• Anterolateral STEMI can cause rupture of the anterolateral papillary muscle.
• The diagnosis is confirmed by echocardiography.
Pericarditis [4] [10]
• Diagnostic criteria:[4]
• Pleuritic chest pain (relieved by sitting or leaning forward)
45
• Pericardial friction rub
• ECG changes: global ST-segment elevation or PR interval depression
• Pericardial effusion.
• Early post-MI pericarditis : usually transient.
• Late post-MI pericarditis : also known as Dressler’s syndrome ; more common after late-
presentation STEMI.
• Both are related to late or failed reperfusion and larger infarct size.
Pericardial effusion [4] [10]
• Secondary to pericarditis.
• Can be a complication of primary percutaneous coronary intervention.
• In the absence of inflammatory signs: rule out subacute left ventricular free wall rupture .
• Look for signs of cardiac tamponade:
• Beck’s triad = hypotension with narrow pulse pressure + raised JVP + muffled heart sounds
• Pulsus paradoxus = exaggerated fall in systolic pressure >10 mmHg during inspiration
• Electrical alternans (and tachycardia) on ECG
• Pleuritic chest pain
• Tachypnoea
• Weakness, anxiety, restlessness.
• Use echocardiography first-line if there a high clinical suspicion of pericardial effusion and/or
tamponade.
Acute MI complications – electrical#

Bradycardia and atrioventricular block [4] [10]
• Sinus bradycardia is common post-STEMI and is usually self-limiting.

• Mobitz type I second-degree atrioventricular (AV) block is associated with inferior STEMI.
• Rarely causes haemodynamic compromise.

DIAGNOSIS
• Mobitz type II second-degree AV block and complete heart block:
• May require pacing.
Practical tip
AV block secondary to inferior STEMI quite often resolves spontaneously or after

coronary reperfusion.
• AV block secondary to anterior STEMI is associated with a high mortality rate and
indicates an extensive area of myocardial damage. It will need consideration of permanent
pacemaker implantation.
• Left bundle branch block or hemiblock suggests an extensive anterior MI.
Supraventricular tachyarrhythmias [4] [10]
• Atrial fibrillation most common.

• Determine the patient’s haemodynamic status and treat accordingly.
Ventricular tachyarrhythmias [4] [10]
• Secondary to ischaemia: unstable, polymorphic, relatively fast ventricular tachycardia degenerating

into ventricular fibrillation.
• Secondary to reperfusion (within 48 hours): ventricular extrasystoles, non-sustained ventricular
tachycardia.
• Usually benign if self-limiting.

• Be aware of incessant ventricular tachycardia/electrical storm despite appropriate
revascularisation.
• It is crucial to identify and treat sustained ventricular arrhythmias in the peri-infarction period to
prevent:
• Further reduction in cardiac output

• Worsening myocardial ischaemia
• Degeneration into ventricular fibrillation.
History and exam

Key diagnostic factors
chest pain (common)
Patients typically present with central chest pain :[1] [4] [29]
• Classically retrosternal, crushing, heavy, severe , and diffuse in nature

• Might be described by the patient as ‘ pressing or squeezing ’
• May occur at rest or on activity
• May be constant or intermittent, or wax and wane in intensity
• Sometimes radiating to the left arm, neck, or jaw
• May be associated with nausea, vomiting, dyspnoea, diaphoresis, lightheadedness,
palpitations, or syncope .[29]
DIAGNOSIS
Always ask about the characteristics of the chest pain as part of your history; in particular
:[29] [41] [42]
• “Have you ever had this type of pain before?”

• Nature, severity, duration of pain
• Radiation
• Associated symptoms
• Time since symptom onset – this is crucial to inform the appropriate reperfusion strategy[4]
[22] [23]
• If symptoms are intermittent, it is important to ask when the last episode of pain
occurred.[29]
Practical tip
The choice of coronary reperfusion strategy depends on time since symptom onset
– but obtaining an exact time for this can be difficult.
• Patients can often give only an approximate idea of when their symptoms began.
47
• Patients sometimes ignore chest pain (or associated symptoms) until they can no longer
tolerate it.
• The reliability of the assessment of time since symptom onset is determined by a combination
of the patient’s ability to give an accurate history and the experience and skill of the clinician
taking the history.
• If you question the patient carefully, they may describe warning signs, or less severe or less
long-lasting symptom episodes preceding the more severe episode that has prompted them
to seek medical help.
Practical tip
Do not rely on a positive patient response to glyceryl trinitrate as a reliable

diagnostic indicator of ischaemic chest pain. [4] [29] [40]
• Response to nitrates can be misleading. Patients who get symptom relief still need
confirmatory ECG testing to inform the diagnosis.
• Complete normalisation of ST-segment elevation along with resolution of chest pain after
buccal or sublingual nitrates suggests coronary vasospasm (with or without associated
MI).[4]
dyspnoea (common)
Dyspnoea is a common feature secondary to pulmonary congestion from left ventricular
systolic dysfunction. [29]
It can also occur due to other mechanical and electrical complications of acute MI, which
occur less commonly in the context of contemporary rapid revascularisation, for example
:
• Left ventricular aneurysm

DIAGNOSIS


• Functional (ischaemic) mitral regurgitation
• Supraventricular tachyarrhythmias
• Ventricular tachyarrhythmias
• Bradycardia and atrioventricular block.
pallor (common)
Pallor is a common feature due to high sympathetic output resulting in peripheral
vasoconstriction.
diaphoresis (common)
Marked sweating is a common feature due to high sympathetic output. [29]
cardiac risk factors (common)
Check for any history of cardiovascular disease: in particular, ischaemic heart disease.
[29]
• Also check for any previous episodes of investigation or treatment for chest pain .
• A history of coronary artery disease should increase your index of suspicion.[4]
A cardiovascular risk factor profile is an important part of your history-taking. Check :[29]
• Smoking status
• Hypertension
• Diabetes mellitus
• Hypercholesterolaemia
• Family history of premature coronary artery disease (<60 years)
• Established coronary artery disease
• Advanced age
• Obesity
• Metabolic syndrome
• Physical inactivity
• Chronic kidney disease
• Cocaine use.
abnormal breath sounds (uncommon)

• Crackles/crepitations or cardiac wheeze would suggest congestive cardiac failure ± pulmonary

oedema.
additional heart sounds (uncommon)

DIAGNOSIS
• Muffled heart sounds could suggest a pericardial effusion or even cardiac tamponade.
• Is there a third (S3) or fourth (S4) heart sound ?
• These added heart sounds could suggest severe heart failure.

• A murmur might suggest:
• Acute ventricular septal defect

• Underlying chronic valvular heart disease.
cardiogenic shock (uncommon)

Cardiogenic shock complicates 6% to 10% of STEMI admissions. [4] [45]
• In-hospital mortality remains high (≥50%).[4]
49
• There is a bimodal presentation: the majority occur within 24 hours; the remainder occur within
the first week.[46]
Seek immediate senior support and specialist input if your clinical assessment suggests
cardiogenic shock.
See our topic Shock .
Patients present with signs of hypoperfusion and/or fulminant heart failure, such as :
• Altered mental status/reduced consciousness

• Tachypnoea
• Severe dyspnoea
• Tachycardia
• Orthopnoea
• Cool peripheries
• Grey, ashen, pale appearance.
Cardiogenic shock is primarily a clinical diagnosis supported by haemodynamic
measures. It is defined as persistent hypotension (systolic blood pressure [SBP] <90
mmHg) together with signs of end-organ hypoperfusion. [4] [26] [27]
• Clinical criteria:[26]
• SBP <90 mmHg despite adequate volume replacement, or if inotropes and/or mechanical
circulatory support are needed to maintain SBP ≥90 mmHg
• Urine output <30 mL/hour
• Cool extremities.
• Haemodynamic criteria:[26]
• 2
Cardiac index ≤2.2 L/minute/m
DIAGNOSIS
• Wedge pressure ≥15 mmHg.

• Cardiogenic shock results from extensive left ventricular infarction and/or
mechanical complications such as :

• Left ventricular free wall rupture leading to pericardial tamponade
• Right ventricular infarction.
Other diagnostic factors

nausea and/or vomiting (common)
Nausea and vomiting are common features. [29]
• These are non-specific symptoms but are commonly associated with inferior-wall STEMI due to
increased vagal tone.
• May be the only indicator of inferior-wall STEMI.
dizziness or light-headedness (common)
Patients commonly report feeling lightheaded or weak/lethargic. [4]
• This is due to cerebral hypoperfusion as a result of hypotension and/or symptomatic

bradycardia.
distress and anxiety (common)

The patient may report an impending sense of doom or death.
palpitations (common)
Some patients present with palpitations. [4]
• Tachycardia

• Ventricular tachyarrhythmias such as ventricular tachycardia
• Bradycardia
• Sinus bradycardia
• Atrioventricular block secondary to inferior STEMI
• Atrioventricular block secondary to anterior STEMI
• Irregular heart beat

• Ventricular extrasystoles
reduced consciousness (uncommon)

Changes in mental status/reduced consciousness are associated with cardiogenic shock
DIAGNOSIS
or bradycardia and hypotension. [27]
hypotension (uncommon)
Hypotension may be present in :
• Cardiogenic shock – systolic blood pressure (SBP) <90 mmHg despite adequate volume
replacement, or if inotropes and/or mechanical circulatory support are needed to maintain SBP
≥90 mmHg[26] [27]
• Inferior STEMI#
• Right ventricular infarction
• Complicating inferior STEMI or an extensive anterior STEMI

• Always think of the triad of hypotension, elevated jugular venous pressure, and clear lung
fields[4] [30]
• Haemodynamically significant atrioventricular block, supraventricular tachyarrhythmias, or
ventricular arrhythmias.
51
atypical location or nature of pain (uncommon)
Be aware of patient groups who are more likely to present atypically. [29]
• Women, older patients, and patients with diabetes are more likely to present with
atypical features.[4] [10] [22] [39]
• Atypical chest pain might be described by the patient as burning, throbbing, tight , or a
feeling like trapped wind .
• The patient may describe indigestion rather than chest pain.

• In the absence of chest pain, there may be epigastric pain, back (interscapular) pain,
neck or jaw pain, or arm pain (typically left-sided).
• Clinical suspicion is key to making the diagnosis. It is, therefore, vital to make a full assessment
based on the history, examination, and serial ECGs.[1] [36] [37]
DIAGNOSIS
Investigations
1st test to order
Test Result
ECG a STEMI is diagnosed in
the appropriate clinical
Perform a 12-lead ECG within 10 minutes of first medical
context (a patient with chest
contact in any patient who presents with chest pain and/or
pain or other symptoms
other signs of possible STEMI. [1] [4]
consistent with myocardial
ischaemia) when there is new
• If the patient presents in the community, obtain a pre-hospital (or increased) and persistent
ECG and send it digitally to the receiving hospital as quickly as ST-segment elevation in at
possible.[4] [29] least two contiguous ECG
• If the ECG is equivocal despite a high clinical suspicion of leads of ≥1 mm in all leads
acute MI, perform serial ECGs in the appropriate hospital other than leads V2-V3 where
setting and compare these with historical ECGs, if available.[1] the following cut-off points
[4] [29] apply:[1]
In the appropriate clinical context (chest pain or other
symptoms of ischaemia), make a clinical diagnosis of STEMI • ≥2.5 mm in men <40
if there is new (or increased) and persistent ST-segment
elevation in two or more contiguous leads. [4] [10] years old
• ≥2 mm in men >40
• Make the diagnosis when these criteria are met in the years old
absence of left ventricular hypertrophy, left bundle • ≥1.5 mm in women
branch block (LBBB), or a paced rhythm on the ECG .
regardless of age
• Severe cases of left ventricular hypertrophy can appear

identical to LBBB.
• A paced rhythm can appear identical to LBBB.
• Note that the presence of left ventricular
hypertrophy, LBBB, or a paced rhythm does
not preclude a diagnosis of STEMI if the patient
DIAGNOSIS
presents with typical symptoms of myocardial ischaemia.
• See Less common ECG presentations below for more
on diagnosis of STEMI in the presence of LBBB.
• Consult a cardiology specialist immediately if the ECG
changes are equivocal.
• An urgent transthoracic echocardiogram to look for

regional wall motion abnormalities is indicated.
Measure ST-segment elevation from the J point. [1] [4]
As soon as a clinical diagnosis of STEMI is made based on

ECG changes together with symptoms or signs of ischaemia,
start treatment and make an immediate assessment of
eligibility for coronary reperfusion therapy (irrespective of age,
ethnicity, sex, or level of consciousness).[4] [10] [23]
• Alert the interventional cardiology team straight away.

• Do not wait for cardiac biomarker results or other
laboratory or imaging investigations. Assessment and
diagnosis of STEMI is a time-critical process .
53
Test Result
• The shortest possible delay from symptom onset
to coronary reperfusion maximises the patient’s
chances of survival and recovery.[1] [4] [10] [20] [21] [22]
[23]
For a library of ECGs with learning points, see the Diagnosis
recommendations section.#
Less common ECG presentations
Posterior STEMI [1] [4]#

• Consider this when there is ST-segment depression in
leads V1-V3 along with characteristic signs and symptoms of
myocardial ischaemia.
• Confirm with posterior lead ECG : ST-segment elevation
≥0.5 mm in V7-V9.
Right ventricular infarction [1] [4] [30]#

• Can complicate an inferior STEMI.
• Check right precordial leads (V3R and V4R).
• Look for ST elevation ≥1 mm in aVR and V1 .
• Confirmation will have an impact on choice of therapeutic
intervention.
Left main coronary obstruction [4] [31]#

• Consider complete left main coronary artery obstruction
if the following are both present, especially if the patient has
haemodynamic compromise:
DIAGNOSIS
• ST depression ≥1 mm in ≥6 surface leads (i.e.,

inferolateral ST depression)
STEMI in the presence of LBBB [33] [62]#

ECG diagnosis of STEMI is problematic in the presence of
LBBB. [4]
• It is often possible to make the diagnosis if marked ST-

segment abnormalities are present.[4]
• The presence of concordant ST-segment elevation

(i.e., in leads with positive QRS deflections) is one
of the best indicators of total coronary occlusion and
ongoing MI in the context of a patient with concomitant
LBBB.[32]
• Manage any patient with LBBB and clinical suspicion
of ongoing myocardial ischaemia in a similar way to
Test Result
STEMI , regardless of whether or not the LBBB was previously
known.[4]
• Presumed new LBBB alone does not indicate the presence of
a STEMI.[34]
• If in doubt, seek immediate input from the cardiology
team .
More info: Sgarbossa criteria for diagnosis of MI in the

presence of LBBB
Consider using the Sgarbossa criteria to improve the diagnostic

accuracy for STEMI in patients who have LBBB at presentation.
Original criteria [1] [33]
• ST elevation of ≥1 mm, concordant with the QRS complex:

5 points.
• ST depression ≥1 mm in leads V1, V2, or V3: 3 points .
• This has a sensitivity of 19% and a specificity of 81%

to diagnose acute MI.[63]
• ST elevation ≥5 mm, discordant with the QRS complex: 2
points .
• This has a sensitivity of 10% and a specificity of 99%

to diagnose acute MI.[63]
• An aggregated score of 3+ is 90% specific for MI but
only 36% sensitive .
Components of the Sgarbossa criteria have high
specificity but low sensitivity so are useful to confirm
acute MI but less useful to rule it out. [64]
• The low sensitivity means you must maintain a high
DIAGNOSIS
index of suspicion if the presentation is consistent
with MI regardless of the criteria score .
• 'Weighted' Sgarbossa criteria rely on the points system;
however, only two of the criteria carry a score ≥3 to make
the diagnosis of acute MI.[65]
• 'Unweighted' Sgarbossa criteria are applied without the
points system – this is more sensitive but less specific.[65]
• The criteria were originally based on the outcome of
acute MI as measured by creatine kinase-MB rather than
angiographic evidence of acute coronary occlusion – further
reducing sensitivity because the criteria encompass both
STEMI and non-ST-elevation MI (NSTEMI).[65]
55
Test Result
Sgarbossa criteria for MI in the presence of LBBB

The modified Sgarbossa criteria have bet ter sensitivity

but worse specificity for STEMI. [65] [66]
• The original rule for >5 mm discordance is replaced with a

proportionately excessive discordance: ST-elevation/S-wave
amplitude ≤-0.25.
• The modified criteria were found to be more sensitive
versus the ‘weighted’ (80% vs. 49%; P <0.001) and
‘unweighted’ (80% vs. 56%; P <0.001) Sgarbossa
criteria.[65]
• Modified criteria specificity is not significantly different

DIAGNOSIS
from the 'weighted' criteria.[65]

• Modified criteria specificity is significantly greater
than the 'unweighted' original criteria.[65]
Test Result
ST/S ratio under the modified Sgarbossa criteria

Previous silent/unrecognised STEMI

Be aware of the possibility that abnormal ECG features might
be due to a previous silent/unrecognised STEMI. [1]
• Residual ST elevation on the ECG from an old STEMI may be

detected either incidentally in an asymptomatic patient who is
having an ECG for another reason, or occasionally in a patient
with symptoms of ischaemia who is experiencing an NSTEMI
DIAGNOSIS
against the background of a previous history of STEMI.
• In such cases, there may be ST-segment elevation on
the current ECG that was already present on old ECGs
(e.g., in the case of left ventricular aneurysm formation). It is
important to distinguish this from new ST elevation as
management will differ.
• The historical STEMI may have been 'silent' and gone

unrecognised at the time. The resulting old ECG
features will usually be fixed .
• It is helpful to take a thorough history, together with diligent
ECG interpretation and comparison with old ECGs (plus
medical records) if available.
• Seek specialist input from the cardiology team.
The following criteria for previous (or silent/unrecognised)
MI can be helpful. There may be :[1]
• Pathological Q waves with or without symptoms, in the

absence of non-ischaemic causes[1]
57
Test Result
• Loss of viable myocardium in a pat tern consistent with
a coronary artery territory (regional wall abnormality) seen
on cardiac imaging :
• Echocardiography
• Myocardial perfusion scintigraphy (MPS)
• Positron emission tomography (PET)
• Cardiac magnetic resonance imaging
• Pathological findings of a healed or healing MI on
cardiac imaging.
Practical tip
A Q wave is defined as any negative deflection

preceding an R wave in the QRS complex.
• A Q wave represents the normal left-to-right depolarisation
across the interventricular septum.
• Small Q waves tend to be normal in most leads (e.g., left-
sided leads such as I, aVL, V5, and V6).
• More pronounced Q waves (>2 mm deep) may be seen in
lead III or aVR as a normal variant.
• Q waves are not usually seen in the right-sided leads (V1-
V3).
• Pathological Q waves can be a sign of previous MI. The
precise definition of pathological Q waves has been
debated. The 2018 Fourth Universal Definition of MI defines
them as follows:[1]
• Any Q wave in leads V2-V3 >20 milliseconds (0.02

seconds) or any QS complex in leads V2 and V3
• Q wave ≥30 milliseconds (0.03 seconds) and ≥1 mm
DIAGNOSIS
deep or QS complex in leads I, II, aVL, aVF, or V4-

V6 in any two leads of a contiguous lead grouping (I,
aVL; V1-V6; II, III, aVF)
• R wave >40 milliseconds (0.04 seconds) in V1-V2
and R/S >1 with a concordant positive T wave in the
absence of a conduction defect.
coronary angiography acute occlusion or critical

After making a clinical diagnosis of STEMI, offer coronary stenosis
angiography, with follow-on primary percutaneous coronary
intervention (PCI) if indicated, as the preferred coronary reperfusion
strategy, if:[23]
• The patient presents within 12 hours of onset of symptoms,

and
• Primary PCI can be delivered within 120 minutes of the time
when fibrinolysis could have been given.
Seek immediate specialist advice from cardiology to discuss
management options for any STEMI patient who presents >12
Test Result
hours after symptom onse t . Coronary angiography ± primary
PCI should be considered if there is:
• Evidence of continuing myocardial ischaemia or cardiogenic

shock[23]
• ECG evidence of continuing ischaemia and/or dynamic
ECG changes, ongoing symptoms of myocardial ischaemia,
symptoms and/or signs of heart failure, shock, or malignant
arrhythmias.[4]
If a patient with acute STEMI has had fibrinolysis, offer angiography:
[23]
• Immediately if an ECG 60-90 minutes after fibrinolysis shows

residual ST-segment elevation
• After seeking specialist cardiology advice if the patient has
recurrent myocardial ischaemia after fibrinolysis
• During the same hospital admission if the patient is stable after
successful fibrinolysis.
Radial arterial access is preferred to femoral access in all patients
undergoing coronary angiography.[23]
cardiac troponin troponin elevated
Request a baseline high-sensitivity cardiac troponin (cTn)
along with your set of routine blood work whenever a patient • acute MI is definitively
presents with a possible acute MI. confirmed by a rise
and/or fall in cardiac
A pathological rise in troponin level followed by a later fall troponin (with at least
provides definitive confirmation of an acute MI in a patient one value >99th
who has clinical/ECG evidence of ongoing myocardial percentile of the
ischaemia (although STEMI can usually be diagnosed by ECG upper reference
alone) . [1] [35] limit ) in a patient who
has symptoms or signs
DIAGNOSIS
• However, do not delay coronary reperfusion to wait for of ischaemia[1] [29]
troponin results .
• Start treatment and immediately assess eligibility for coronary
reperfusion therapy as soon as a clinical diagnosis of STEMI is
made based on ECG signs in a patient with chest pain or other
symptoms consistent with myocardial ischaemia.[1] [29]
Troponin I and T are the preferred biomarkers for definitive
confirmation of an MI, with high-sensitivity assays preferred
to standard ones. [1] [29]
• Cardiac troponins are biological markers of cardiac muscle

death (cardiomyocyte necrosis) that are released into the
circulation when damage to cardiac muscle has occurred.[1]
[35] [36]
• Creatine kinase-MB fraction is less sensitive and less specific
and is now rarely used or measured.[1]
Troponin level deviations and normal cut-offs are assay-
specific so check local protocols.
• Note there is significant variability in :[1]
59
Test Result
• The time to peak value – levels usually begin to rise
around 2-3 hours after onset of myocardial ischaemia
but this varies according to the underlying mechanism
• The time when a normal value may become greater than
the 99th percentile of the upper range limit[67]
• The 99th percentile threshold is designated as

the decision level for the presence of myocardial
injury
• It varies between men and women and is
established separately for each specific assay[1]
[29]
• The time window to observe a fluctuating pattern of
values.
• Because assays are not standardised, values from one
assay cannot be compared with those from a different
assay .[1]
Always interpret troponin values in the context of :[1] [29]
• Current and previous ECGs

• Signs and symptoms reported by the patient (in particular, the
time since symptom onset )
• The possibility of an alternative cause for an elevated
troponin . This may be cardiac (e.g., myocarditis, aortic
dissection, severe heart failure) or non-cardiac (e.g.,
pulmonary embolism, impaired renal function, underlying
sepsis)[29]
• The demonstration of a rising and/or falling pat tern

is important to distinguish acute myocardial injury from a
chronically elevated cTn[1]
DIAGNOSIS
• Historical troponin levels recorded for the individual patient

(e.g., measured during previous admissions)
• Some patients may have a higher baseline

compared with the general population.[29]
Test Result
Cardiac troponin kinetics after acute myocardial injury including acute MI

glucose normal or elevated plasma
Look for uncontrolled hyperglycaemia in all patients (not glucose
just those with diabetes). [4]
• Hyperglycaemia is common in the setting of acute MI, with or

without a history of diabetes.
• Also check for hypoglycaemia in critically ill patients.
Do not delay coronary reperfusion treatment to wait for
blood results. [4]
full blood count normal range but can be
Look for anaemia, which may influence the duration of dual elevated or reduced
antiplatelet therapy prescribed.
DIAGNOSIS
Raised inflammatory markers may be a direct result of
the acute-phase response to acute MI or may point to a
concomitant infection.
Do not delay coronary reperfusion treatment to wait for

blood results. [4] #
electrolytes, urea, creatinine, and estimated glomerular normal range but can be
filtration rate (eGFR) elevated or reduced
Potassium, calcium, and magnesium homeostasis is
crucially important to prevent both bradyarrhythmias and
tachyarrhythmias during the peri-infarct interval.
Baseline renal function at the time of hospital admission

will provide a benchmark for:
• Subsequent up-titration of medications

• Identification of contrast-induced nephropathy after primary
angioplasty (if the patient is eligible for coronary reperfusion
therapy)
61
Test Result
• Note patients on potentially nephrotoxic drugs on
admission, especially if they are eligible for primary
angioplasty.
Aim to record an eGFR as early as possible to help guide

contrast load and specific contrast agent used during
primary percutaneous coronary intervention. [4]
• Also note that chronic kidney disease is a cardiac risk factor.
C-reactive protein (CRP) normal range or elevated

May be raised as a direct result of the acute-phase response
to acute MI but may also point to a concomitant infection.
• Not useful in the acute period of STEMI management but

an elevated level may inform assessment of the patient’s
continued risk for recurrent cardiovascular events.[68]
• In a secondary analysis of the VISTA-16 trial, elevated levels
of high-sensitivity CRP during the index admission and the
subsequent 16 weeks after an acute coronary syndrome were
associated with a higher risk of the combined end point of
cardiovascular death, myocardial infarction, non-fatal stroke,
unstable angina, and all-cause death.[68]
serum lipids normal range or elevated

Not useful in the acute period of STEMI management but
will inform assessment of the patient’s risk factor profile for
recurrent cardiovascular events.
Cholesterol levels may be lowered by high catecholamine

levels mediated by an acute MI in its early phases.
• Serum lipids should, therefore, be repeated in 30-60 days.

DIAGNOSIS
• Irrespective of serum lipid levels, high-intensity statins are

mandated after STEMI.
Other tests to consider
Test Result
arterial blood gas oxygen is indicated when:[4]
Patients may be hypoxaemic and require supplemental
ox ygen. • arterial oxygen
saturation (SaO 2 )
• Check arterial blood gases only when there is severe <90% or
• PaO 2 <60 mmHg
dyspnoea, hypoxia, and/or clinical evidence of pulmonary
oedema or cardiogenic shock, and in survivors of cardiac
arrest.
• Patients may require airway stabilisation and oxygen
supplementation before proceeding to primary percutaneous
coronary intervention.
• This should not be performed routinely and must not delay
coronary reperfusion therapy if there is no current or impending
objective respiratory compromise.
• Taking an arterial blood gas may cause trauma to the

radial artery, which is typically the access point for
coronary angiography.
chest x-ray possible findings:

Use a chest x-ray to exclude alternative causes and to aid
indirect assessment of cardiac function. [29] • pulmonary oedema
• widened mediastinum
• Widened mediastinum may indicate acute aortic dissection. • cardiomegaly
• Pulmonary oedema suggests impaired left ventricular systolic • permanent pacemaker
function. • biventricular
• A large globular cardiac contour or significantly increased
DIAGNOSIS
pacemaker
cardiothoracic ratio may suggest pericardial effusion. • sternal wires
Imaging tests must not delay coronary reperfusion therapy. • clear lung fields
• normal cardiac contour
point-of-care transthoracic echocardiogram • left ventricular

Use a point-of-care transthoracic echocardiogram to :[1] [4] regional wall motion
abnormalities
• Look for regional wall motion abnormalities of the left
• valvular defects
ventricle in patients with an atypical presentation or
equivocal ECG • right ventricular
• Assess the patient’s eligibility for coronary reperfusion therapy function
in the event of a delayed presentation • pericardial effusion
• left ventricular mural
• In practice, however, the patient's clinical status and
thrombus
the presence of pathological Q waves in the ECG are
usually enough to assess their eligibility for coronary
reperfusion therapy if presentation is delayed
• Look for mechanical complications of acute MI:
63
Test Result
• Left ventricular function
• Right ventricular function
• Cardiac tamponade.
An echocardiogram can also be used to :
• Exclude STEMI in patients who present with global saddle-

shaped ST-segment elevation (as seen with acute
pericarditis)
• Confirm the diagnosis of takotsubo cardiomyopathy
(usually after normal coronary arteries are found on a STEMI
angiogram).[1]
Imaging tests must not delay coronary reperfusion therapy.
A pre-discharge echocardiogram is indicated for all patients

post-acute MI to assess left ventricular function after
coronary reperfusion therapy. [10] [23]
Emerging tests
Test Result
cardiac myosin-binding protein C (cMyC) elevated
CMyC may perform bet ter than cardiac troponin T or I in
patients who present early after symptom onset. [71]
DIAGNOSIS
• CMyC is a cardiac-restricted protein that is released more

rapidly than cardiac troponin after acute MI.
• CMyC is also more abundant than cardiac troponins.
• It may become the gold standard test for the early diagnosis of
acute MI.
Differentials
Condition Differentiating signs / Differentiating tests

symptoms
Unstable angina • Clinical presentation may not • ECG may show non-specific
differentiate. ST-segment and T-wave
changes.
• Cardiac biomarkers are
normal.
Non-ST-elevation • Clinical presentation may not • ECG may show non-specific

myocardial infarction differentiate. ST-segment and T-wave
changes, but does not show
ST-segment elevation.
• Cardiac biomarkers are
elevated in both non-ST-
elevation MI and STEMI.
Aortic dissection • Patients typically present • CXR may show a widened

with tearing chest pain, mediastinum.
notably between the • ECG may be unremarkable,
shoulder blades. show sinus tachycardia, or
• They can be in show ST-segment changes
considerable distress and if the dissection extends
haemodynamically unstable. proximally and involves the
• Peripheral pulses may be coronary ostium.
unequal or absent distally. • A CT of chest and abdomen
with intravenous contrast
showing the presence of a
dissection flap and a true
lumen and false lumen
is diagnostic for aortic
dissection.
• A trans-oesophageal
DIAGNOSIS
echocardiogram may also
show the dissection flap with
the true and false lumens.
Pulmonary embolism (PE) • Patients classically present • Patients are hypoxic with an
with acute onset of sharp increased arterial-alveolar
stabbing chest pain that gradient on the arterial blood
is pleuritic in nature and gas.
associated with shortness of • ECG may show sinus
breath. tachycardia or right
• A background of increased ventricular strain with
clotting tendency, such prominent S wave in lead
as known hereditary I, prominent Q in lead
thrombophilia or connective III, and flipped T in lead
tissue disease; known deep III (S1Q3T3), or can be
venous thrombosis; or unremarkable.
previous PE increases the • D-dimer is useful for risk
likelihood of the diagnosis. stratifications. In a patient
• Other risk factors with a low probability of PE
include recent prolonged on clinical scoring, with a
immobilisation and limb non-elevated d-dimer, a PE
trauma. can be excluded; if elevated,
65

symptoms
further work-up is required to
confirm PE.
• For patients with a high
probability of PE on clinical
scoring (i.e., PE is likely)
or an abnormal D-dimer,
imaging is required. The
multiple-detector CT
pulmonary angiography
scanning of the chest is the
imaging study of choice.
Pneumothorax • Patients present with sudden • CXR shows a visceral

onset of pleuritic chest pleural line.
discomfort and shortness of
breath.
• Tachycardia, hypotension,
and cyanosis suggest a
tension pneumothorax.
• Known underlying medical
conditions that predispose
to pneumothorax, such
as chronic obstructive
pulmonary disease,
connective tissue disease,
or recent chest trauma, may
support this diagnosis.
Pneumonia • Patients usually have • WBC count is usually

an insidious onset of elevated with neutrophilia.
fevers, cough (that may be • CXR shows increased
productive of sputum), and alveolar markings.
shortness of breath. • Blood and sputum cultures
DIAGNOSIS
• Chest discomfort may be may be positive for an

pleuritic in nature. infective organism.
• Examination will usually
confirm pneumonic
consolidation with decreased
resonance, decreased air
entry, and crackles over the
affected lung.
Pericarditis • Patients can present with • ECG may have diffuse ST-
chest pain of varying quality segment elevation that
that is typically better on is concave up ('saddle-
sitting up and leaning shaped') with PR segment
forwards and worse with depression.[79]
lying down. • Cardiac biomarkers
• There may be a history of can be elevated if
recent viral syndrome and inflammation extends into
a pericardial friction rub on the myocardium.
clinical examination. • Inflammatory markers such
as CRP and erythrocyte
sedimentation rate may be
elevated.

symptoms
• CXR demonstrating a
globular cardiac shadow is
suggestive.
• Echocardiogram may show
a pericardial effusion or may
be unremarkable.
Myocarditis • Patients often have a • ECG changes and cardiac

recent history of influenza- biomarkers can mimic MI.
like illness or underlying • Inflammatory markers
autoimmune condition (erythrocyte sedimentation
such as systemic lupus rate and CRP) and
erythematosus. autoimmune assays may be
• They are likely to be young elevated.
and often do not have risk • Test of choice is cardiac
factors for coronary artery magnetic resonance
disease. imaging, with delayed
• Myocarditis is more likely enhancement imaging
to present with symptoms showing an epicardial or
of cardiac failure than with mid-myocardial involvement.
chest pain.
Gastro-oesophageal reflux • Patients present with burning • Diagnosis is usually clinical.

disease retrosternal discomfort that is • Cardiac biomarkers, ECG,
relieved by antacids. and CXR are normal.
• Discomfort/pain is usually • Oesophagogastroduodenoscopy
non-exertional. is indicated for patients
with persistent or atypical
symptoms and may show
oesophagitis (erosions,
ulcerations, strictures) or
Barrett's oesophagus.
Oesophageal spasm • Patients present with • Cardiac biomarkers, ECG,
DIAGNOSIS
squeezing retrosternal and CXR are normal.
discomfort that may be • Oesophageal manometry or
relieved by glyceryl trinitrate barium swallow may show
(due to relaxation of the evidence of dysmotility.
spasm).
• Discomfort/pain is usually
non-exertional.
Costochondritis • Musculoskeletal chest wall • Cardiac biomarkers, ECG,

discomfort that is worse with and CXR are normal.
certain movement and deep
breaths.
• Focal tenderness over the
costochondral joints may be
present.
Anxiety or panic at tack • Normal examination; • Cardiac biomarkers, ECG,

however, evidence and CXR are all normal.
of hyperventilation is
sometimes present.
67
Criteria
ST elevation on ECG[1]
New (or increased) and persistent ST-segment elevation in at least two contiguous leads of ≥1 mm
in all leads, other than leads V2-V3 where the following cut points apply :[1]

Criteria for acute, evolving, or recent MI[2]

Either one of the following criteria:
1. Typical rise of biomarkers of myocardial necrosis (troponin or creatine kinase-MB) with at least one of
the following:
• Ischaemic symptoms
• Development of pathological Q waves on ECG
• ECG changes indicative of ischaemia (ST-segment elevation or depression)
• Coronary artery intervention (e.g., coronary angiography).
2. Pathological findings of acute MI.
Criteria for established MI[2]

Any one of the following:
1. Development of pathological Q waves on serial ECGs. The patient may or may not remember previous
DIAGNOSIS
symptoms. Biochemical markers of myocardial necrosis may have normalised, depending on the
length of time that has passed since the infarct developed.
2. Pathological findings of a healed or healing MI.
3. Cardiac magnetic resonance imaging with delayed enhancement imaging showing a classic sub-
endocardial or transmural infarct in a coronary artery distribution.
Screening
The NHS in England offers all people aged 40 to 74 years an NHS Health Check once every 5 years, which
includes a formal assessment of cardiovascular risk. NHS England has estimated this could prevent 1600
myocardial infarctions per year, saving at least 650 lives.[80]
ST-elevation myocardial infarction Management
Recommendations
Urgent
as possible , unless they have aspirin hypersensitivity. [23]
• Check your local protocol or discuss the patient with a senior colleague if they have hypersensitivity
to aspirin.
Make a clinical diagnosis of STEMI and start treatment if the patient has signs and symptoms
of myocardial ischaemia plus persistent/increasing ST elevation in two or more contiguous
leads on the ECG .[4]
• Do not wait for cardiac troponin levels to confirm a STEMI.

Perform all of the following in tandem as soon as a clinical diagnosis of STEMI has been made.[4]
[10] [23]
• Immediately assess the patient’s eligibility for coronary reperfusion therapy (irrespective of
age, ethnicity, sex, or level of consciousness).[23]
• For most patients the best option will be primary percutaneous coronary intervention (PCI);
fibrinolysis is reserved for those without access to timely primary PCI.[4] [23]
• If eligible, take steps to ensure reperfusion is administered as quickly as possible .[4]
[23]
• If not eligible, offer conservative medical management.[23]
• Gain intravenous access and start continuous haemodynamic monitoring and pulse
oximetry .[4]
• Avoid placing a cannula that obstructs access to the right radial artery (the commonest entry
site for primary PCI).
• Give pain relief : an intravenous opioid (e.g., morphine, diamorphine) is recommended plus a
concomitant intravenous anti-emetic to prevent vomiting.
• Give ox ygen therapy only if oxygen saturation is <90% .[4]
• Give dual antiplatelet therapy by adding a P2Y 12 inhibitor to aspirin.[23]
• If the patient is having primary PCI, use prasugrel if they are not already taking an oral
anticoagulant, or clopidogrel if they are already taking oral anticoagulation.[23]
• Consider an intravenous nitrate (e.g., glyceryl trinitrate, isosorbide dinitrate) if the
patient has:[4] [29]
• Persistent chest pain despite administration of sublingual (or buccal) glyceryl trinitrat
MANAGEMENT
• Sustained hypertension
• Clinical and/or radiographic evidence of congestive heart failure .
• Do not give an intravenous nitrate if there is :
69
• Hypotension secondary to any one of: right ventricular infarction (usually

complicating an inferior or extensive anterior STEMI); severe aortic stenosis or
left ventricular outflow tract obstruction; pre-existing cardiomyopathy
• Persistent hypotension secondary to another cause
• Use of a phosphodiesterase-5 inhibitor (e.g., avanafil, sildenafil, tadalafil,
vardenafil) for erectile dysfunction within the last 48 hours.
• Seek immediate specialist input from the interventional cardiology team .[4]
• If you are managing the patient at a non-PCI capable hospital , contact the interventional
cardiology team at your designated PCI-capable hospital to discuss immediate transfer .
Do not give anticoagulant therapy if the patient is likely to be eligible for primary PCI. [4] [10]
• Anticoagulation will be started by the interventional cardiology team in the catheterisation

laboratory.
• If the patient is having fibrinolysis , start anticoagulation at the same time.[4] [10] [23] Select
enoxaparin or unfractionated heparin (unless streptokinase is used for thrombolysis, in which case
choose fondaparinux). Continue anticoagulation until revascularisation (if fibrinolysis is followed by
PCI) or for the duration of hospital stay up to a maximum of 8 days.[4] [10]
In a patient who has had a return of spontaneous circulation (ROSC) after an out-of-hospital
cardiac arrest :[4] [81] [82] [83] [84] [85]
• Primary PCI is the treatment of choice if there is ST-segment elevation on the post-ROSC
ECG or life-threatening arrhythmia#
• If there is no ST-segment elevation on the post-ROSC ECG then:
• Exclude non-coronary causes of cardiac arrest

• Perform urgent echocardiography
• Strongly consider a referral to cardiology for urgent angiography if there is a high index of
suspicion of ongoing myocardial ischaemia despite no ST-segment elevation
• When deciding whether to take a survivor of cardiac arrest (with or without ST-segment elevation)
to the catheterisation laboratory for urgent angiography ± PCI:[4]
• Consider each case on its individual merits and seek senior advice
• Take account of factors associated with the cardiac arrest that will influence the chance of a
good neurological outcome .
If your STEMI patient has cardiogenic shock , seek urgent senior support – coronary angiography ±
PCI is indicated.[4] [23]
Key Recommendations
MANAGEMENT
If there is a high clinical suspicion of STEMI or a clinical diagnosis of STEMI has been made,
seek immediate specialist input from cardiology .
The established cornerstone of STEMI management is a combined strategy of:[4] [23]
• Coronary reperfusion therapy – primary PCI or fibrinolysis plus

• Antithrombotic therapy – with dual antiplatelet therapy and anticoagulation.
• Dual antiplatelet therapy is started immediately and normally continued for at least 12
months.[4] [23]
MANAGEMENT
71
Choice of coronary reperfusion therapy
MANAGEMENT
Selection of the most appropriate reperfusion strategy. PPCI, primary percutaneous coronary intervention
For most patients with STEMI, primary PCI is the preferred reperfusion strategy provided it can
be delivered within 120 minutes of the time when fibrinolysis could have been given .[23] [28]
• Multiple trials have shown it has bet ter outcomes (in terms of reduced mortality, reinfarction, or
stroke) and less intracranial bleeding than fibrinolysis if administered in a timely manner
by an experienced team.
Select primary PCI as the preferred reperfusion strategy in patients with acute STEMI, if both the
following apply:[23] [28]
• Symptom onset <12 hours ago AND

• PCI can be delivered as soon as possible and at the latest within 120 minutes of the time
when fibrinolysis could have been given .
Give fibrinolysis (unless contraindicated) if there is a lack of access to timely primary PCI.[4] [23]
Give anticoagulation at the same time as giving fibrinolysis. Give dual antiplatelet therapy immediately
afterwards.[23]
• The UK National Institute for Health and Care Excellence recommends a fibrin-specific drug such
as alteplase or tenecteplase . It also recommends streptokinase (a non-fibrin-specific drug) as
an option in some patients. Check local protocols for advice on choice of fibrinolytic drug.[86]
• Fibrinolysis can be administered as part of the pre-hospital management of STEMI, in which case
an intravenous bolus dose of tenecteplase (or reteplase if available) is preferred as the other drugs
are administered by intravenous infusion.[4] [86]
• If your patient is not at a PCI-capable hospital, transfer them to one immediately after
fibrinolysis has been given.
• Assess the success of fibrinolysis with an ECG after 60-90 minutes.[23]
• If it has failed, offer immediate coronary angiography, with follow-on PCI if

indicated. Do not repeat fibrinolytic therapy .[4] [23]
If primary PCI cannot be delivered within 120 minutes of STEMI diagnosis and the patient’s
symptom onset was >2-3 hours ago, seek a specialist cardiology opinion to support your choice
of reperfusion strategy.[4] [10] [87]
• The clinical efficacy of thrombolysis diminishes as the time from symptom onset increases.[20] [88]
• Therefore, the later the patient presents (particularly if >2-3 hours) the more consideration should
be given to transferring for primary PCI instead, even if the delay is likely to exceed 120
minutes.[4] [22]
If your patient experiences spontaneous resolution of ST-segment elevation and complete
symptom relief after taking glyceryl trinitrate :[4]
• Refer to cardiology
• Aim for early coronary angiography within 24 hours.
Seek immediate specialist advice from cardiology for any patient who presents >12 hours
after symptom onset.
MANAGEMENT
• Coronary angiography ± primary PCI should be considered if there is:
73
• ECG evidence of continuing ischaemia and/or dynamic ECG changes, ongoing symptoms
of myocardial ischaemia, symptoms and/or signs of heart failure, shock, or malignant
arrhythmias.[4]
If your patient has ongoing ischaemic symptoms suggestive of MI BUT no ST-segment

elevation on the ECG, primary PCI should be considered if one or more of the following is
present :[4]
• Cardiogenic shock or haemodynamic instability

• Acute heart failure
• Ongoing or recurrent chest pain refractory to pharmacological treatment
• Cardiac arrest or life-threatening arrhythmia
• Signs and symptoms suggestive of mechanical complications of acute MI
• Dynamic ST-segment or T-wave changes, especially intermittent ST-segment elevation.
Time targets for the management of STEMI

The benefits of reperfusion in reducing mortality and improving myocardial salvage decline
rapidly with time. [4] [23]
• It is, therefore, vital to take every step possible to ensure the chosen reperfusion strategy
(primary PCI or fibrinolysis) is delivered as quickly as possible .
The 2017 European Society of Cardiology STEMI guideline sets widely accepted maximum
time-to-treatment targets as follows . [4]
MANAGEMENT
Interval Target
First medical contact to ECG and STEMI ≤10 minutes

diagnosis
STEMI diagnosis to primary PCI ≤120 minutes
If this time target cannot be met, consider

fibrinolysis
STEMI diagnosis to primary PCI if the patient’s ≤60 minutes if the patient presents to or is in a
first medical contact is at a hospital PCI-capable hospital
≤90 minutes if the patient presents to or

is in a non-PCI-capable hospital and needs
transferring
STEMI diagnosis to administration of a bolus/ ≤10 minutes

infusion of a fibrinolytic drug (if primary PCI
cannot be accessed within 120 minutes)
Start of fibrinolysis to ECG assessment of its 60-90 minutes

success or failure
If fibrinolysis is successful, time interval 2-24 hours

from starting fibrinolysis to early coronary
angiography
Long-term management of STEMI

Long-term management should include aspirin (plus a P2Y 12 inhibitor for up to 12 months as part of dual
antiplatelet therapy), an ACE inhibitor, a beta-blocker, and a statin, as well as cardiac rehabilitation and
modification of risk factors for cardiovascular disease.[15] [23]
Full Recommendations
Treatment goals
The established cornerstone of STEMI management is a combined strategy of :[4] [23]
• Coronary reperfusion therapy – either primary percutaneous coronary intervention or

fibrinolysis
AND
• Antithrombotic therapy – with dual antiplatelet therapy and anticoagulation.

MANAGEMENT
The aim is to restore myocardial blood flow as quickly as possible and within guideline-
mandated target times to :[4] [10] [21] [22]
• Achieve pain relief
75
• Limit myocardial damage/necrosis
• Reduce subsequent myocardial remodelling, which can have an adverse effect on predominantly
left ventricular and overall function
• Minimise morbidity and mortality by preventing or limiting the effect of both electrical and
mechanical complications of acute MI.
Initial treatment for all patients with suspected STEMI

as possible , unless they have aspirin hypersensitivity.[23]
• Aspirin can be given orally (or via nasogastric tube if oral ingestion is not possible).[4] An
intravenous loading dose is used in some countries; however, this formulation is not available in the
UK.
Check your local protocol or discuss the patient with a senior colleague if they have hypersensitivity to
aspirin.
After the loading dose, continue with a lower maintenance dose of aspirin as part of ongoing dual
antiplatelet therapy unless contraindicated.
Initial treatment for all patients with a clinical diagnosis

of STEMI
Start treatment for STEMI immediately after making a clinical diagnosis – do not wait for
cardiac troponin levels to confirm it. [4]
• Make a clinical diagnosis of STEMI based on a combination of:
• Signs and symptoms of myocardial ischaemia, plus

• Persistent or increasing ST elevation on the ECG .
Perform all of the following in tandem as soon as a clinical diagnosis of STEMI has been
made. [4] [10] [23]
• Immediately assess the patient’s eligibility for coronary reperfusion therapy. [4] [23]
• If eligible, take steps to ensure coronary reperfusion therapy is delivered as quickly as

possible – see Choice of coronary reperfusion therapy below.
• Do not allow the patient’s age, ethnicity, or sex to influence your assessment of their
suitability for reperfusion therapy.[23] Evidence suggests that women tend to receive
reperfusion therapy less frequently and/or in a more delayed fashion than men, even though
it has equal benefits for both sexes.[4]
• Gain intravenous access and start continuous haemodynamic monitoring and pulse
oximetry. [4]
MANAGEMENT
Practical tip
When placing an intravenous cannula, avoid placing it in the right hand or right wrist area
as the right radial artery is the usual route used to perform primary percutaneous coronary
intervention.
• Give pain relief. [4] [23]
• Titrated intravenous opioids (e.g., morphine, diamorphine) are the most commonly used
option. Give an intravenous anti-emetic concomitantly to prevent vomiting.
• Pain relief is crucial not just for the comfort of the patient but also because the pain is
associated with sympathetic activation, which causes vasoconstriction and increases the
workload of the heart.[4]
• Consider an intravenous nitrate (e.g., glyceryl trinitrate, isosorbide dinitrate). [4] [23]
• Routine use of an intravenous nitrate in STEMI is not recommended as there is no evidence

to support its benefits. However, an intravenous nitrate may be useful in patients who
have:[4]
• Persistent chest pain despite administration of sublingual (or buccal)

glyceryl trinitrate (which the patient may have received before arriving at hospital)
• Clinical and/or radiographic evidence of congestive heart failure .
• Titrate the rate of infusion according to the patient’s blood pressure and
wider clinical response.
• Do not give an intravenous nitrate when there is:
• Hypotension secondary to right ventricular infarction (usually complicating an inferior

or extensive anterior STEMI)
• Hypotension secondary to severe aortic stenosis or left ventricular outflow tract
obstruction
• Hypotension secondary to pre-existing cardiomyopathy
• Persistent hypotension secondary to other causes
• Use of a phosphodiesterase-5 inhibitor (e.g., avanafil, sildenafil, tadalafil, vardenafil)
for erectile dysfunction within the last 48 hours.
• Give ox ygen therapy only if saturations are <90% on pulse oximetry. [4]
• Routine supplemental oxygen is not indicated if arterial oxygen saturation (SaO 2 ) ≥90%.[89]
[90] [91]
Evidence: Ox ygen therapy in patients with acute MI
There is no evidence from randomised controlled trials (RCTs) to support the routine use of inhaled
MANAGEMENT
oxygen in people with acute MI without hypoxia, but guidelines vary on their specific recommendations.
There are different recommendations in guidelines on the thresholds for starting ox ygen
therapy. Guidelines also vary on recommended upper limits for ox ygen saturation once
ox ygen has been started.#
77
• The 2017 ESC guideline on the management of STEMI recommends that routine oxygen
is not given if the arterial oxygen saturation is ≥90%.[4] The evidence underpinning this
recommendation includes the AVOID study, a Cochrane review, and the protocol for the
DETO2X-AMI (all discussed below).[89] [90] [91] This guideline recommends oxygen therapy for
hypoxic patients with an oxygen saturation <90% (based on limited evidence).
• A 2018 BMJ Rapid Recommendation also recommends that oxygen therapy is not initiated in
patients with acute MI if the oxygen saturation is ≥90%.[92] This is based on the findings from
a large systematic review and meta-analysis that liberal oxygen therapy was associated with
higher mortality than conservative oxygen therapy in adults with acute illness (see below).[93]
• The NICE guideline on chest pain of recent onset, last updated in 2016, recommends that
supplemental oxygen is not routinely offered to patients with suspected acute coronary
syndrome.[29] It recommends oxygen therapy if the patient has an oxygen saturation <94%
and is not at risk of hypercapnic respiratory failure, aiming for a saturation of 94% to 98%. For
patients with COPD who are at risk of hypercapnic respiratory failure, it recommends a target
oxygen saturation of 88% to 92%, until blood gas analysis is available.[29]
• The 2016 Scottish Intercollegiate Guidelines Network (SIGN) guideline on acute coronary
syndrome does not include a specific recommendation on the use of oxygen but does refer to a
2013 Cochrane review stating that it found no conclusive evidence to support the routine use of
inhaled oxygen in patients with acute MI.[94] [95]
There is a lack of evidence to support the routine use of ox ygen in patients with acute MI
when there is no hypoxia, although ox ygen therapy has commonly been used as part of
the initial management of patients with STEMI.
• A 2018 systematic review and meta-analysis including 7 randomised trials and a total of 7702
patients with acute MI without hypoxaemia found that routine supplemental oxygen did not
reduce:[96]
• Mortality
• Arrhythmias
• Heart failure
• Recurrent ischaemic events.
• The DETO2X-AMI multicentre RCT (published in 2017) compared supplemental oxygen therapy
(6 L/min) with ambient air in 6629 patients with suspected acute MI and an oxygen saturation
level of ≥90% on pulse oximetry and found no significant difference in death from any cause at 1
year (hazard ratio 0.97; 95% CI 0.79 to 1.21; P=0.80).[97]
• A 2016 Cochrane review including 5 RCTs compared oxygen with air in 1173 people within 24
hours of onset of suspected or proven acute MI (STEMI or non-STEMI). It found no difference
in mortality, pain, or infarct size and the authors stated that they could not rule out a harmful
effect.[91]
• One 2015 RCT of 441 patients with proven STEMI (the AVOID study, included in the Cochrane
review above) found that patients receiving oxygen (at 8 L/min) had similar mean peak troponin
levels but significantly increased creatine kinase levels compared with those receiving air.[89]
MANAGEMENT
Patients randomised to receive air, were given oxygen via nasal cannula (4 L/min) or face mask
(8 L/min) if their oxygen saturation fell below 94%, to maintain a target level of 94%. Infarction
size on cardiac magnetic resonance at 6 months was increased in patients with oxygen therapy
compared with air.[89]
Regarding the upper limit for target ox ygen saturation once ox ygen has been started,
evidence from a large systematic review and meta-analysis on ox ygen use in acutely ill
adults not at risk of hypercapnic respiratory failure (including those with MI) supports a
96% upper limit for target ox ygen saturation.#
• A large systematic review (published in 2018) of 25 RCTs and over 16,000 patients, including
a meta-analysis, found that in adults with acute illness (including MI, but also including sepsis,
critical illness, stroke, trauma, cardiac arrest, and emergency surgery), liberal oxygen therapy
(broadly equivalent to a target saturation >96%) is associated with higher mortality than
conservative oxygen therapy (broadly equivalent to a target saturation ≤96%).[93]
• In-hospital mortality was 11 per 1000 higher with liberal oxygen therapy versus conservative
oxygen therapy (95% CI 2 to 22 per 1000 more). Mortality at 30 days was also higher with
liberal oxygen (RR 1.14; 95% CI 1.01 to 1.29). Studies that were limited to people with chronic
respiratory illness or psychiatric illness, on extracorporeal life support, receiving hyperbaric
oxygen therapy, or having elective surgery were all excluded from the review.[93]
A lower target ox ygen saturation of 88% to 92% is appropriate if the patient is at risk of
hypercapnic respiratory failure. [98]
• Give a P2Y 12 inhibitor in addition to aspirin given in the initial phase, as part of dual
antiplatelet therapy.
• Check your local protocol when deciding which P2Y 12 inhibitor to use and the timing of this.
• The UK National Institute for Health and Care Excellence (NICE) recommends the
following:[23]
• If the patient is eligible for primary percutaneous coronary intervention (PCI),

start dual antiplatelet therapy during PCI :
• Prasugrel, in combination with aspirin, if the patient is not already taking an oral
anticoagulant
• For patients aged 75 years and over, the bleeding risk of using prasugrel
needs to be weighed up against its effectiveness. If the bleeding risk from
prasugrel is a concern in these patients, ticagrelor or clopidogrel may be
used as alternatives
Practical tip
At present, many hospitals in the UK use ticagrelor rather than prasugrel

in patients who are not already on an oral anticoagulant. This 2020
guidance update from NICE will require a change in current practice in the
UK.
• Clopidogrel, in combination with aspirin, if the patient is already taking an oral
MANAGEMENT
anticoagulant
• If the patient is having fibrinolysis, start dual antiplatelet therapy immediately
afterwards :
79
• Ticagrelor, in combination with aspirin, unless the patient has a high bleeding
risk
• Clopidogrel, in combination with aspirin, or aspirin alone, for patients with a high
bleeding risk.
• Seek immediate specialist input from the interventional cardiology team. [4]
• If you are managing the patient within a PCI-capable hospital, this team will be available on
site. If not, call the interventional cardiology team at your designated PCI-capable hospital to
discuss immediate transfer for coronary reperfusion therapy.
Practical tip
D o not give anticoagulation therapy if the patient is likely to be eligible for primary PCI.
[4] [10]
• This will be given by the interventional cardiology team in the cardiac catheterisation laboratory.
Practical tip
Administration of an intravenous nitrate should not delay transfer to the

catheterisation laboratory.
• An intravenous nitrate can be given in the catheterisation laboratory by the interventional
cardiology team, if needed.
• Recanalisation of the occluded infarct artery is the most effective way of relieving refractory
chest pain, so the priority is to get the patient to primary PCI as quickly as possible.
Choice of coronary reperfusion therapy for different

patient groups
For most patients with STEMI, primary percutaneous coronary intervention (PCI) is the
preferred reperfusion strategy. [4] [23] [28]
• Multiple randomised controlled trials have shown that primary PCI has bet ter outcomes
(in terms of reducing mortality, reinfarction, or stroke) and less intracranial bleeding than
fibrinolysis provided it can be delivered in a timely manner by an experienced team.[4] [99] [100]
[101] [102] [103] [104]
• However, fibrinolysis may be more appropriate when there is a lack of access to timely
PCI.[4] [23]
The most appropriate coronary reperfusion strategy will depend on :[4] [10] [22]
• Duration of ischaemic symptoms

• Persistence or resolution of ST-segment elevation on serial ECGs
• Availability of timely access to primary PCI
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• Whether a patient is first assessed in a PCI-capable or non-PCI-capable hospital

• Estimated transfer time from a non-PCI-capable to a PCI-capable hospital
• Whether there was a pre-hospital STEMI diagnosis made by trained and fully equipped paramedic
team who can administer initial pharmacotherapy
• The quality and expertise of the regional network infrastructure in place for STEMI management.
Many patients who present with STEMI are already taking long-term oral anticoagulation for
various indications. [4]
• This is a relative contraindication for fibrinolysis .

• For any such patient, choose a primary PCI strategy for coronary reperfusion therapy,
regardless of the anticipated time to access this intervention.[4]
Concurrent anticoagulation and dual antiplatelet therapy is given alongside coronary
reperfusion, regardless of whether primary PCI or fibrinolysis is used.
• Seek specialist advice if the patient has a separate indication for ongoing oral anticoagulation.
The flowchart below summarises the choice of coronary reperfusion strategy according to time since the
patient’s symptom onset and the anticipated time to access primary PCI.[4] [23]
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Selection of the most appropriate reperfusion strategy. PPCI, primary percutaneous coronary intervention
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Patients presenting <12 hours from symptom onset
Primary PCI
Select primary PCI as the preferred reperfusion strategy for any patient who had symptom
onset <12 hours ago and has :[4] [23] [99] [100] [101] [102] [105]
• Ongoing signs and symptoms of myocardial ischaemia, AND

• Persistent (or increasing) ST-segment elevation on ECG.
Take steps to ensure that primary PCI will be delivered within 120 minutes of the time when
fibrinolysis could have been given. [23] [28]
• Primary PCI involves immediate transfer to the catheterisation laboratory with the intention of
opening the artery with stent placement. Drug-eluting stents are recommended by the European
Society of Cardiology (ESC) and National Institute for Health and Care Excellence guidelines.[4]
[23]
• Many hospitals have round-the-clock PCI capability . If yours does not, then arrange
immediate transfer to your designated PCI-capable hospital .
• If it is not possible to ensure primary PCI within 120 minutes of the time when
fibrinolysis could be started, offer fibrinolysis (if not contraindicated) . [23] #
• If your patient has STEMI with cardiogenic shock, seek urgent senior support. Coronary
angiography ± primary PCI is indicated.[4] [23]
• If the patient’s coronary anatomy is unsuitable for PCI, or PCI fails, emergency coronary artery
bypass graft ( CABG ) is recommended.[4]
• See our topic Shock for more information on supportive management.
Practical tip
If your patient experiences a spontaneous resolution of ST-segment elevation, along

with complete symptom relief, after taking glyceryl trinitrate, this is suggestive of
coronary spasm with or without associated MI. [4]
• Refer to cardiology.
• Aim for early coronary angiography (within 24 hours).
More info: PCI angiograms – inferior STEMI case example
Left main coronary artery: right anterior oblique view MANAGEMENT
83
Left main coronary artery: right anterior oblique view

• 70-year-old man admitted with crushing central chest pain

• Inferior ST elevation on ECG
• This would suggest a right coronary artery (RCA) occlusion so an angiogram of the left coronary
artery system with a diagnostic catheter are taken first
• Bear in mind an inferior STEMI can also be associated with a left circumflex (LCx) occlusion
• This view allows you to see:
• Left main stem (LMS) (blue arrow)

• Proximal left anterior descending (LAD) artery (orange arrow)
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• True atrioventricular circumflex (AVCx) (red arrow), which is a small vessel in this case
• A large obtuse marginal (OM) branch artery of the LCx
Left main coronary artery: posterior anterior cranial view
Left main coronary artery: posterior anterior cranial view

• This view shows the LAD artery

• The LAD artery here is diffusely diseased throughout its mid course (purple arrows)
• Septal branches of the LAD artery are indicated by the turquoise arrows
• The red arrow corresponds to a diagonal branch of the LAD artery
• The LMS is shown by the blue arrow
Right coronary artery: left anterior oblique view
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85
Right coronary artery: left anterior oblique view

• As the initial left coronary artery angiogram showed no occlusion, we would typically assume
the occlusion is in the RCA
• Therefore, a guide catheter (stiffer and larger calibre compared with a diagnostic catheter) would
be used to intubate the RCA ostium
• Here the initial angiogram confirms an acute total occlusion of the mid RCA (blue arrow)
Coronary guidewire deployment
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Coronary guidewire deployment

• Before introducing any equipment into a coronary artery, the patient is given a bolus dose of
unfractionated heparin anticoagulation, adjusted according to weight
• A coronary guidewire is then deployed into the distal RCA (red arrow)
• Introduction of the guidewire already starts to restore coronary flow (green arrows)
First balloon dilatation
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87
First balloon dilatation

• A balloon is passed over the coronary guidewire and inflated across the point of the original
acute occlusion (blue arrow)
Restoration of coronary flow
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Restoration of coronary flow

• The first balloon inflation restores flow to the RCA

• Now the full outline of the artery can be seen
• The area of stenosis and likely atherosclerotic plaque rupture is shown by the blue arrow
Stent positioning
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89
Stent positioning
• The proximal (red arrow) and distal (blue arrow) stent markers are shown here
• A decision has been made to stent from what is perceived to be ‘normal’ artery to ‘normal’ artery
covering the culprit lesion
Stent deployed
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Stent deployed
• The stent is sized according to diameter and length in millimetres

• Stent deployment transiently re-occludes the vessel, which can cause pain for the patient and
haemodynamic changes
After stent deployment
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91
After stent deployment

• The stent is now expanded within the RCA

• There remains an area of underexpanded stent as shown by the blue arrow
• Underexpansion can be seen directly using intravascular ultrasound (IVUS) or optical coherence
tomography (OCT)
• Here the underexpansion assumption is based solely on angiographic appearance
Stent post-dilatation
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Stent post-dilatation
• A post-stent balloon dilatation (blue arrow) is performed to ensure adequate stent expansion
• Underexpansion of a stent can lead to acute stent thrombosis
RCA primary angioplasty: final result
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93
RCA primary angioplasty: final result

• There is an excellent angiographic result

• The stent appears fully expanded angiographically with reference to the proximal and distal
vessel
Left anterior descending artery pre-dilatation
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Left anterior descending artery pre-dilatation image 1

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95

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97

• Complete versus infarct-related artery-only (IRA) revascularisation in patients with multi-vessel

disease during STEMI remains an area of open debate
• The ESC STEMI guideline advocates non-IRA revascularisation in patients with cardiogenic
shock[4]
• Otherwise the ESC recommends routine revascularisation of non-IRA lesions before hospital
discharge rather than during the index primary angioplasty procedure
• In this case the decision was made to revascularise the LAD during the index procedure
• A coronary guidewire is deployed in the distal LAD (image 1)
• The mid (image 2) and proximal (image 3) LAD is then dilated with a balloon
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• Image 4 shows the LAD after the serial balloon dilatations

Mid-LAD artery stent deployment
Mid-LAD artery stent deployment image 1 - stent positioned in the mid-LAD artery

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99
Mid-LAD artery stent deployment image 2 - stent balloon inflated

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Mid-LAD artery stent deployment image 3 - post mid-LAD stent deployed

Proximal LAD stent deployment
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101
Proximal LAD stent deployment image 1 - following the mid-

LAD stent deployment the proximal vessel is pre-dilated
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Proximal LAD stent deployment image 2 - proximal stent is positioned with the distal marker
(blue arrow) overlapping/within the proximal end of the previously deployed mid-LAD stent
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103
Proximal LAD stent deployment image 3 - proximal stent deployed

Post-dilatation of overlapping stents

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Post-dilatation of overlapping stents

• The same balloon of the proximal stent is then used to post-dilate the overlap between the
proximal and mid-LAD stents
Final LAD stenting result
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Final LAD stenting result: posterior anterior cranial view

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Final LAD stenting result: right anterior oblique cranial view

Conclusion :
• The patient had complete coronary revascularisation with primary angioplasty to the occluded
RCA and non-IRA angioplasty to the LAD artery. The patient made an excellent recovery and
was discharged home 72 hours after admission.
Fibrinolysis
Give fibrinolysis (unless contraindicated) if primary PCI cannot be delivered within 120
minutes of the time when fibrinolysis could be given. [23] [28]
MANAGEMENT
• The ESC recommends that fibrinolysis should be given within 10 minutes of making the clinical
diagnosis of STEMI.[4]
107
• Check your local protocols for advice on the preferred fibrinolytic drug and how it should be
administered. See Choice of fibrinolytic drug below.
• Start anticoagulation at the same time as giving fibrinolysis and start dual antiplatelet therapy
immediately afterwards.[4] [10] [23] See Antithrombotic co-therapy given with fibrinolysis below.
If primary PCI cannot be delivered within 120 minutes of STEMI diagnosis and the patient
has presented >2-3 hours after symptom onset, seek a specialist cardiology opinion to
support your choice of reperfusion strategy. [4] [10] [87]
• The greatest benefit of fibrinolysis is observed when given <2 hours after symptom onset. Its
clinical efficacy diminishes as time from symptom onset increases .[20] [88]
• Therefore, the later the patient presents (particularly >2-3 hours), the more consideration should be
given to transferring for primary PCI instead – discuss the options with cardiology.[4] [22]
If your patient is not already at a PCI-capable hospital, transfer them to one immediately
after giving fibrinolysis. [4]
• This is so that rescue PCI can be performed if fibrinolysis fails or angiography ± PCI can be
arranged if fibrinolysis is effective.
Use an ECG 60-90 minutes after administering fibrinolysis to assess whether it has been
successful. [4] [23]
• If fibrinolysis has failed (<50% ST-segment resolution at 60-90 minutes), offer immediate
coronary angiography, with follow-on PCI if indicated. Do not repeat fibrinolytic therapy
.[4] [23]
• If fibrinolysis is successful , consider angiography during the same hospital admission for
patients who are clinically stable.[23]
• The ESC guidelines recommend arranging angiography ± PCI of the infarct-related artery
within 2-24 hours .[4]
• Several randomised trials and two meta-analyses have shown that early routine angiography
(with PCI if needed) after fibrinolysis reduces the rate of reinfarction and recurrent ischaemia
compared with a watchful waiting strategy. The benefits of early routine PCI following
fibrinolysis were seen across patient subgroups and without any increased risk of adverse
events such as stroke or major bleeding.[106] [107] [108]
• If the patient has recurrent myocardial ischaemia after fibrinolysis, seek immediate
specialist advice from cardiology . PCI may be indicated.[23]
The ESC guideline recommends immediate rescue PCI if, at any time following fibrinolysis,
the patient develops haemodynamic or electrical instability or worsening ischaemia. [4]
Emergency angiography ± PCI is recommended if, at any time following fibrinolysis, the
patient has :
• Heart failure or cardiogenic shock [4]

MANAGEMENT
• Recurrent ischaemia or evidence of re-occlusion after initially successful fibrinolysis.[4] [109]

[110]
Practical tip
The ESC STEMI guideline lists the contraindications to fibrinolytic therapy as follows
:[4]
• Absolute contraindications
• History of intracranial haemorrhage or stroke of unknown origin at any time

• Ischaemic stroke in the last 6 months
• Central nervous system damage, neoplasm, or arteriovenous malformation
• Major trauma/surgery/head injury within the last 1 month
• Gastrointestinal bleeding within the last 1 month
• Bleeding disorder
• Aortic dissection
• Non-compressible punctures within the last 24 hours (e.g., liver biopsy, lumbar puncture)
• Relative contraindications
• Chronic oral anticoagulant therapy

• Pregnancy or within 1 week postnatal
• Refractory hypertension (systolic BP >180 mmHg and/or diastolic BP >110 mmHg)
• Transient ischaemic attack in the last 6 months
• Advanced liver disease
• Infective endocarditis
• Active peptic ulcer
• Prolonged or traumatic cardiopulmonary resuscitation.
If primary PCI is not available within 120 minutes but your patient has a
contraindication to fibrinolysis :
• It is important to weigh up the potentially life-saving benefits of fibrinolysis against its potentially
life-threatening adverse effects, bearing in mind alternative treatment options such as delayed
primary PCI.[4] Seek immediate advice from the interventional cardiology team
• For a patient with an absolute contraindication to fibrinolysis, primary PCI will normally be the
preferred management strategy despite the delay in accessing it.
Evidence: Role of fibrinolysis in STEMI
Fibrinolytic therapy remains an important evidence-based intervention in settings where primary PCI
cannot be offered in a timely manner.
Two landmark studies demonstrated the benefits of fibrinolysis in patients with STEMI
(prior to the advent of primary PCI).
• The Fibrinolytic Therapy Trialists’ Collaborative Group (1994) demonstrated highly

significant benefits in saving lives and helped to establish the time window when fibrinolytic
therapy is most effective.[88]
MANAGEMENT
• The study demonstrated highly significant absolute mortality reductions from fibrinolysis of
about:
109
• 30 per 1000 for those presenting within 0-6 hours of symptom onset
• 20 per 1000 for those presenting 7-12 hours after symptom onset.
• There was a statistically uncertain benefit of about 10 per 1000 for those presenting at
13-18 hours (with more randomised evidence needed in this group to assess reliably the
net effects of treatment).
• The 1993 GUSTO trial [111] [112] compared different fibrinolysis strategies.
• It demonstrated a benefit of 14% reduction in mortality (95% CI, 5.9% to 21.3%) for
an accelerated tissue plasminogen activator (t-PA) versus streptokinase (the standard
fibrinolytic treatment at the time). Alteplase (recombinant t-PA) was used in the trial.
• The trial randomly assigned 41,021 patients with evolving acute MI to 4 different
fibrinolytic strategies. The data for the primary end point of 30-day mortality for each
treatment arm was as follows:
• Streptokinase plus subcutaneous heparin = 7.2%

• Streptokinase plus intravenous heparin = 7.4%
• t-PA plus intravenous heparin = 6.3%
• Streptokinase plus t-PA plus intravenous heparin = 7.0%.
• A significant excess of haemorrhagic strokes was observed for accelerated t-PA (P =
0.03) and for the combination strategy (P <0.001), as compared with streptokinase only.
The 2013 STREAM trial provided further support for fibrinolysis as an appropriate
reperfusion strategy for STEMI when primary PCI cannot be delivered in a timely manner
– especially if followed by routine early angiography ± PCI (a 'pharmacoinvasive strategy').
[104]
• The STREAM trial was conducted at a time when primary PCI was established as the standard
of care for STEMI.
• In the trial, 1892 STEMI patients presenting within 3 hours of symptom onset but unable to have
primary PCI within 1 hour were randomly assigned to:
• Primary PCI or
• Pre-hospital bolus tenecteplase (with a half-dose used in patients ≥75 years) plus
clopidogrel plus enoxaparin before transport to a PCI-capable hospital
• Patients had emergency angiography if fibrinolysis failed

• If fibrinolysis was successful, patients had routine angiography within 6-24 hours
after randomisation.
• There was no significant difference between the primary PCI and fibrinolysis groups in the
primary composite end point of death, shock, congestive heart failure, or reinfarction within 30
days.
MANAGEMENT
• More intracranial haemorrhages occurred in the fibrinolysis group.
• The median time from randomisation to bolus of fibrinolytic was 9 minutes, which
has served as the basis for the ESC guideline recommendation that fibrinolysis
should be given within 10 minutes of STEMI diagnosis. [4]
The extent to which the delay-to-PCI time diminishes the advantages of primary PCI over
fibrinolysis has been widely debated, and more research is needed .[4]
• It is clear that if delay to treatment is similar, primary PCI is superior to fibrinolysis in reducing
mortality, reinfarction, or stroke.[4]
• However, fibrinolysis can be administered expeditiously and the longer the delay to
primary PCI, the lower the benefits over fibrinolysis. The exact cut-off point at which the
delay to access PCI makes fibrinolysis the better reperfusion strategy is based on weak
evidence.
Patients presenting >12 hours from symptom onset

Seek immediate specialist advice from cardiology to discuss management options for any
STEMI patient who presents >12 hours after symptom onset.
• Coronary angiography ± primary PCI should be considered if there is:

• ECG evidence of continuing ischaemia and/or dynamic ECG changes, ongoing symptoms
of myocardial ischaemia, symptoms and/or signs of heart failure, shock, or malignant
arrhythmias.[4]
If your patient has ongoing ischaemic symptoms suggestive of MI but no ongoing ST-
segment elevation on the ECG, primary PCI should be considered if one or more of the
following is present :[4]
• Cardiogenic shock or haemodynamic instability

• Ongoing or recurrent chest pain refractory to pharmacological treatment
• Cardiac arrest or life-threatening arrhythmia
• Signs and symptoms suggestive of mechanical complications of acute MI
• Dynamic ST-segment or T-wave changes, especially intermittent ST-segment elevation.
Discuss urgently with cardiology any patient who presents >12 hours after symptom onset
but has no ongoing symptoms .[4] [113]
• Routine primary PCI strategy should still be considered in patients presenting between 12 and 48
hours after symptom onset. However, if the time since symptom onset is >48 hours and the patient
is now asymptomatic, routine PCI of an occluded infarct-related artery is not recommended.
• Fibrinolysis is not indicated.
MANAGEMENT
Survivors of out-of-hospital cardiac arrest

Primary PCI is the treatment of choice for any patient in whom a return of spontaneous
circulation (ROSC) is achieved after cardiac arrest and who has :[4] [81] [82] [83] [84] [85]
111
• ST-segment elevation on their post-ROSC ECG , or

• Life-threatening arrhythmia .
In a patient who has been resuscitated from cardiac arrest but has no ST-segment elevation
on their post-ROSC ECG :[4]
• Exclude non-coronary causes of cardiac arrest:
• Non-cardiogenic shock
• Respiratory failure
• Cerebrovascular event
• Pulmonary embolism
• Hypothermia
• Hypoglycaemia
• Intoxication/poisoning
• Perform urgent echocardiography [4]
• Look for regional left ventricular wall motion abnormalities

• Identify other mechanical complications of acute MI
• Consider referral to cardiology for urgent angiography if there is a high index of
suspicion of ongoing myocardial ischaemia despite no ST-segment elevation, for example:
• Chest pain prior to cardiac arrest

• Presence of cardiac risk factors
• Established coronary artery disease or previous myocardial infarction
• Ambiguous or abnormal post-ROSC ECG.
To make a decision on whether to take a survivor of cardiac arrest (with or without ST-
segment elevation) to the catheterisation laboratory for urgent angiography ± PCI :[4]
• Consider each case on its individual merits and seek senior advice
• Take account of factors associated with a greater chance of a good neurological
outcome , including:
• A witnessed cardiac arrest

• Immediate bystander cardiopulmonary resuscitation and/or early arrival of emergency
medical services (<10 minutes)
• An initial shockable rhythm
• Sustained ROSC achieved within 20 minutes.
See our topic Cardiac arrest .
Target times for administering coronary reperfusion

The benefits of reperfusion in reducing mortality and improving myocardial salvage decline
MANAGEMENT
rapidly with time. [4] [23]
• It is, therefore, vital to take every step possible to ensure the chosen reperfusion strategy (primary
percutaneous coronary intervention [PCI] or fibrinolysis) is delivered as quickly as possible.
The 2017 European Society of Cardiology STEMI guideline sets widely accepted maximum
time-to-treatment targets as follows :[4]
Interval Target
First medical contact to ECG and STEMI ≤10 minutes

diagnosis
STEMI diagnosis to primary PCI ≤120 minutes
If this time target cannot be met, consider

fibrinolysis
STEMI diagnosis to primary PCI if the patient’s ≤60 minutes if the patient presents to or is in a
first medical contact is at a hospital PCI-capable hospital
≤90 minutes if the patient presents to or

is in a non-PCI-capable hospital and needs
transferring
STEMI diagnosis to administration of a bolus/ ≤10 minutes

infusion of a fibrinolytic drug (if primary PCI
cannot be accessed within 120 minutes)
Start of fibrinolysis to ECG assessment of its 60-90 minutes

success or failure
If fibrinolysis is successful, time interval 2-24 hours

from starting fibrinolysis to early coronary
angiography
Antithrombotic co-therapy for primary PCI
Choice of antiplatelet therapy for patients undergoing primary

PCI
Give any patient who will undergo primary percutaneous coronary intervention (PCI) dual antiplatelet
therapy with a P2Y 12 inhibitor plus aspirin .[23]
• After the initial aspirin loading dose, reduce the aspirin to a lower daily maintenance dose.
• Check your local protocol when deciding which P2Y 12 inhibitor to use, the timing of this, and the
recommended initial loading and ongoing daily doses.
The UK National Institute for Health and Care Excellence (NICE) recommends the following:[23]
MANAGEMENT
• Prasugrel, in combination with aspirin, if the patient is not already taking an oral anticoagulant
• For patients aged 75 years and over, the bleeding risk of using prasugrel needs to be
weighed up against its effectiveness. If the bleeding risk from prasugrel is a concern in these
patients, ticagrelor or clopidogrel may be used as alternatives
113
Practical tip
At present, many hospitals in the UK use ticagrelor rather than prasugrel in patients
who are not already on an oral anticoagulant. This new guidance by NICE will require a
change in current practice in the UK.
• Clopidogrel, in combination with aspirin, if the patient is taking an oral anticoagulant.

The European Society of Cardiology guideline recommends prasugrel or ticagrelor (in combination with
aspirin) as first-line options in patients undergoing primary PCI, with clopidogrel only indicated when
neither of these drugs is available or they are contraindicated.[4]
Cangrelor may be considered if the patient either has not yet received a loading dose of an
oral P2Y 12 inhibitor at the time primary PCI starts or is unable to ingest an oral drug. [4]
However, always follow your local protocol when deciding which P2Y 12 inhibitor to use and the timing of
this.
• Cangrelor is an intravenous reversible P2Y 12 inhibitor that has been shown to significantly reduce
periprocedural ischaemic complications at the time of PCI when compared with clopidogrel or
placebo.[114] [115] [116] [117]
• Much like ticagrelor and prasugrel, it increases the risk of bleeding given its greater antiplatelet
potency compared with clopidogrel.
• NICE has yet to make any recommendation on the use of cangrelor.
Practical tip
Do not use either ticagrelor or prasugrel in patients who :[4]

• Have a history of haemorrhagic stroke
• Have moderate to severe liver disease
• Are already taking chronic oral anticoagulation.
Prasugrel is also :[4]
• Contraindicated in patients with previous stroke or transient ischaemic attack
• Not generally recommended in patients aged ≥75 years or those with body weight <60 kg
• If prasugrel is recommended by the interventional cardiology team for these patient

groups, then a lower maintenance dose is advised.[4]
Do not give a glycoprotein IIb/IIIa inhibitor or fibrinolytics prior to primary PCI. [23]
• Glycoprotein IIb/IIIa inhibitors (e.g., eptifibatide, tirofiban, abciximab) may be used by the
interventional cardiology team during the PCI procedure to tackle a high thrombus burden or
no-reflow phenomenon. Abciximab is not currently available in the UK, and shortages in other
countries have been reported.
Evidence: Choice of P2Y 12 inhibitor for patients undergoing PCI

MANAGEMENT
Third-generation P2Y 12 inhibitors prasugrel and ticagrelor are preferred to clopidogrel as part of a dual
antiplatelet therapy regimen with aspirin for the treatment of STEMI in patients undergoing primary PCI
who are not already on oral anticoagulation.
In November 2020 the UK National Institute for Health and Care Excellence (NICE) updated its acute
coronary syndromes guidance. This included a network meta-analysis of dual antiplatelet therapy
that found prasugrel and ticagrelor were more effective than clopidogrel at both 30 days and 1 year.
Although there was some uncertainty at 30 days, prasugrel was more effective than ticagrelor at 1
year, especially for reducing all-cause mortality and reinfarction.[23] These results were driven by 3
large trials, as follows.
• In the TRITON-TIMI 38 trial, 13,608 acute coronary syndrome (ACS) patients awaiting PCI were
randomised to loading and maintenance doses of prasugrel versus clopidogrel.
• There was a significant reduction in favour of prasugrel in the combined primary end point
of cardiovascular mortality, non-fatal myocardial infarction (MI), or non-fatal stroke (9.9%
vs. 12.1%; hazard ratio [HR] 0.81, 95% CI 0.73 to 0.90; P <0.001).[118]
• The PLATelet inhibition and patient Outcomes (PLATO) trial randomised 18,624 patients
admitted to hospital with an ACS (with or without ST-segment elevation) to loading and
maintenance doses of ticagrelor versus clopidogrel.
• There was a significant reduction in favour of ticagrelor in the 12-month primary efficacy
end point of cardiovascular death, MI, or stroke (9.8% vs. 11.7%; HR 0.84, 95% CI 0.77
to 0.92; P <0.001).
• Of note, the ticagrelor group also had significantly lower all-cause mortality (4.5% vs.
5.9%, P <0.001).[119]
• The ISAR-REACT 5 trial, in which 4018 ACS patients awaiting PCI were randomised to
ticagrelor versus prasugrel.
• There was a significant reduction in favour of prasugrel in the 12-month primary efficacy
end point of all-cause mortality, MI, or stroke (9.3% with ticagrelor vs. 6.9% with
prasugrel; HR 1.36, 95% CI 1.09 to 1.70; P = 0.006).[120]
The faster onset of action and greater antiplatelet potency of prasugrel and ticagrelor
(compared with clopidogrel) means they carry a greater risk of bleeding. Therefore,
clopidogrel is preferred in people already taking an oral anticoagulant.
• In the TRITON-TIMI trial, the prasugrel group had a higher risk of life-threatening bleeding
versus the clopidogrel group (1.4% vs. 0.9%; P = 0.01).[118]
• In the PLATO trial, ticagrelor was associated with a higher rate of major bleeding unrelated to
coronary artery bypass grafting compared with clopidogrel (4.5% vs. 3.8%).[119]
• In the ISAR-REACT 5 trial there was no significant difference in major bleeding between
ticagrelor versus prasugrel (HR 1.12, 95% CI 0.83 to 1.51).[120]
The evidence is less certain for people aged 75 years and over and a reduced dose of
prasugrel or alternative treatment should be considered on an individual basis.
• NICE noted that the TRITON-TIMI trial adverse events, including major bleeding, were more
MANAGEMENT
common with prasugrel than with clopidogrel in people aged 75 years and over. Subsequent
trials used a reduced dose of prasugrel in this age group and did not find an increased risk of
bleeding.
115
• NICE also stated that more research is required comparing the efficacy of prasugrel,
ticagrelor, and clopidogrel in people aged 75 years and over.[23]
The European Society of Cardiology guideline recommends prasugrel or ticagrelor (in combination
with aspirin) as first-line options in patients undergoing primary PCI, with clopidogrel only indicated
when neither of these drugs is available or they are contraindicated.[4]
Choice of anticoagulant therapy for patients undergoing primary

PCI
Anticoagulation is routinely given during primary PCI.
• This will be started by the interventional cardiology team in the cardiac catheterisation
laboratory.
• Therefore, do not start anticoagulation if your patient is likely to be eligible for primary
PCI.
The recommended options for intravenous anticoagulation are :
• Unfractionated heparin, for patients undergoing primary PCI with radial access[4] [23]
• Bivalirudin (a direct thrombin inhibitor), for patients undergoing PCI with femoral access[4] [23]
• Enoxaparin.[4]
Fondaparinux is not recommended as an adjunctive anticoagulant during primary PCI. [4]
• It was associated with catheter thrombosis at the time of primary PCI in the OASIS-6 trial.[121]
Routine post-procedural anticoagulation is not required after primary PCI unless there is a
separate indication for it, for example:[121]
• Full-dose anticoagulation:
• Atrial fibrillation
• Mechanical heart valve
• Left ventricular thrombus
• Prophylactic-dose anticoagulation:
• Patients at high risk of venous thromboembolism.
Choice of fibrinolytic drug

If the delay to primary percutaneous coronary intervention (PCI) means fibrinolysis is
selected as the most appropriate reperfusion strategy, check your local protocols regarding
the choice of fibrinolytic drug.
MANAGEMENT
The UK National Institute for Health and Care Excellence recommends a fibrin-specific drug such as
alteplase or tenecteplase .[23] It also recommends streptokinase (a non-fibrin-specific drug) as an
option in some patients.[86]
The European Society of Cardiology guideline recommends the same drugs plus reteplase (no longer
available in the UK).[4] According to these guidelines, you should consider a half-dose of tenecteplase if
the patient is aged 75 years or older.[4]
When choosing a fibrinolytic drug take account of:[86]
• Balancing the benefit and harm (e.g., stroke risk) of each drug for the individual patient
• The importance of avoiding giving streptokinase to a patient who has received it in the past
(patients treated with streptokinase may develop antibodies that neutralise the drug if repeat
treatment is given)
• Your local hospital protocol for reducing delays in the administration of thrombolysis.
To shorten the time to treatment, fibrinolysis can be administered as part of the pre-hospital
management of STEMI. [4] [86]
• This may be part of the emergency care treatment pathway where geographical considerations
mean the anticipated time to primary PCI will be >120 minutes.
• In such cases, a bolus dose of tenecteplase ( or reteplase if available) is preferred for the
sake of practicality as the other fibrinolytic drug options are administered by intravenous infusion.
Transfer to a PCI-capable hospital is indicated in all patients immediately after
administration of fibrinolysis.
Antithrombotic co-therapy given with fibrinolysis

Antithrombotic co-therapy with fibrinolysis consists of a combination of :
• Dual antiplatelet therapy with a P2Y 12 inhibitor, in addition to aspirin given in the initial phase
• Parenteral anticoagulation.
Give any patient having fibrinolysis anticoagulation at the same time as giving fibrinolysis and
start dual antiplatelet therapy immediately afterwards (see below). [23]
The choice of parenteral anticoagulation can be any one of: [4]
• Enoxaparin – an intravenous bolus dose initially, followed by subcutaneous dosing in patients

<75 years of age (patients ≥75 years of age are given subcutaneous dosing only). The European
Society of Cardiology (ESC) guideline recommends this as the first-choice anticoagulant for
patients undergoing fibrinolysis[4] [122] [123] [124]
• Unfractionated heparin – a weight-adjusted intravenous bolus followed by an intravenous
infusion
• Fondaparinux (only if streptokinase is used for fibrinolysis) – an intravenous dose initially,
followed by the first subcutaneous dose given 24 hours later.[125]
Ensure anticoagulation co-therapy for any patient undergoing fibrinolysis continues :[4] [10]
• Up to the point of coronary revascularisation with percutaneous coronary intervention

MANAGEMENT
(PCI; if performed), or
• For at least the first 48 hours but ideally up until hospital discharge for a maximum of 8
days in total if revascularisation is not performed. [4]
If a pharmacoinvasive strategy is adopted (fibrinolysis followed by angiography ± PCI), then
one regimen that is supported by robust data is composed of :[4] [104] [109] [126] [127]
117
• Fibrinolysis with intravenous tenecteplase, plus

• Oral aspirin and clopidogrel, plus
• Intravenous enoxaparin at the time of fibrinolysis, plus
• Subcutaneous enoxaparin until the time of revascularisation by PCI.
Give the patient dual antiplatelet therapy with a P2Y 12 inhibitor plus aspirin immediately after
giving fibrinolysis .[23]
• After the initial aspirin loading dose, reduce the aspirin to a lower daily maintenance dose.
• Check your local protocol when deciding which P2Y 12 inhibitor to use, the timing of this, and the
recommended initial loading and ongoing daily doses.
The UK National Institute for Health and Care Excellence recommends the following:[23]
• Ticagrelor, in combination with aspirin, unless the patient has a high bleeding risk
• Clopidogrel, in combination with aspirin, or aspirin alone for patients with a high bleeding risk.
The ESC guideline recommends clopidogrel as the preferred agent.[4]
Evidence: Choice of P2Y 12 inhibitor for patients not undergoing PCI
Ticagrelor, a third-generation P2Y 12 inhibitor, is preferred to clopidogrel as part of a dual antiplatelet

therapy regimen with aspirin for the treatment of STEMI in patients who are not undergoing PCI.
In November 2020 the UK National Institute for Health and Care Excellence (NICE) updated its acute
coronary syndromes guidance. This included a network meta-analysis of dual antiplatelet therapy.[23]
• As prasugrel is only licensed for patients undergoing primary PCI the guideline committee
considered the evidence for ticagrelor versus clopidogrel for patients not undergoing PCI.
• Most of the evidence was from patients with unstable angina or non-STEMI, as the majority of
people with STEMI are managed with PCI; however, this mostly indirect population was felt to
be appropriate due to similarities in the basic pathophysiology and the consistent benefits of
ticagrelor over clopidogrel in all patients not undergoing PCI.
• Ticagrelor reduced reinfarction at 30 days and 1 year. There was some uncertainty around
mortality at 30 days but ticagrelor reduced all-cause and cardiac mortality at 1 year.
• Ticagrelor also reduced the need for revascularisation at 30 days and 1 year, and stent
thrombosis events at 1 year.
• Overall, the evidence did not show a clinically important harm with ticagrelor over
clopidogrel in terms of bleeding (major or minor) at 30 days or 1 year.
• There was a possible increased risk of stroke with ticagrelor compared with clopidogrel,
but the absolute difference in number of events was small and the confidence intervals
were wide.
• Breathing adverse events (e.g., shortness of breath) were more common with ticagrelor
MANAGEMENT
at 30 days and 1 year. However, the guideline committee considered these to be mostly
reversible.
• NICE reported a cost-effectiveness analysis study that showed in medically managed people
ticagrelor was cost-effective compared with clopidogrel.
The faster onset of action and greater antiplatelet potency of ticagrelor compared with clopidogrel
means it may carry a greater risk of bleeding.
• In the PLATelet inhibition and patient Outcomes (PLATO) trial, ticagrelor was associated with
a higher rate of major bleeding unrelated to coronary artery bypass grafting compared with
clopidogrel (4.5% vs. 3.8%).[119]
• The NICE guideline committee noted that most other studies excluded older people or other
groups of people at higher risk of bleeding, and was concerned about the trade off between
benefit and harm in these subgroups.
• Therefore, the committee agreed that clopidogrel plus aspirin or aspirin alone may be
more appropriate for people with a higher risk of bleeding.[23]
Patients not receiving immediate coronary reperfusion

therapy
Offer conservative medical management to any patient who is ineligible for any reperfusion therapy.[23]
Ensure the patient still receives dual antiplatelet therapy, anticoagulation, and all appropriate secondary
prevention therapies.[4] [23]
Check your local protocol when deciding which P2Y 12 inhibitor to use and the timing of this.
The UK National Institute for Health and Care Excellence recommends the following options for dual
antiplatelet therapy in patients who are not treated with percutaneous coronary intervention:[23]
• Ticagrelor, in combination with aspirin, unless the patient has a high bleeding risk
• Clopidogrel, in combination with aspirin, or aspirin alone for patients with a high bleeding risk.
Arrange early echocardiography assessment of left ventricular ejection fraction for any patient who does
not receive coronary reperfusion in the acute phase.[4]
Long-term management
Ensure all patients are given the following (while taking into account any contraindications).
• Dual antiplatelet therapy with aspirin and a P2Y 12 inhibitor (unless the patient has a separate
indication for anticoagulation - seek specialist advice).[23] Continue the P2Y 12 inhibitor used
in the acute phase for up to 12 months (unless contraindicated).[23] The National Institute for
Health and Care Excellence (NICE) in the UK recommends:[23]
• For patients who had undergone percutaneous coronary intervention (PCI):
• Prasugrel in those not taking an oral anticoagulant. However, follow your local
protocol. At present, many hospitals in the UK use ticagrelor rather than prasugrel in
MANAGEMENT
these patients. This new guidance by NICE will require a change in current practice
in the UK. Consider ticagrelor or clopidogrel in patients aged 75 years or older if the
bleeding risk from prasugrel is a concern
• Clopidogrel in those taking an oral anticoagulant.
119
• For patients who had fibrinolysis:
• Ticagrelor unless the patient has a high bleeding risk

• Clopidogrel or aspirin alone if the patient has a high bleeding risk.
In the UK, it is clinical practice to check the patient’s clinical report, which includes an
individualised plan written by the interventional cardiology team specifying what antiplatelet
therapy is advised for long-term management depending on the interventions performed.
Continue aspirin indefinitely unless the patient has hypersensitivity.
More info: Antiplatelet therapy for patients with a separate indication for anticoagulation
Seek specialist advice when deciding the duration and type (dual or single) of antiplatelet therapy in
the 12 months after STEMI for patients with a separate indication for anticoagulation (e.g., in patients
with ongoing atrial fibrillation).
The National Institute for Health and Care Excellence (NICE) in the UK recommends taking account of
all of the following when deciding about the duration and type (dual or single) of antiplatelet therapy in
patients with a separate indication for anticoagulation:[23]
• Bleeding risk
• Thromboembolic risk
• Cardiovascular risk
• Patient's wishes.
Be aware that long-term continuation of aspirin, clopidogrel, and oral anticoagulation (triple therapy)
significantly increases bleeding risk.
For patients already on anticoagulation who had PCI :[23]
• Continue anticoagulation and clopidogrel for up to 12 months

• If the patient is taking a direct oral anticoagulant, adjust the dose according to bleeding risk,
thromboembolic risk, and cardiovascular risk.
For patients with a new indication for anticoagulation who had PCI :[23]
• Offer clopidogrel (to replace prasugrel or ticagrelor) for up to 12 months and an oral
anticoagulant licensed for the indication, which best matches the patient's bleeding risk,
thromboembolic risk, cardiovascular risk, and wishes.
For patients already on anticoagulation, or those with a new indication, who did not have PCI :[23]
• Continue anticoagulation and, unless there is a high risk of bleeding, consider continuing aspirin
(or clopidogrel for patients with contraindication for aspirin) for up to 12 months.
Do not routinely offer prasugrel or ticagrelor in combination with anticoagulation in patients with
a separate indication for anticoagulation.[23]
MANAGEMENT
• An ACE inhibitor
• Start this as soon as the patient is haemodynamically stable and continue it indefinitely.
Complete upwards dose titration within 4-6 weeks of hospital discharge.[23]
• Offer an angiotensin-II receptor antagonist as an alternative if the patient is intolerant to an
ACE inhibitor.[23]
• Measure renal function, serum electrolytes, and blood pressure before starting an ACE
inhibitor or angiotensin-II receptor antagonist.[23] In practice, if the patient has abnormal
renal function or blood pressure, start with a low dose and titrate this carefully with close
monitoring.
• A beta-blocker
• Start this as soon as the patient is haemodynamically stable.[23]

• Continue the beta-blocker for at least 12 months if the patient does not have reduced left
ventricular ejection fraction (LVEF).[23]
• Continue the beta-blocker indefinitely if the patient has reduced LVEF.[23]
• Evidence shows that a beta-blocker may reduce the short-term risk of a reinfarction and
the long-term risk of all‐cause mortality and cardiovascular mortality in patients with acute
myocardial infarction.[128] [129]
• High-intensity statin therapy.[15] [23]
Give an aldosterone antagonist (e.g., eplerenone, spironolactone) to any patient with signs or symptoms
of heart failure and reduced LVEF.[23]
• Start this within 3-14 days of a STEMI and preferably after starting an ACE inhibitor.[23]
Calcium-channel blockers and potassium-channel activators
• Do not routinely give calcium-channel blockers.[23]

• Consider a non-dihydropyridine calcium-channel blocker, such as verapamil, in a patient without
pulmonary congestion or reduced LVEF who has a contraindication to beta-blockers (or when these
need to be discontinued).[23]
• Do not offer nicorandil (a potassium-channel activator).
Offer cardiac rehabilitation to all patients. This should include an exercise component, health education,
stress management, and psychological and social support. Advise all patients on lifestyle changes such
as:[23]
• Changes to diet
• Reduction of alcohol consumption
• Smoking cessation
• Weight management
• Physical exercise.
Treatment algorithm overview

Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
MANAGEMENT
121
Acute ( summary )
suspected or clinical diagnosis of
STEMI (symptoms of myocardial
ischaemia + ST elevation on ECG)
1st aspirin
plus assess eligibility for coronary reperfusion

therapy
plus analgesia
plus anti-emetic
consider ox ygen
consider intravenous nitrate
<12 hours since symptom plus primary PCI

onset: primary PCI
available within 120
minutes
plus P2Y12 inhibitor
plus parenteral anticoagulation
consider glycoprotein IIb/IIIa inhibitor
<12 hours since symptom plus fibrinolysis

onset: primary PCI NOT
minutes of the time when
fibrinolysis could be
given AND patient is
eligible for fibrinolysis
plus angiography with or without PCI
<12 hours since symptom plus consult interventional cardiology team to

onset: primary PCI discuss primary PCI
NOT available within
120 minutes AND
patient has absolute
contraindication to
fibrinolysis
>12 hours since symptom plus primary PCI

onset: with ongoing
MANAGEMENT
evidence of myocardial
ischaemia (symptoms
and/or signs on ECG)
Acute ( summary )
>12 hours since symptom plus seek immediate cardiology advice to

onset: no ongoing discuss management options
ischaemia (no symptoms
Ongoing ( summary )
post-STEMI
1st continue dual antiplatelet therapy
plus start or continue beta-blocker or non-

dihydropyridine calcium-channel blocker
plus start or continue ACE inhibitor or

angiotensin-II receptor antagonist
plus statin
consider aldosterone antagonist
plus cardiac rehabilitation
MANAGEMENT
123
Treatment algorithm
Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
MANAGEMENT
Acute
suspected or clinical diagnosis of
STEMI (symptoms of myocardial
ischaemia + ST elevation on ECG)
1st aspirin
Primary options
» aspirin: 300 mg orally (chewed or dispersed

in water) as a loading dose, followed by
75-100 mg once daily thereafter
The loading and maintenance dose varies
across guidelines and locations; check local
protocols for further guidance on dose.
» Give all patients with suspected STEMI

a single loading dose of aspirin as soon
as possible, unless they have aspirin
hypersensitivity.[23]
• Aspirin can be given orally (or via

nasogastric tube if oral ingestion is not
possible).[4] An intravenous loading dose
is used in some countries; however, this
formulation is not available in the UK.
» Check your local protocol or discuss the
patient with a senior colleague if they have
hypersensitivity to aspirin.
» Start treatment for STEMI immediately

after making a clinical diagnosis - do not
wait for cardiac troponin levels to confirm
it. [4]
» After the loading dose, continue with a lower

maintenance dose of aspirin as part of ongoing
dual antiplatelet therapy unless contraindicated.
plus assess eligibility for coronary reperfusion
therapy
Treatment recommended for ALL patients in
selected patient group
» Make an immediate assessment of
the patient’s eligibility for coronary
reperfusion therapy as soon as a clinical
diagnosis of STEMI has been made. [4] [23]
• If eligible, take steps to ensure

coronary reperfusion therapy (primary
percutaneous coronary intervention
MANAGEMENT
or fibrinolysis) is delivered as quickly

as possible . If not eligible, offer
conservative medical management.[23]
• Do not allow the patient’s age, ethnicity,
or sex to influence your assessment of
their suitability for reperfusion therapy.[23]
125
Acute
Evidence suggests that women tend to
receive reperfusion therapy less frequently
and/or in a more delayed fashion than
men, even though it has equal benefits for
both sexes.[4]
» For most patients with STEMI, primary
(PCI) is the preferred reperfusion strategy
provided it can be delivered within 120
minutes of the time when fibrinolysis
could have been given. [23] [28]
• Multiple randomised controlled trials

have shown that primary PCI has
bet ter outcomes (in terms of reducing
mortality, reinfarction, or stroke) and
less intracranial bleeding than
fibrinolysis provided it can be delivered
in a timely manner by an experienced
team.[4] [99] [100] [101] [102] [103] [104]
• However, fibrinolysis may be more
appropriate when there is a lack of
access to timely PCI.[4] [23]
Practical tip
The European Society of Cardiology

(ESC) STEMI guideline lists the
contraindications to fibrinolytic
therapy as follows: [4]
• History of intracranial
haemorrhage or stroke of
unknown origin at any time
• Ischaemic stroke in the last 6
months
• Central nervous system damage,
neoplasm, or arteriovenous
malformation
• Major trauma/surgery/head injury
within the last 1 month
• Gastrointestinal bleeding within
the last 1 month
• Non-compressible punctures
MANAGEMENT
within the last 24 hours (e.g.,

liver biopsy, lumbar puncture)
Acute
• Chronic oral anticoagulant
therapy
• Pregnancy or within 1 week
postnatal
• Refractory hypertension (systolic
BP >180 mmHg and/or diastolic
BP >110 mmHg)
• Transient ischaemic attack in the
last 6 months
• Prolonged or traumatic
cardiopulmonary resuscitation.
» Seek immediate specialist input from the

interventional cardiology team .[4]
• If you are managing the patient within

a PCI-capable hospital, this team
will be available on site. If not, call
the interventional cardiology team at
your designated PCI-capable hospital
to discuss immediate transfer for
coronary reperfusion therapy.
• Also take the earliest opportunity
to gain intravenous access and
start continuous haemodynamic
monitoring and pulse oximetry .[4]
Practical tip
When placing an intravenous cannula,

avoid placing it in the right hand or right
wrist area as the right radial artery is the
usual route used to perform primary PCI.
» Concurrent anticoagulation and dual

antiplatelet therapy is given alongside
coronary reperfusion, regardless of
whether primary PCI or fibrinolysis
is used. The benefits of reperfusion
in reducing mortality and improving
myocardial salvage decline rapidly with
time. [4] [23]
• It is, therefore, vital to take every step

MANAGEMENT
possible to ensure the chosen reperfusion

strategy (primary PCI or fibrinolysis) is
delivered as quickly as possible.
127
Acute
Practical tip
Do not give anticoagulation therapy if

the patient is likely to be eligible for
primary PCI. [4] [10]
• This will be given by the interventional
cardiology team in the cardiac
» The ESC STEMI guideline has set widely

accepted maximum time-to-treatment
targets as follows: [4]
Interval Target
First medical contact ≤10 minutes

to ECG and STEMI
diagnosis
STEMI diagnosis to ≤120 minutes

primary PCI
If this time target
cannot be met,
consider fibrinolysis
STEMI diagnosis to ≤60 minutes if the

primary PCI if the patient presents to or
is in a PCI-capable
patient’s first medical hospital
contact is at a hospital
≤90 minutes if the
patient presents to
or is in a non-PCI-
capable hospital and
needs transferring
STEMI diagnosis to ≤10 minutes

administration of a
bolus/infusion of a
fibrinolytic drug (if
primary PCI cannot be
accessed within 120
minutes)
Start of fibrinolysis to 60-90 minutes

ECG assessment of its
MANAGEMENT
success or failure
If fibrinolysis is 2-24 hours

successful, time
interval from starting
Acute
Interval Target
fibrinolysis to early
coronary angiography
» The most appropriate coronary

reperfusion strategy will depend on :[4] [10]
[22]
• Duration of ischaemic symptoms

• Persistence or resolution of ST-segment
elevation on serial ECGs
• Availability of timely access to primary PCI
• Whether a patient is first assessed

in a PCI-capable or non-PCI-
capable hospital
• Estimated transfer time from a
non-PCI-capable to a PCI-capable
hospital
• Whether there was a pre-hospital STEMI
diagnosis made by trained and fully
equipped paramedic team who can
administer initial pharmacotherapy
• The quality and expertise of the regional
network infrastructure in place for STEMI
management.
» Many patients who present with
STEMI are already taking long-term oral
anticoagulation for various indications. [4]
• This is a relative contraindication for

fibrinolysis .
• For any such patient, choose a primary
PCI strategy for coronary reperfusion
therapy, regardless of the anticipated time
to access this intervention.[4]
More info: Summary flowchart – choice

of coronary reperfusion strategy
The flowchart below summarises the choice

of coronary reperfusion strategy according to
time since the patient’s symptom onset and
MANAGEMENT
the anticipated time to access primary PCI.[4]

[23]
129
Acute
Selection of the most appropriate

reperfusion strategy. PPCI, primary
plus analgesia
Primary options
» morphine sulfate: 2.5 to 10 mg

intravenously initially, followed by 2.5 to 10
mg if required (at a rate of 1-2 mg/minute)
The lower end of the dose range is
recommended in elderly and frail patients.
OR
» diamorphine: 2.5 to 5 mg intravenously

initially, followed by 1.25 to 5 mg if required
(at a rate of 1-2 mg/minute)
The lower end of the dose range is
recommended in elderly and frail patients.
MANAGEMENT
» Give pain relief. [4] [29]
• Titrated intravenous opioids (e.g.,

morphine or diamorphine) are the most
commonly used option for analgesia.
Acute
• Pain relief is crucial not just for the comfort
of the patient but also because the pain
is associated with sympathetic activation,
which causes vasoconstriction and
increases the workload of the heart.[4]
plus anti-emetic
Primary options
» ondansetron: 4-8 mg intravenously as a

single dose
OR
» metoclopramide: body weight <60 kg: up to

500 micrograms/kg/day intravenously given in
3 divided doses; body weight ≥60 kg: 10 mg
intravenously up to three times daily
OR
» cyclizine: 50 mg intravenously three times

daily
» Give an anti-emetic concomitantly with

the opioid analgesic to prevent the patient
vomiting the oral loading dose of dual
antiplatelet therapy.
consider ox ygen
Treatment recommended for SOME patients in
» Give ox ygen therapy only if saturations
are <90% on pulse oximetry. [4]
• Routine supplemental oxygen is not

indicated if arterial oxygen saturation (SaO
2 ) ≥90%.[89] [90] [91]
consider intravenous nitrate

Primary options
» glyceryl trinitrate: 15-20 micrograms/

minute intravenous infusion initially, adjust
MANAGEMENT
dose according to response, maximum 400

micrograms/minute
OR
131
Acute
» isosorbide dinitrate: 2-10 mg/hour
intravenous infusion initially, adjust dose
according to response, maximum 20 mg/hour
» Routine use of an intravenous nitrate in

STEMI is not recommended as there is no
evidence to support its benefits. [4]
• In practice, a sublingual (or buccal) dose

is often given after a STEMI diagnosis has
been made (and sometimes before the
patient arrives at hospital).
Practical tip
If your patient experiences a

spontaneous resolution of ST-
segment elevation, along with
complete symptom relief, after taking
glyceryl trinitrate, this is suggestive
of coronary spasm with or without
associated MI. [4]
• Refer to cardiology.
• Aim for early coronary angiography
(within 24 hours).
» Consider an intravenous nitrate if the

patient has:[4] [29]
• Persistent chest pain despite

administration of sublingual (or
buccal) glyceryl trinitrate
• Clinical and/or radiographic evidence of
congestive heart failure .
» Titrate the rate of infusion according to
the patient’s blood pressure and wider clinical
response.
» Do not give an intravenous nitrate when

there is :
• Hypotension secondary to right

ventricular infarction (usually complicating
an inferior or extensive anterior STEMI)
• Hypotension secondary to severe aortic
stenosis or left ventricular outflow tract
obstruction
MANAGEMENT
• Hypotension secondary to pre-existing

cardiomyopathy
• Persistent hypotension secondary to other
causes
Acute
• Use of a phosphodiesterase-5
inhibitor (e.g., avanafil, sildenafil,
tadalafil, vardenafil) for erectile
dysfunction within the last 48 hours.
Practical tip
Administration of intravenous nitrate

should not delay transfer to the
• An intravenous nitrate can be given
in the catheterisation laboratory by
the interventional cardiology team, if
needed.
• Recanalisation of the occluded infarct
artery is the most effective way of
relieving refractory chest pain so the
priority is to get the patient to primary
percutaneous coronary intervention as
quickly as possible.
<12 hours since symptom plus primary PCI

onset: primary PCI
minutes
» Select primary percutaneous coronary
intervention (PCI) as the preferred
reperfusion strategy for any patient who
had symptom onset <12 hours ago and has
:[4] [23] [28] [99] [100] [101] [102] [105]
• Ongoing signs and symptoms of

myocardial ischaemia, AND
• Persistent (or increasing) ST-
segment elevation on ECG.
» Take steps to ensure that primary PCI
will be delivered within 120 minutes of the
time when fibrinolysis could have been
given. [23] [28]
» Primary PCI involves immediate transfer

to the catheterisation laboratory with
the intention of opening the artery with
stent placement. Drug-eluting stents are
recommended by the European Society of
Cardiology and the UK National Institute for
Health and Care Excellence.[4] [23]
MANAGEMENT
• Many hospitals have round-the-clock

PCI capability . If yours does not, then
arrange immediate transfer to your
designated PCI-capable hospital .
133
Acute
• If it is not possible to ensure primary
PCI within 120 minutes, offer
fibrinolysis (if not contraindicated).[23]
• If your patient has STEMI with
cardiogenic shock, seek urgent
senior support. Coronary angiography ±
primary PCI is indicated.[23]
• If the patient’s coronary anatomy
is unsuitable for PCI, or PCI fails,
emergency coronary artery bypass graft (
CABG ) is recommended.[4]
• See our topic Cardiogenic shock for more
information on supportive management.

Primary options
» prasugrel: <75 years of age and body

weight <60 kg: 60 mg orally as a loading
dose, followed by 5 mg once daily thereafter;
<75 years of age and body weight ≥60 kg: 60
mg orally as a loading dose, followed by 10
mg once daily thereafter; ≥75 years of age:
60 mg orally as a loading dose, followed by 5
mg once daily thereafter
OR
» clopidogrel: <75 years of age: 300-600 mg

orally as a loading dose, followed by 75 mg
once daily thereafter; ≥75 years of age: 75
mg orally once daily
The licensed loading dose in the UK is 300
mg. The ESC guideline recommends a
higher loading dose of 600 mg for patients
proceeding to PCI. While this higher
dose is not licensed in the UK, it is widely
used in practice. 28886621 Ibanez B,
James S, Agewall S, et al; ESC Scientific
Document Group. 2017 ESC guidelines
for the management of acute myocardial
infarction in patients presenting with ST-
segment elevation. Eur Heart J. 2018 Jan
7;39(2):119-77. https://academic.oup.com/
eurheartj/article/39/2/119/4095042
OR
MANAGEMENT
» ticagrelor: 180 mg orally as a loading dose,

followed by 90 mg twice daily thereafter
» Give any patient who will undergo primary

percutaneous coronary intervention (PCI) dual
Acute
antiplatelet therapy with a P2Y 12 inhibitor
plus aspirin .[23]
• After the initial aspirin loading dose,

reduce the aspirin to a lower daily
maintenance dose.
• Check your local protocol when deciding
which P2Y 12 inhibitor to use, the timing of
this and the recommended initial loading
and ongoing daily doses.
» The UK National Institute for Health and Care
Excellence (NICE) recommends the following for
any patient undergoing PCI:[23]
• Prasugrel, in combination with aspirin, if

the patient is not already taking an oral
anticoagulant
• For patients aged 75 years and

older, the bleeding risk of using
prasugrel needs to be weighed
up against its effectiveness. If the
bleeding risk from prasugrel is a
concern in these patients, ticagrelor
or clopidogrel may be used as
alternatives
Practical tip
At present, many hospitals in

the UK use ticagrelor rather
than prasugrel in patients
who are not already on an
oral anticoagulant. This new
guidance by NICE will require
a change in current practice in
the UK.
• Clopidogrel, in combination with aspirin,
if the patient is already taking an oral
anticoagulant.
» The European Society of Cardiology guideline
recommends prasugrel or ticagrelor (in
combination with aspirin) as first-line options
in patients undergoing primary PCI, with
clopidogrel only indicated when neither of these
MANAGEMENT
drugs is available or they are contraindicated.[4]

135
Acute
Primary options
» heparin: no glycoprotein IIb/IIIa inhibitor use

planned: 70-100 units/kg intravenous bolus;
glycoprotein IIb/IIIa inhibitor use planned:
50-70 units/kg intravenous bolus
Monitor activated clotting time (ACT) during
procedure. Further doses may be required to
maintain ACT.
OR
» enoxaparin: 0.5 mg/kg intravenous bolus

Some centres may continue with
subcutaneous dosing after this initial
intravenous dose; consult local protocols for
further guidance.
OR
» bivalirudin: 0.75 mg/kg intravenous

bolus initially, followed by 1.75 mg/kg/hour
intravenous infusion during procedure and
for up to 4 hours after procedure, reduce to
0.25 mg/kg/hour for a further 4-12 hours if
necessary
» Anticoagulation is routinely given

during primary percutaneous coronary
intervention (PCI).
• This will be started by the

interventional cardiology team in the
cardiac catheterisation laboratory.
• Therefore, do not start

anticoagulation if your patient is
likely to be eligible for primary PCI.
» The recommended options for

intravenous anticoagulation are :
• Unfractionated heparin for patients

undergoing primary PCI with radial
access[4] [23]
• Bivalirudin (a direct thrombin inhibitor)
for patients undergoing PCI with femoral
access[4] [23]
• Enoxaparin.[4]
» Fondaparinux is not recommended
MANAGEMENT
as an adjunctive anticoagulant during

primary PCI. [4]
Acute
• It was associated with catheter thrombosis
at the time of primary PCI in the OASIS-6
trial.[121]
» Routine post-procedural anticoagulation
is not required after primary PCI unless
there is a separate indication for it, for
example:[4]
• Patients at high risk of venous

thromboembolism
• Consult local protocols for full- and
prophylactic-dose regimens for these
indications. The doses presented here are
the doses used during primary PCI only.

Primary options
» eptifibatide: consult specialist for guidance

on dose
OR
» tirofiban: consult specialist for guidance on

dose
» A glycoprotein IIb/IIIa inhibitor (e.g.,

eptifibatide, tirofiban, abciximab) may
be used by the interventional cardiology
team during the percutaneous coronary
intervention procedure. [4] Abciximab is not
currently available in the UK, and shortages in
other countries have been reported.
• This can help to tackle a high thrombus

burden or no-reflow phenomenon.
MANAGEMENT
<12 hours since symptom plus fibrinolysis

onset: primary PCI NOT
minutes of the time when
fibrinolysis could be
137
Acute
given AND patient is
Primary options
eligible for fibrinolysis
» tenecteplase: body weight <60 kg: 30 mg
(6000 units) intravenous bolus as a single
dose; body weight 60 to <70 kg: 35 mg (7000
units) intravenous bolus as a single dose;
body weight 70 to <80 kg: 40 mg (8000
body weight 80 to <90 kg: 45 mg (9000
body weight ≥90 kg: 50 mg (10,000 units)
intravenous bolus as a single dose
Dose should be halved in patients ≥75 years
of age due to a higher bleeding risk in these
patients. Tenecteplase is only licensed in the
UK for use within 6 hours of symptom onset.
OR
» alteplase: accelerated regimen (if started

within 6 hours of symptom onset): 15 mg
intravenous bolus, followed by 0.75 mg/
kg (maximum 50 mg/dose) intravenous
infusion over 30 minutes, then 0.5 mg/kg
(maximum 35 mg/dose) intravenous infusion
over 60 minutes, maximum 100 mg total
dose over 90 minutes; regular regimen (if
started within 6-12 hours of symptom onset):
10 mg intravenous bolus, followed by 50 mg
intravenous infusion over 60 minutes, then
10 mg intravenous infusion over 30 minutes
for four infusions, maximum 100 mg total
dose over 3 hours and maximum 1.5 mg/kg in
patients with body weight <65 kg
The ESC guideline recommends the
accelerated regimen as the preferred
regimen. 28886621 Ibanez B, James
S, Agewall S, et al; ESC Scientific
Secondary options
» streptokinase: 1.5 million units intravenous

infusion given over 30-60 minutes
» Give fibrinolysis (unless

MANAGEMENT
contraindicated) if primary percutaneous

coronary intervention (PCI) cannot be
delivered within 120 minutes of the time
when fibrinolysis could be given. [23] [28]
Acute
» Start anticoagulation at the same
time as giving fibrinolysis and start
dual antiplatelet therapy immediately
afterwards. [4] [10] [23]
» Check your local protocols regarding the

choice of fibrinolytic drug.
• The UK National Institute for Health and

Care Excellence recommends a fibrin-
specific drug such as alteplase or
tenecteplase .[23] It also recommends
streptokinase (a non-fibrin-specific drug)
as an option in some patients.[86]
• The European Society of Cardiology
(ESC) guideline recommends the same
fibrin-specific drugs plus reteplase (no
longer available in the UK).[4] According
to these guidelines, consider a half-dose
of tenecteplase if the patient is aged 75
years or older.[4]
• When choosing a fibrinolytic drug take
account of:[86]
• Balancing the benefit and harm

(e.g., stroke risk) of each drug for
the individual patient
• The importance of avoiding
giving streptokinase to a
patient who has received it
in the past (patients treated
with streptokinase may develop
antibodies that neutralise the drug if
repeat treatment is given)
• Your local hospital protocol
for reducing delays in the
administration of thrombolysis.
» To shorten the time to treatment,

fibrinolysis can be administered as part of
the pre-hospital management of STEMI. [4]
[86]
• This may be part of the emergency care

treatment pathway where geographical
considerations mean the anticipated time
to primary PCI will be >120 minutes.
• In such cases, a bolus dose of
tenecteplase ( or reteplase if available)
MANAGEMENT
is preferred for the sake of practicality

as the other fibrinolytic drug options are
administered by intravenous infusion.
139
Acute
» If your patient is not already at a PCI-
capable hospital, transfer them to one
immediately after giving fibrinolysis. [4]
• This is so that rescue PCI can be

performed if fibrinolysis fails or
angiography ± PCI can be arranged if
fibrinolysis is effective.
» If primary PCI cannot be delivered
within 120 minutes of STEMI diagnosis
and the patient has presented >2-3 hours
after symptom onset, seek a specialist
cardiology opinion to support your choice
of reperfusion strategy. [4] [10] [87]
• The greatest benefit of fibrinolysis is

observed when given <2 hours after
symptom onset. Its clinical efficacy
diminishes as time from symptom
onset increases .[20] [88]
• Therefore, the later the patient presents
(particularly >2-3 hours), the more
consideration should be given to
transferring for primary PCI instead –
discuss the options with cardiology.[4]
[22]
Practical tip
The ESC STEMI guideline lists the

therapy as follows :[4]
months
malformation
the last 1 month
MANAGEMENT
Acute

therapy
postnatal
BP >110 mmHg)
last 6 months
Evidence: Role of fibrinolysis in STEMI
Fibrinolytic therapy remains an important

evidence-based intervention in settings where
primary PCI cannot be offered in a timely
manner.
Two landmark studies demonstrated

the benefits of fibrinolysis in patients
with STEMI (prior to the advent of
primary PCI).
• The Fibrinolytic Therapy Trialists’

Collaborative Group (1994)
demonstrated highly significant
benefits in saving lives and helped
to establish the time window
when fibrinolytic therapy is most
effective.[88]
• The study demonstrated highly

significant absolute mortality
reductions from fibrinolysis of
about:
• 30 per 1000 for those

presenting within 0-6
MANAGEMENT
hours of symptom onset

• 20 per 1000 for those
presenting 7-12 hours
after symptom onset.
141
Acute
• There was a statistically
uncertain benefit of about 10
per 1000 for those presenting
at 13-18 hours (with more
randomised evidence needed in
this group to assess reliably the
net effects of treatment).
• The 1993 GUSTO trial [111]
[112] compared different fibrinolysis
strategies.
• It demonstrated a benefit of 14%

reduction in mortality (95% CI,
5.9% to 21.3%) for accelerated
tissue plasminogen activator
(t-PA) versus streptokinase
(the standard fibrinolytic
treatment at the time). Alteplase
(recombinant t-PA) was used in
the trial.
• The trial randomly assigned
41,021 patients with evolving
acute MI to 4 different fibrinolytic
strategies. The data for the
primary end point of 30-day
mortality for each treatment arm
was as follows:
• Streptokinase plus
subcutaneous heparin =
7.2%
• Streptokinase plus
intravenous heparin =
7.4%
• t-PA plus intravenous
heparin = 6.3%
• Streptokinase plus t-PA
plus intravenous heparin =
7.0%.
• A significant excess of
haemorrhagic strokes was
MANAGEMENT
observed for accelerated t-

PA (P = 0.03) and for the
combination strategy (P <0.001),
Acute
as compared with streptokinase
only.
The 2013 STREAM trial provided

further support for fibrinolysis as
an appropriate reperfusion strategy
for STEMI when primary PCI cannot
be delivered in a timely manner –
especially if followed by routine early
angiography ± PCI (a 'pharmacoinvasive
strategy'). [104]
• The STREAM trial was conducted

at a time when primary PCI was
established as the standard of care for
STEMI.
• In the trial, 1892 STEMI patients
presenting within 3 hours of symptom
onset but unable to have primary PCI
within 1 hour were randomly assigned
to:
• Primary PCI or
• Pre-hospital bolus tenecteplase
(with a half-dose used in
patients ≥75 years) plus
clopidogrel plus enoxaparin
before transport to a PCI-
capable hospital
• Patients had emergency

angiography if fibrinolysis
failed
• If fibrinolysis was
successful, patients had
routine angiography
within 6-24 hours after
randomisation.
• There was no significant difference

between the primary PCI and
fibrinolysis groups in the primary
composite end point of death, shock,
congestive heart failure, or reinfarction
MANAGEMENT
within 30 days.
143
Acute
• More intracranial haemorrhages
occurred in the fibrinolysis
group.
• The median time from
randomisation to bolus of
fibrinolytic was 9 minutes, which
has served as the basis for the
ESC guideline recommendation
that fibrinolysis should be given
within 10 minutes of STEMI
diagnosis. [4]
The extent to which the delay-to-PCI
time diminishes the advantages of
primary PCI over fibrinolysis has been
widely debated and more research is
needed. [4]
• It is clear that if delay to treatment

is similar, primary PCI is superior
to fibrinolysis in reducing mortality,
reinfarction, or stroke.[4]
• However, fibrinolysis can be

administered expeditiously and
the longer the delay to primary
PCI, the lower the benefits
over fibrinolysis. The exact cut-
off point at which the delay to
access PCI makes fibrinolysis
the better reperfusion strategy is
based on weak evidence.

Primary options
» enoxaparin: <75 years of age: 30 mg

intravenous bolus, followed by 1 mg/
kg subcutaneously every 12 hours until
revascularisation or hospital discharge for up
to 8 days, maximum 100 mg/dose for each
of the first 2 subcutaneous doses; ≥75 years
of age: 0.75 mg/kg subcutaneously every
MANAGEMENT
12 hours until revascularisation or hospital

discharge for up to 8 days, maximum 75 mg/
dose for each of the first 2 subcutaneous
doses
OR
Acute
» heparin: 60 units/kg (maximum 4000

units) intravenous bolus, followed by 12
units/kg/hour (maximum 1000 units/hour)
intravenous infusion for 24-48 hours; adjust
dose according to aPTT
Secondary options
» fondaparinux: 2.5 mg intravenously once

daily on the first day, followed by 2.5 mg
subcutaneously once daily for up to 8 days
(or hospital discharge if sooner)
Only use fondaparinux when streptokinase is
used for fibrinolysis.
» Start anticoagulation at the same time

as fibrinolysis. [4] [10] [23]
» The choice of parenteral

anticoagulation can be any one of :[4]
• Enoxaparin (the European Society of

Cardiology guideline recommends this as
the first-choice anticoagulant for patients
undergoing fibrinolysis)[4] [122] [123]
[124]
• Unfractionated heparin
• Fondaparinux (only if streptokinase
is used for fibrinolysis). [125]
» Ensure anticoagulation for any patient
undergoing fibrinolysis continues :[4] [10]
• Up to the point of coronary

revascularisation with percutaneous
coronary intervention (if performed), or
• For at least the first 48 hours but ideally
up until hospital discharge for a maximum
of 8 days in total if revascularisation is not
performed.[4]

Primary options

OR
MANAGEMENT
» clopidogrel: <75 years of age: 300 mg orally

as a loading dose, followed by 75 mg once
daily thereafter; ≥75 years of age: 75 mg
orally once daily
145
Acute
» Give the patient dual antiplatelet therapy
with a P2Y 12 inhibitor plus aspirin
immediately after giving fibrinolysis .[23]

maintenance dose.
Excellence recommends the following:[23]
• Ticagrelor, in combination with aspirin,

unless the patient has a high bleeding risk
• Clopidogrel, in combination with aspirin,
or aspirin alone for patients with a high
bleeding risk.
recommends clopidogrel as the preferred
agent.[4]
plus angiography with or without PCI
» Use an ECG 60-90 minutes after
administering fibrinolysis to assess
whether it has been successful. [4] [23]
» If fibrinolysis has failed (<50% ST-

segment resolution at 60-90 minutes),
offer immediate coronary angiography,
with follow-on percutaneous coronary
intervention (PCI) if indicated. [23]
• Do not repeat fibrinolytic therapy.[23]

» If the patient has recurrent myocardial
ischaemia after fibrinolysis, seek immediate
specialist advice from cardiology . PCI may
be indicated.[23]
» If fibrinolysis is successful , consider

angiography before discharge for patients who
are clinically stable.[23]
• Several randomised trials and two meta-

MANAGEMENT
analyses have shown that early routine

angiography (with PCI if needed)
after fibrinolysis reduces the rate of
reinfarction and recurrent ischaemia
compared with a watchful waiting strategy.
The benefits of early routine PCI following
Acute
fibrinolysis were seen across patient
subgroups and without any increased risk
of adverse events such as stroke or major
bleeding.[106] [107] [108]
recommends immediate rescue PCI if, at any
time following fibrinolysis, the patient develops
haemodynamic or electrical instability or
worsening ischaemia.[4]
» Emergency angiography ± PCI is

recommended if, at any time following
fibrinolysis, the patient has :
• Heart failure or cardiogenic shock [4]

• Recurrent ischaemia or evidence of
re-occlusion after initially successful
fibrinolysis.[4] [109] [110]
<12 hours since symptom plus consult interventional cardiology team to

onset: primary PCI NOT discuss primary PCI
minutes AND patient has
absolute contraindication
to fibrinolysis » If primary percutaneous coronary
intervention (PCI) is not available within
120 minutes but your patient has a
contraindication to fibrinolysis :
• It is important to weigh up the

potentially life-saving benefits of
fibrinolysis against its potentially life-
threatening adverse effects , bearing
in mind alternative treatment options such
as delayed primary PCI[4]
• Seek immediate advice from the
interventional cardiology team
• For a patient with an absolute
contraindication to fibrinolysis, primary
PCI will normally be the preferred
management strategy despite the delay
in accessing it.
Practical tip
The European Society of Cardiology

STEMI guideline lists the
therapy as follows :[4]
MANAGEMENT
147
Acute
months
malformation
the last 1 month

therapy
postnatal
BP >110 mmHg)
last 6 months
» If primary PCI is undertaken, the

interventional cardiology team will
start parenteral anticoagulation in the
» Arrange early echocardiography assessment

of left ventricular ejection fraction for any patient
who does not receive coronary reperfusion in the
acute phase.[4]
MANAGEMENT

Primary options

Acute
OR

OR

» Give the patient dual antiplatelet therapy

with a P2Y 12 inhibitor plus aspirin .[23]

maintenance dose.
Excellence recommends the following:[23]
• If the patient is eligible for primary

percutaneous coronary intervention (PCI):
MANAGEMENT
• Prasugrel, in combination with

aspirin, if they are not already taking
an oral anticoagulant
149
Acute
• For patients aged 75 years
and older, the bleeding risk
of using prasugrel needs to
be weighed up against its
effectiveness. If the bleeding
risk from prasugrel is a
concern in these patients,
ticagrelor or clopidogrel may
be used as alternatives
Practical tip
At present, many
hospitals in the UK
use ticagrelor rather
than prasugrel in
patients who are not
already taking an oral
anticoagulant. This new
guidance by NICE will
require a change in
current practice in the
UK.
• Clopidogrel, in combination with
aspirin, if they are taking an oral
anticoagulant.
• If the patient is not having primary PCI:
• Ticagrelor, in combination with

aspirin, unless the patient has a
high bleeding risk
aspirin, or aspirin alone, for patients
with a high bleeding risk.

>12 hours since symptom plus primary PCI

onset: with ongoing
MANAGEMENT
ischaemia (symptoms
and/or signs on ECG) » Seek immediate specialist advice
from cardiology to discuss management
options for any STEMI patient who
presents >12 hours after symptom onset.
Acute
• Coronary angiography ± primary
percutaneous coronary intervention (PCI)
should be considered if there is:
• Evidence of continuing myocardial

ischaemia or cardiogenic shock[23]
• ECG evidence of continuing
ischaemia and/or dynamic ECG
changes, ongoing symptoms of
myocardial ischaemia, symptoms
and/or signs of heart failure, shock,
or malignant arrhythmias.[4]
» If your patient has ongoing ischaemic

symptoms suggestive of MI but no
ongoing ST-segment elevation on the ECG,
primary PCI should be considered if one or
more of the following is present: [4]
• Cardiogenic shock or haemodynamic

instability
• Ongoing or recurrent chest pain refractory
to pharmacological treatment
• Cardiac arrest or life-threatening
arrhythmia
• Signs and symptoms suggestive of
mechanical complications of acute MI
• Dynamic ST-segment or T-wave changes,
especially intermittent ST-segment
elevation.

Primary options

MANAGEMENT
OR

151
Acute
OR

» Give any patient who will undergo primary

percutaneous coronary intervention (PCI) dual
antiplatelet therapy with a P2Y 12 inhibitor
plus aspirin .[23]

maintenance dose.
Excellence (NICE) recommends the following for
any patient undergoing PCI:[23]
• Prasugrel, in combination with aspirin,

if they are not already taking an oral
anticoagulant
• For patients aged 75 years and

older, the bleeding risk of using
prasugrel needs to be weighed
up against its effectiveness. If the
concern in these patients, ticagrelor
or clopidogrel may be used as
alternatives
MANAGEMENT
Practical tip
At present, many hospitals in

the UK use ticagrelor rather
Acute
than prasugrel in patients
who are not already taking an
oral anticoagulant. This new
guidance by NICE will require
a change in current practice in
the UK.
• Clopidogrel, in combination with aspirin, if
the patient is taking an oral anticoagulant.
» The European Society of Cardiology
Primary options
» heparin: no glycoprotein IIb/IIIa inhibitor use

planned: 70-100 units/kg intravenous bolus;
glycoprotein IIb/IIIa inhibitor use planned:
50-70 units/kg intravenous bolus
Monitor activated clotting time (ACT) during
procedure. Further doses may be required to
maintain ACT.
OR
» enoxaparin: 0.5 mg/kg intravenous bolus

Some centres may continue with
subcutaneous dosing after this initial
intravenous dose; consult local protocols for
further guidance.
OR
» bivalirudin: 0.75 mg/kg intravenous

bolus initially, followed by 1.75 mg/kg/hour
intravenous infusion during procedure and
for up to 4 hours after procedure, reduce to
0.25 mg/kg/hour for a further 4-12 hours if
necessary
» Anticoagulation is routinely given

during primary percutaneous coronary
intervention (PCI).
MANAGEMENT
• This will be started by the

interventional cardiology team in the
cardiac catheterisation laboratory.
153
Acute
• Therefore, do not start
anticoagulation if your patient is
likely to be eligible for primary PCI.
» The recommended options for

intravenous anticoagulation are :
• Unfractionated heparin for patients

undergoing primary PCI with radial
access[4] [23]
• Bivalirudin (a direct thrombin inhibitor)
for patients undergoing PCI with femoral
access[4] [23]
• Enoxaparin.[4]
» Fondaparinux is not recommended
as an adjunctive anticoagulant during
primary PCI. [4]
• It was associated with catheter thrombosis

at the time of primary PCI in the OASIS-6
trial.[121]
» Routine post-procedural anticoagulation
is not required after primary PCI unless
there is a separate indication for it, for
example:[4]
• Patients at high risk of venous

thromboembolism
• Consult local protocols for full- and
prophylactic-dose regimens for these
indications. The doses presented here are
the doses used during primary PCI only.

Primary options
MANAGEMENT
» eptifibatide: consult specialist for guidance

on dose
OR
Acute
» tirofiban: consult specialist for guidance on
dose
» A glycoprotein IIb/IIIa inhibitor (e.g.,

eptifibatide, tirofiban, abciximab) may
be used by the interventional cardiology
team during the percutaneous coronary
intervention procedure. [4] Abciximab is not
currently available in the UK, and shortages in
other countries have been reported.
• This can help to tackle a high thrombus

burden or no-reflow phenomenon.
>12 hours since symptom plus seek immediate cardiology advice to

onset: no ongoing discuss management options
ischaemia (no symptoms
» Discuss urgently with cardiology any
patient who presents >12 hours after
symptom onset but has no ongoing
symptoms. [4] [113]
• Routine primary percutaneous coronary

intervention (PCI) strategy should still
be considered in patients presenting
between 12 and 48 hours after symptom
onset. However, if the time since symptom
onset is >48 hours and the patient is now
asymptomatic, routine PCI of an occluded
infarct-related artery is not recommended.
• Fibrinolysis is not indicated.

Primary options

MANAGEMENT
OR

155
Acute
OR

» Give the patient dual antiplatelet therapy with a

P2Y 12 inhibitor plus aspirin .[23]

maintenance dose.
» The UK National Institute for Health and
Care Excellence (NICE) recommends the
following:[23]
• If the patient is eligible for primary

• Prasugrel, in combination with

aspirin, if they are not already taking
an oral anticoagulant
• For patients aged 75 years

and older, the bleeding risk
of using prasugrel needs to
be weighed up against its
effectiveness. If the bleeding
MANAGEMENT
risk from prasugrel is a

concern in these patients,
ticagrelor or clopidogrel may
be used as alternatives
Acute
Practical tip
At present, many
hospitals in the UK
use ticagrelor rather
than prasugrel in
patients who are not
already taking an oral
anticoagulant. This new
guidance by NICE will
require a change in
current practice in the
UK.
aspirin, if the patient is taking an
oral anticoagulant.
• If the patient is not having primary PCI:
• Ticagrelor, in combination with

aspirin, unless the patient has a
high bleeding risk
aspirin, or aspirin alone, for patients
with a high bleeding risk.

in patients undergoing primary PCI, and
clopidogrel as the preferred agent for patients
having fibrinolysis.[4]
MANAGEMENT
157
Ongoing
post-STEMI
1st continue dual antiplatelet therapy

Primary options
» aspirin: 75-100 mg once daily thereafter

--AND--
weight <60 kg: 5 mg orally once daily; <75
years of age and body weight ≥60 kg: 10
mg orally once daily; ≥75 years of age: 5 mg
orally once daily
-or-
» ticagrelor: 90 mg orally twice daily
-or-
» clopidogrel: 75 mg orally once daily
Secondary options
» clopidogrel: 75 mg orally once daily
» Ensure all patients are given dual antiplatelet

therapy with aspirin and a P2Y 12 inhibitor
(while taking into account any contraindications;
seek specialist advice if the patient has a
separate indication for anticoagulation. See
more info panel below).[23]
» Continue the P2Y 12 inhibitor used in the

acute phase for up to 12 months (unless
contraindicated).[23] The National Institute for
Health and Care Excellence (NICE) in the UK
recommends:[23]
• For patients who had undergone

• Prasugrel in those not taking an

oral anticoagulant. However, follow
your local protocol. At present,
many hospitals in the UK use
ticagrelor rather than prasugrel in
these patients. This new guidance
by NICE will require a change in
current practice in the UK. Consider
ticagrelor or clopidogrel in patients
aged 75 years or older if the
MANAGEMENT

concern
• Clopidogrel in those taking an oral
anticoagulant.
Ongoing
• For patients who had fibrinolysis:
• Ticagrelor unless the patient has a

high bleeding risk
• Clopidogrel or aspirin alone if the
patient has a high bleeding risk.
» Continue aspirin indefinitely unless the

patient has hypersensitivity.
More info: Antiplatelet therapy for

patients with a separate indication for
anticoagulation
Seek specialist advice when deciding

the duration and type (dual or single) of
antiplatelet therapy in the 12 months after
STEMI for patients with a separate indication
for anticoagulation (e.g., in patients with
ongoing atrial fibrillation).
The National Institute for Health and Care

Excellence (NICE) in the UK recommends
taking account of all of the following when
deciding about the duration and type (dual or
single) of antiplatelet therapy in patients with
a separate indication for anticoagulation:[23]
• Bleeding risk
• Thromboembolic risk
• Cardiovascular risk
• Patient's wishes.
Be aware that long-term continuation of
aspirin, clopidogrel, and oral anticoagulation
(triple therapy) significantly increases
bleeding risk.
For patients already on anticoagulation

who had PCI :[23]
• Continue anticoagulation and

clopidogrel for up to 12 months
• If the patient is taking a direct
oral anticoagulant, adjust the
dose according to bleeding
risk, thromboembolic risk, and
MANAGEMENT
cardiovascular risk.
For patients with a new indication for
anticoagulation who had PCI :[23]
159
Ongoing
• Offer clopidogrel (to replace prasugrel
or ticagrelor) for up to 12 months and
an oral anticoagulant licensed for the
indication, which best matches the
patient's bleeding risk, thromboembolic
risk, cardiovascular risk, and wishes.
For patients already on anticoagulation, or
those with a new indication, who did not
have PCI :[23]
• Continue anticoagulation and,

unless there is a high risk of
bleeding, consider continuing aspirin
(or clopidogrel for patients with
contraindication for aspirin) for up to 12
months.
Do not routinely offer prasugrel
or ticagrelor in combination with
anticoagulation in patients with a separate
indication for anticoagulation.[23]
plus start or continue beta-blocker or non-

dihydropyridine calcium-channel blocker
Primary options
» bisoprolol: 1.25 mg orally once daily initially

for 1 week, increase gradually according to
response, maximum 10 mg/day
OR
» carvedilol: 3.125 mg orally twice daily

initially, increase gradually according to
response, maximum 50 mg/day (body weight
<85 kg) or 100 mg/day (body weight >85 kg)
Secondary options
» verapamil: 240 mg orally (modified-release)

in the morning and 120 mg in the evening; or
120 mg orally (modified-release) three times
daily
» Ensure all patients are given a beta-

MANAGEMENT
blocker (while taking into account any

contraindications).[23]
• Start this as soon as the patient is

haemodynamically stable.[23]
Ongoing
• Continue the beta-blocker for at least
12 months if the patient does not have
reduced left ventricular ejection fraction
(LVEF).[23]
» Continue the beta-blocker indefinitely if the
patient has reduced LVEF.[23]
» Do not routinely give calcium-channel blockers

after STEMI.[23]
• Consider a non-dihydropyridine calcium-

channel blocker, such as verapamil, in a
patient without pulmonary congestion or
reduced LVEF who has a contraindication
to beta-blockers (or when these need to
be discontinued).[23]
» Do not offer nicorandil (a potassium-channel
activator) after STEMI.[23]
plus start or continue ACE inhibitor or
angiotensin-II receptor antagonist
Primary options
» enalapril: 2.5 mg orally once daily initially,

increase gradually according to response,
usual dose 10-20 mg twice daily, maximum
40 mg/day
OR
» ramipril: 2.5 mg orally twice daily for 3 days,

maximum 10 mg/day
OR
» lisinopril: 2.5 to 5 mg orally once daily

Secondary options
» valsartan: 20 mg orally twice daily initially,

maximum 320 mg/day
OR
MANAGEMENT
» losartan: 12.5 mg orally once daily initially,

maximum 150 mg/day
OR
161
Ongoing
» candesartan: 4 mg orally once daily initially,

maximum 32 mg/day
» Ensure all patients are given an ACE inhibitor

(while taking into account any contraindications).
• Start this as soon as the patient is

haemodynamically stable and continue
it indefinitely. Complete upwards dose
titration within 4-6 weeks of hospital
discharge.[23]
• Offer an angiotensin-II receptor antagonist
as an alternative if the patient is intolerant
to an ACE inhibitor.[23]
• Measure renal function, serum
electrolytes, and blood pressure before
starting an ACE inhibitor or angiotensin-
II receptor antagonist.[23] In practice, if
the patient has abnormal renal function or
blood pressure, start with a low dose and
titrate this carefully with close monitoring.
plus statin
Primary options
» atorvastatin: 40-80 mg orally once daily
OR
» rosuvastatin: 20-40 mg orally once daily
» Ensure all patients are given a high-

intensity statin (while taking into account any
contraindications).[15] [23]
consider aldosterone antagonist
Primary options
» eplerenone: 25 mg orally once daily initially,

maximum 50 mg/day
OR
MANAGEMENT
» spironolactone: 25 mg orally once daily

Ongoing
» Give an aldosterone antagonist to any patient
with signs or symptoms of heart failure and
reduced left ventricular ejection fraction.[23]
• Start this within 3-14 days of a STEMI

and preferably after starting an ACE
inhibitor.[23]
plus cardiac rehabilitation

» Offer cardiac rehabilitation to all patients.
This should include an exercise component,
health education, stress management, and
psychological and social support. Advise all
patients on lifestyle changes such as:[23]
• Changes to diet
MANAGEMENT
163
Emerging
Factor Xa inhibitors
These are being studied for acute coronary syndromes.[207] Rivaroxaban is a factor Xa inhibitor that has
been shown to reduce cardiovascular events when given in addition to dual antiplatelet therapy to stabilised
STEMI patients, but increases bleeding events.[208] One review and meta-analysis found that direct oral
anticoagulants in combination with antiplatelet therapy were associated with a reduced risk of ischaemic
events at the cost of an increase in major bleedings compared with antiplatelet therapy alone in patients with
STEMI.[209]
Primary prevention
Use a systematic approach among people aged 40 years and above to identify those who are likely to be at
high risk of cardiovascular disease (CVD).[15] [16] This may be based on an estimate of 10-year risk, lifetime
risk, or a combination of the two.
• Current National Institute for Health and Care Excellence (NICE) guidance recommends the use of the
QRISK2 tool to assess 10-year CVD risk for primary prevention in individuals up to and including 84
years of age.[15] [QRISK2]
• An evidence review by NICE concluded that the updated QRISK3 version of the tool performs
better in identifying those at greatest risk of heart disease and stroke.[17] [QRISK2]
• The European Society of Cardiology guideline on CVD prevention recommends an assessment of
lifetime risk using the country-specific SCORE risk charts.[16] [SCORE risk charts]
• The JBS3 calculator recommended by the Joint British Societies guideline can be used to estimate
both 10-year and lifetime risk of CVD for an individual.[18] [JBS3 risk calculator]
• NICE recommends treating any person aged 85 years or older as being at high risk of CVD based on
age alone, and especially if the person smokes and/or has high blood pressure.[15]
• Some groups of patients are unsuitable for calculator-based risk assessment so check the guidance
for each tool carefully.
Offer a statin to any individual whose CVD risk score puts them at increased risk of CVD.
• NICE recommends offering atorvastatin for primary prevention to anyone whose 10-year CVD risk
is estimated to be 10% or higher, using the QRISK tool (after modification of lifestyle and other
modifiable risk factors).[15]
• The Scottish Intercollegiate Guidelines Network (SIGN) has concluded that a 10-year CVD risk of 20%
or higher is a more appropriate threshold for offering statin treatment for primary prevention.[19]
• This was based on concerns about the practical challenges associated with the lower treatment
threshold recommended by NICE. SIGN’s analysis found 95% of all individuals aged 60 to 64 in
Scotland would be eligible for treatment under a 10% or higher 10-year risk threshold.
Encourage all individuals to adopt a healthy lifestyle and take steps to modify any major risk factors for CVD
regardless of their 10-year or lifetime risk score.[15] [16]
• Advise smokers to stop and offer support to help them do so.

• Offer antihypertensive medication as appropriate.
• Advise weight loss if the person is overweight or obese.
MANAGEMENT
• Encourage a cardioprotective diet.

• Offer advice on ways of increasing activity levels to the recommended minimum (150 minutes of
moderate intensity or 75 minutes of vigorous intensity aerobic physical activity each week).
Aspirin is not recommended for the primary prevention of CVD because the increased risk of major bleeding
is considered to outweigh any potential benefits.[16] [18] [19]
Secondary prevention
Offer cardiac rehabilitation to all patients. This should include an exercise component, health education,
stress management, and psychological and social support. Advise all patients on lifestyle changes such
as:[23]
• Changes to diet
The most important preventive actions involve combined dietary and lifestyle changes (stopping smoking;
increasing physical activity; losing weight; increasing consumption of fish, fruits, vegetables, fibre, and nuts;
reducing salt intake).
Patients should switch to a heart-healthy diet. If overweight, patients should lose weight and maintain a
healthy body weight. Patients should consume a diet rich in vegetables and fruits. Patients should be advised
to choose wholegrain, high-fibre foods and to eat fish, especially oily fish, at least twice a week. Excess
sugars, trans-fats, salt, and foods with excess cholesterol should be limited.
For a smoker, cessation is the single most crucial step that can be taken to reduce heart-related and all-
cause death. This includes avoiding second-hand smoke. Many different support programmes, medicines,
and alternative therapies are available to help. Data from the EVITA (Evaluation of Varenicline in Smoking
Cessation for patients post Acute Coronary Syndrome) trial suggest that pharmacotherapy with varenicline
started in hospital at the time of an acute coronary syndrome may be efficacious for smoking cessation;
however, further studies to assess safety end points are needed.[223]
Improving physical fitness through aerobic exercise is extremely important. It is recommended that patients
engage in ≥30 minutes of moderate-intensity physical activity on most, and preferably all, days of the week.
Likewise, patients should engage in multiple short bouts of physical activity daily, such as walking the dog or
taking the stairs instead of the lift.
Family members can be very helpful and should become involved along with other support systems to help
remind patients of, and to reinforce, lifestyle changes. Patients should use the resources that are available
(e.g., written materials, the Internet, educational classes, regular counselling) and be in close communication
with healthcare providers.
Patient discussions
Patients should schedule a follow-up appointment with their doctor in 1-2 weeks. Patients should be
given prescriptions and detailed discharge instructions including a list of medicines to take (e.g., dual
antiplatelet therapy, ACE inhibitor, beta-blocker, statin). These instructions should inform the patient what
MANAGEMENT
to do if they experience any recurrent signs or symptoms and should include restrictions on physical
activity. Before discharge, patients should also receive instruction and prescriptions for any additional
testing that is needed by the physician. If one is available, patients should enter a cardiac rehabilitation
programme. Cardiac rehabilitation is a structured programme that provides myocardial infarction survivors
with the tools, motivation, and support needed to change behaviour and increase chance of survival.
165
Typically, cardiac rehabilitation programmes use group therapy to supervise and promote beneficial
exercise, as well as to provide emotional support.
Patients should return to the nearest accident and emergency department or call their physician if they
develop recurring chest pain or discomfort, shortness of breath, sweating, gastrointestinal symptoms,
lightheadedness, palpitations, or other symptoms suggesting another myocardial infarction or heart
condition.
MANAGEMENT
ST-elevation myocardial infarction Follow up
Monitoring
Monitoring
FOLLOW UP
Survivors of acute MI should be closely followed up to ensure adequate modification of risk factors and
optimisation of (and adherence to) pharmacotherapy for secondary prevention, as well as to monitor for
the development of post MI complications and/or residual angina symptoms. Patients should be evaluated
within 2 to 3 weeks of discharge and evaluated periodically based on the extent of myocardial damage
and patient condition.
Initiating risk-factor modification and aggressive medical management prior to discharge has been
associated with increased patient adherence. All patients should continue the optimal medical regimen
indefinitely. This includes dual antiplatelet therapy with aspirin plus ticagrelor, prasugrel, or clopidogrel (for
at least 1 year); beta-blockers; statins; and ACE inhibitors (especially in patients with decreased ejection
fraction).
Ejection fraction is assessed by echocardiography during the index hospital admission, possibly 3
months after the acute episode (depending on physician discretion and/or institutional protocols) and then
periodically thereafter, depending on left ventricular (LV) function and symptoms. Patients with ejection
fraction <35% at 3 months' follow-up should be referred to an electrophysiologist for consideration of
an implantable cardioverter defibrillator (ICD), as there is a high risk for arrhythmias in this population.
Patients who develop diminished LV function and congestive heart failure should be followed up and
managed appropriately.
Patients with a history of MI are at increased risk for recurrent infarction. They should be evaluated by
stress testing or cardiac catheterisation if symptoms develop. Routine periodic ischaemic evaluations with
stress echocardiography or myocardial perfusion studies are controversial.
167
Complications
Complications Timeframe Likelihood

FOLLOW UP
sinus bradycardia, first-degree heart block, and type I short term medium
second-degree heart block
Usually develop with occlusion of the right coronary artery, and are caused by infarction of the
atrioventricular node and the conduction system above the His bundle or by increased vagal tone.
These arrhythmias are usually benign and transient and do not require any treatment. If the heart rate
goes below 50 bpm and the patient is symptomatic, give intravenous atropine.
Temporary pacing may be required if heart failure, syncope or angina develop.
complete heart block with anterior MI short term medium
Can develop acutely in patients with anterior infarcts and may lead to ventricular asystole.
Complete heart block in anterior infarcts occurs because of infarction and necrosis of the bundle branches
in the septum.
Trans-cutaneous or, preferably, trans-venous pacing should be carried out in these patients immediately
after conduction defects are noticed. Permanent pacing is usually required.
recurrent chest pain short term medium
Chest pain may occur in as many as 50% of patients after percutaneous coronary intervention.[216]
Angina-like symptoms should be assessed with ECG changes for escalation of medical therapy, and an
intra-aortic balloon pump and repeat angiography considered.[10]
type II second-degree heart block with anterior MI short term low
Usually occurs from a defect in the conduction system below the His bundle and can rapidly progress into
complete heart block in patients with anterior MI.
Trans-cutaneous or more preferably trans-venous cardiac pacing should be carried out in these patients
immediately after conduction defects are noted.
complete heart block with inferior MI short term low
Can develop in patients with inferior infarcts caused by vagal stimulation.
Usually transient or resolved with atropine.
Temporary pacing may be required if heart failure, syncope, or angina develop. Permanent pacing is rarely
required.
acute mitral regurgitation short term low
Inferior MI can cause rupture of the posteromedial papillary muscle, while anterolateral infarctions can
cause rupture of the anterolateral papillary muscle.

Right ventricular papillary muscle rupture is rare and can cause life-threatening tricuspid regurgitation.
FOLLOW UP
Complete papillary muscle rupture causes wide-open mitral regurgitation and is usually fatal.
Patients with incomplete papillary muscle rupture require emergency cardiac surgery.
Inotropic support and an intra-aortic balloon pump should be considered for transient stabilisation before
emergency surgery.
ventricular septal defects (VSD) short term low
Interventricular septal rupture causing a VSD can occur.
Rupture associated with anterior infarction is more apical in location, while inferior infarctions are
associated with more basal septal perforations and a much worse prognosis.
Rupture of the septum is more likely to be associated with complete heart block or right bundle branch
block.
These patients require emergency cardiac surgery either via open heart surgery or percutaneously using a
closure device.
Survival depends on early recognition, defect size, and degree of impairment of ventricular function.
acute pericardial tamponade short term low
Ventricular free wall rupture causing acute pericardial tamponade accounts for up to 10% of in-hospital
mortality from STEMI.
Thinness of the apical wall with marked intensity of necrosis at the terminal end of blood flow and shearing
effect of muscular contraction are proposed causes.
Tamponade most often occurs in patients without previous infarction and usually occurs at the junction of
the infarct and normal muscle.
There is an increased risk of ventricular wall rupture involving anterior and lateral walls after anterior MI.
Incomplete rupture can result in the development of a pseudoaneurysm.
Acute or complete rupture is rarely treatable.
Patients require emergency surgery for surgical resection of necrotic myocardium and primary
reconstruction.
Inotropic support and intra-aortic balloon counterpulsation for transient stabilisation should be considered
before surgery.
post-infarction pericarditis (Dressler's syndrome) short term low
Occurs in 5% to 10% of patients with MI.
169

Aspirin is the treatment of choice, as other non-steroidal anti-inflammatory drugs impair scar formation in
animal studies.[217]
FOLLOW UP
congestive heart failure long term high
Congestive heart failure caused by decreased left ventricular (LV) function occurs frequently after MI
because of myocardial damage, infarct progression, and LV remodelling after the acute episode.
Appropriate use of medications, including beta-blockers, ACE inhibitors, angiotensin-II receptor

antagonists, and diuretics, when appropriate, decreases the incidence and progression of congestive heart
failure.
Biventricular pacing with or without an implantable cardioverter defibrillator should be considered if

appropriate criteria are met.
ventricular arrhythmias variable high
Ventricular tachycardia and ventricular fibrillation can occur during ischaemia and reperfusion and can
be lethal. They can also occur at any stage following a MI because of re-entry circuits at the border of
myocardial scar and normal myocardium, and are commonly seen in patients with decreased ejection
fraction.
Electrolytes should be optimised, especially potassium and magnesium, as electrolyte imbalance

increases the risk of ventricular arrhythmias. Potassium should be maintained at >4 millimol/L (4 mEq/L)
and magnesium at >1 millimol/L (2 mEq/L).
Appropriate therapy should be initiated with direct current cardioversion and anti-arrhythmic therapy.
Optimal medical management (in particular, beta-blockers) decreases incidence of ventricular arrhythmias.
Implantable cardioverter defibrillator should be considered for all patients with persistently decreased left
ventricular ejection fraction (<35%) if there has been no response to 3 months of intensive medical therapy
after MI.[214]
recurrent ischaemia and infarction variable high
Patients with acute MI can have recurrent ischaemia or infarction caused by further plaque rupture and
progression of atherosclerosis.
Recurrence should be treated in the same manner as the initial presentation.
Aggressive risk factor modification after the initial presentation decreases incidence of recurrences.
depression variable high
Common complication post MI, and patients should routinely be screened for it.[215]
Management with antidepressants or psychological therapies may be necessary.
in-stent thrombosis variable low

Dual antiplatelet therapy is recommended for at least 12 months in all patients whether they have been
stented or not. In-stent thrombosis is often precipitated by premature cessation of dual antiplatelet
FOLLOW UP
therapy, but can also be caused by technical factors and other comorbidities such as diabetes mellitus.
Patients and their family should be strongly cautioned in hospital and in follow-up appointments about the
importance of dual antiplatelet therapy for 12 months.[218]
left ventricular (LV) thrombus variable low
LV thrombus can be seen in the early days of acute MI, especially large anterior MI with dyskinesia of the
apex. In early studies, LV thrombus was visualised by echocardiography in about one third of patients with
large anterior MI[219] [220] [221] in the absence of early revascularisation. The rate of embolism was low
even in patients with LV thrombus (4.5%). In a more recent study, in the era of early reperfusion therapy,
LV thrombus was identified in 8.8% of patients with cardiac magnetic resonance imaging (MRI).[222]
The majority of patients (88%) had resolution of LV thrombus on follow-up cardiac MRI. Large baseline
infarct size is a risk factor for LV thrombus formation. Anticoagulation with vitamin K antagonists may be
considered in patients with LV mural thrombus.[10]
LV aneurysm variable low
The incidence of LV aneurysm formation after acute MI is low (<5%) in the era of reperfusion therapy,
and it is seen more frequently in large anterior MI. The presence of LV aneurysm may increase the risk
for thrombo-embolic complications and arrhythmia, although surgery is rarely needed to correct the
aneurysm.[10]
Prognosis
Prognosis for patients with STEMI varies depending on time to presentation after onset of chest pain
and time to treatment after presentation. Survival rates have improved significantly over the last 20 years
but mortality remains substantial. The in-hospital mortality of unselected STEMI patients in national
registries of European countries ranges from 4% to 12%, while reported 1-year mortality of STEMI patients
in angiography registries is around 10%.[4] Prognosis is improved by early reperfusion, adherence to
appropriate medical therapy, and risk factor modification. Patients with elevated troponin levels have a worse
prognosis than those with normal troponin levels.[210] Adherence to evidence-based medicine has been
shown to have better patient outcomes.[211] In-hospital death and reinfarction can affect 5% to 10% of
patients.[212] Major bleeding as defined by the Bleeding Academic Research Consortium (BARC) or the
Thrombolysis in Myocardial Infarction (TIMI) bleeding score is associated with worse 1-year mortality.[213]
171
ST-elevation myocardial infarction Guidelines
Diagnostic guidelines
United Kingdom
Acute coronary syndromes

Published by: National Institute for Health and Care Excellence Last published: 2020
Europe
Fourth universal definition of myocardial infarction

Published by: European Society of Cardiology Last published: 2018
2018 ESC/EACTS guidelines on myocardial revascularization

Published by: European Society of Cardiology; European Association Last published: 2018
for Cardio-Thoracic Surgery
GUIDELINES
Management of acute myocardial infarction in patients presenting with ST-

segment elevation
2017 ESC focused update on dual antiplatelet therapy in coronary artery

disease developed in collaboration with EACTS
North America
2015 ACCF/AHA/SCAI focused update on primary percutaneous coronary

intervention for patients with ST-elevation myocardial infarction
Published by: American College of Cardiology Foundation; American Last published: 2015
Heart Association; Society for Cardiovascular Angiography and
Interventions
2013 ACCF/AHA guideline for the management of ST-elevation myocardial

infarction
Heart Association
Treatment guidelines
United Kingdom
Acute coronary syndromes

Recent-onset chest pain of suspected cardiac origin: assessment and

diagnosis
Ticagrelor for the treatment of acute coronary syndromes

Endoaortic balloon occlusion for cardiac surgery
GUIDELINES
Acute coronary syndrome

Published by: Joint Royal Colleges Ambulance Liaison Committee Last published: 2007
Europe
2018 ESC/EACTS guidelines on myocardial revascularization

Published by: European Society of Cardiology; European Association Last published: 2018
for Cardio-Thoracic Surgery
2017 ESC focused update on dual antiplatelet therapy in coronary artery

disease developed in collaboration with EACTS
Management of acute myocardial infarction in patients presenting with ST-

segment elevation
European Resuscitation Council guidelines 2021.

Published by: European Resuscitation Council Last published: 2021
Pre-hospital treatment of STEMI patients

Published by: Working Group Acute Cardiac Care of the European Last published: 2011
Society of Cardiology
173
North America
Clinical policy: emergency department management of patients needing

reperfusion therapy for acute ST-segment elevation myocardial infarction
Published by: American College of Emergency Physicians Last published: 2017
ACC/AHA/SCAI focused update on primary percutaneous coronary

intervention for patients with ST-elevation myocardial infarction: an update
of the 2011 ACCF/AHA/SCAI guideline for percutaneous coronary intervention
and the 2013 ACCF/AHA guideline for the management of ST-elevation
Published by: American College of Cardiology; American Heart Last published: 2015
Association; Society for Cardiovascular Angiography and Interventions;
American College of Emergency Physicians
Acute coronary syndromes: 2015 American Heart Association guidelines for

GUIDELINES
cardiopulmonary resuscitation and emergency cardiovascular care science

Published by: American Heart Association Last published: 2015
ACCF/AHA guideline for the management of ST-elevation myocardial

infarction
Heart Association
2013 AHA/ACC guideline on lifestyle management to reduce cardiovascular

risk
Association
2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce

atherosclerotic cardiovascular risk in adults
Association
2012 ACCF/AHA/HRS focused update of the 2008 guidelines for device-based

therapy of cardiac rhythm abnormalities
Association
AHA/ACCF secondary prevention and risk reduction therapy for patients with
coronary and other atherosclerotic vascular disease: 2011 update
Published by: American Heart Association; American College of Last published: 2011
Cardiology Foundation
2011 ACCF/AHA/SCAI guideline for percutaneous coronary intervention

Heart Association; Society for Cardiovascular Angiography and
Interventions
North America
Effectiveness-based guidelines for the prevention of cardiovascular disease

in women - 2011 update
Published by: American Heart Association Last published: 2011
Focused updates to guidelines in ST-elevation myocardial infarction

and percutaneous coronary intervention: application to interventional
cardiology
Published by: American College of Cardiology Interventional Scientific Last published: 2010
Council
Asia
API expert consensus document on management of ischemic heart disease
GUIDELINES
Published by: Association of Physicians of India Last published: 2006
Oceania
Guidelines for the management of acute coronary syndromes

Published by: National Heart Foundation of Australia; Cardiac Society Last published: 2016
of Australia and New Zealand
ST-elevation myocardial infarction: New Zealand management guidelines

Published by: ST-Elevation Myocardial Infarction Guidelines Group; Last published: 2013
New Zealand Branch of the Cardiac Society of Australia and New
Zealand
175
ST-elevation myocardial infarction Online resources
Online resources
1. QRISK2 (external link)
2. SCORE risk charts (external link)
3. JBS3 risk calculator (external link)

ONLINE RESOURCES
ST-elevation myocardial infarction References
Key articles
• Thygesen K, Alpert JS, Jaffe AS, et al. Fourth universal definition of myocardial infarction (2018). Glob
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Heart. 2018 Dec;13(4):305-38. Full text Abstract
• Ibanez B, James S, Agewall S, et al; ESC Scientific Document Group. 2017 ESC guidelines for the
management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur
Heart J. 2018 Jan 7;39(2):119-77. Full text Abstract
• National Institute for Health and Care Excellence. Acute coronary syndromes. November 2020
[internet publication]. Full text
• National Institute for Health and Care Excellence. Recent-onset chest pain of suspected cardiac origin:
assessment and diagnosis. November 2016 [internet publication]. Full text
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193
ST-elevation myocardial infarction Images
Images
IMAGES
Figure 1: Identifying the J point on the ECG

IMAGES
Figure 2: 12-lead ECG placement
Created by Npatchett (own work) [CC BY-SA 4.0], via Wikimedia Commons
195
IMAGES ST-elevation myocardial infarction Images
Figure 3: Coronary anatomy and ECG leads

Figure 4: Coronary anatomy and ECG leads table

IMAGES
Figure 5: Sgarbossa criteria for MI in the presence of LBBB
197
Figure 6: ST/S ratio under the modified Sgarbossa criteria

Figure 7: Anterior STEMI

Figure 8: Anterolateral STEMI example I

IMAGES
Figure 9: High lateral STEMI
Figure 10: Inferoposterior STEMI example II

199
Figure 11: Inferoposterolateral STEMI example III

IMAGES
Figure 12: Anterolateral STEMI example II

Figure 13: Anteroseptal STEMI example I

Figure 14: Anteroseptal STEMI example II

IMAGES
Figure 15: Left bundle branch block example I
201
Figure 16: Left bundle branch block example II

IMAGES
Figure 17: Left bundle branch block example III

Figure 18: Inferoposterior STEMI example I

IMAGES
Figure 19: Inferoposterolateral STEMI example I
203
Figure 20: Inferoposterolateral STEMI example II

Figure 21: Possible’ inferolateral STEMI

IMAGES
Figure 22: Possible’ inferolateral STEMI: ST-segment shift
205
Figure 23: Inferior STEMI example I

IMAGES
Figure 24: Inferior STEMI example II

Figure 25: Inferior STEMI example III

Figure 26: Paced rhythm example I

IMAGES
Figure 27: Paced rhythm example II
Figure 28: Paced rhythm example III

207
Figure 29: Left ventricular hypertrophy example I

IMAGES
Figure 30: Left ventricular hypertrophy example II

IMAGES
Figure 31: Acute pericarditis
209
Figure 32: Cardiac troponin kinetics after acute myocardial injury including acute MI
IMAGES
Figure 33: Selection of the most appropriate reperfusion strategy. PPCI, primary percutaneous coronary
intervention
211
Figure 34: Left main coronary artery: right anterior oblique view
IMAGES
Figure 35: Left main coronary artery: posterior anterior cranial view
213
Figure 36: Right coronary artery: left anterior oblique view

IMAGES
Figure 37: Coronary guidewire deployment
215
Figure 38: First balloon dilatation

IMAGES
Figure 39: Restoration of coronary flow
217
Figure 40: Stent positioning

IMAGES
Figure 41: Stent deployed
219
Figure 42: After stent deployment

IMAGES
Figure 43: Stent post-dilatation
221
Figure 44: RCA primary angioplasty: final result

IMAGES
Figure 45: Left anterior descending artery pre-dilatation image 1
223

IMAGES
225

IMAGES
Figure 49: Mid-LAD artery stent deployment image 1 - stent positioned in the mid-LAD artery
227
Figure 50: Mid-LAD artery stent deployment image 2 - stent balloon inflated
IMAGES
Figure 51: Mid-LAD artery stent deployment image 3 - post mid-LAD stent deployed
229
Figure 52: Proximal LAD stent deployment image 1 - following the mid-LAD stent deployment the proximal
vessel is pre-dilated
IMAGES
Figure 53: Proximal LAD stent deployment image 2 - proximal stent is positioned with the distal marker (blue
arrow) overlapping/within the proximal end of the previously deployed mid-LAD stent
231
Figure 54: Proximal LAD stent deployment image 3 - proximal stent deployed
IMAGES
Figure 55: Post-dilatation of overlapping stents
233
Figure 56: Final LAD stenting result: posterior anterior cranial view
IMAGES
Figure 57: Final LAD stenting result: right anterior oblique cranial view
235
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• ≥2.5 mm in men <40 years old

• 1 mm = 1 small square (at a standard ECG calibration of 10 mm/mV).

Characterised by glucose intolerance, hyperinsulinaemia, elevated triglycerides, low HDL-cholesterol,

established coronary artery disease

family history of premature coronary artery disease

STEMI is more common in men than in women.[4]

age >50 years

Fourth Universal Definition of Myocardial Infarction[1]

• Acute myocardial infarction (types 1, 2, and 3 MI)

• Includes STEMI and NSTEMI

• Includes vasospasm, coronary microvascular dysfunction, and non-atherosclerotic

• Type 4a MI – related to percutaneous coronary intervention

• Cardiogenic shock complicates 6% to 10% of STEMI admissions . Look for persistent

As soon as a clinical diagnosis of STEMI is made, make an immediate assessment of

• Characteristics of symptoms of myocardial ischaemia (including time since symptom onset

• Confirm a STEMI diagnosis

• ≥2.5 mm in men <40 years old

• 1 mm = 1 small square (at a standard ECG calibration of 10 mm/mV)

• ST depression ≥1 mm in ≥6 surface leads (i.e., inferolateral ST depression)

Practical diagnosis of STEMI

1. ST-segment elevation in at least two contiguous leads on a 12-lead ECG of ≥1 mm in all

• ≥2.5 mm in men <40 years old

Formal diagnostic criteria for STEMI

• Symptoms of acute myocardial ischaemia

• Classically retrosternal, crushing, heavy, severe, and diffuse in nature

• Dyspnoea is a common feature secondary to pulmonary congestion from left ventricular

• Left ventricular aneurysm

• Left ventricular free wall rupture

• Supraventricular tachyarrhythmias such as atrial fibrillation

• Supraventricular tachyarrhythmias such as atrial fibrillation

• The patient may describe indigestion rather than chest pain.

Do not rely on a positive patient response to glyceryl trinitrate as a reliable diagnostic

• Characteristics of symptoms ; in particular, chest pain:[29]

• “Have you ever had this type of pain before?”

• Nature, severity, and duration of pain

• Your priorities are to establish the following as quickly as possible :[29]

• Confirm the STEMI diagnosis

• Blood pressure, heart rate, and heart rhythm

• Congestive cardiac failure

• These added heart sounds could suggest severe heart failure.

• Acute ventricular septal defect

• This would suggest congestive cardiac failure ± pulmonary oedema.

Check for peripheral oedema and hepatomegaly.

• Killip class I = no signs of heart failure/pulmonary congestion

Evidence: Killip class and prognosis

Risk of death is strongly correlated to Killip class.

• In-hospital mortality remains high (≥50%.)

See our topic Shock .

• Altered mental status/reduced consciousness

• Papillary muscle rupture

Important differentials to consider

• Aortic dissection (ST elevation can be present on the ECG)

• A minority can present in cardiogenic shock (2% to 5%).[48] [49]

• 26% to 87% of patients with SCAD present with STEMI

• Conservative management with close ongoing monitoring is preferred for most