Stemi, Stemi Equivalents and STEMI Mimics: Kyaw Soe Win
Stemi, Stemi Equivalents and STEMI Mimics: Kyaw Soe Win
Stemi, Stemi Equivalents and STEMI Mimics: Kyaw Soe Win
STEMI
on ECG
Conventional STEMI
• In V2-3
• ≥ 0.2mV in men ≥ 40 years
• ≥ 0.25mV in men <40 years
• ≥ 0.15mV in women
examples of ST-elevation in MI
• In other leads
• ≥ 0.1mV for both sexes
General pitfalls
Beware of baseline ECG abnormalities ( Artefacts) that may obscure interpretation
Sinus tachycardia
STEMI location
• septal
• V1, V2
• inferior
• II, III, aVF
• reciprocal changes: I, aVL
• lateral
• I, aVL, V5, V6
• reciprocal changes: II, III, aVF
• anterior
• V3, V4
• anteroseptal
• V1, V2, V3, V4
• anterolateral
• I, aVL, V3, V4, V5, V6
• reciprocal changes: II, III, aVF
• posterior
• V7, V8, V9
ECG 1
Anterolateral STEMI
ECG 2
Inferior STEMI
ECG 3
Inferolateral STEMI
+ Horizontal ST depression V1-3
+ Tall R waves, upright T-waves V2-3
ECG 3 + posterior leads
Inferior-lateral-posterior STEMI
ECG 3 + RV leads
RV leads
Inferior-lateral-posterior-RV STEMI
Overview of Infarcts
Location of Infarct Arterial Supply Indicative Reciprocal
Changes Changes
Anterior LAD V1-V4 II, III, aVF
Inferior RCA II, III, aVF I, aVL
Lateral Circumflex I, aVL, V5, V6 V1
Posterior Posterior Descending None V1, V2
(RCA)
Septal Septal Perforating Loss of R wave in V1, None
(LAD) V2, or V3
Posterior Descending
(RCA
The ECG in ST Elevation MI
The Hyper-acute Phase
Less than 12 hours
• “ST segment elevation is the hallmark ECG abnormality of acute myocardial
infarction” (Quinn, 1996)
• The ECG changes are evidence that the ischaemic myocardium cannot completely
depolarize or repolarize as normal
• Usually occurs within a few hours of infarction
• May vary in severity from 1mm to ‘tombstone’ elevation
The Fully Evolved Phase
24 - 48 hours from the onset of a myocardial infarction
• ST segment elevation is less (coming back to baseline).
• T waves are inverting.
• Pathological Q waves are developing (>2mm)
The Chronic Stabilised Phase
• Isoelectric ST segments
• T waves upright.
• Pathological Q waves.
• May take months or weeks.
Reciprocal Changes
• Changes occurring on the opposite side of the myocardium that is
infarcting
Reciprocal Changes ie S-T
depression in some leads in MI
STEMI equivalents
STEMI equivalents
B B
• Hyperacute T waves L B
• De Winter ST T complex ew
= N
• Wellens T waves t s
l en
• Posterior MI
i va
• Shark T q u
I E
• Diffuse ST depression with aVR ST elevation EM
ST
• Persistent Pain e r
ng
• Sgarbossa Criteria
Lo
• Left Ventricular Hypertrophy No
• Hyperacute T waves
• Tall , often asymmetrical, broad- based anterior T waves often associated
with reciprocal ST depression
• Wellens T waves
• These ECG patterns are not always yet accompanied by chest pain and usually
precede overt ST elevation myocardial infarction. They can be interpreted as
an early sign of impending coronary occlusion ( with 24 hr)
• Type A: deeply- inverted anterior T waves
• Type B: biphasic anterior T waves
• Posterior MI
• 0.05 mV ST depression in V1-3 especially associated with positive T waves (0.05 mV elevation in
V7-9)
• Shark T
• J point depression transitioning in a convex ST segment
• Diffuse ST depression
• aVR /V1= 0.1mV + 8 leads with ST depression = 0.1mV is moderately suggestive of left main
coronary artery occlusion.
• Persistent Pain
• Persistent pain despite medical treatment, especially in the presence of RBBB or pace maker
rhyhthm should be regarded as a possible coronary occlusion in the absence of a clear alternative
explanation
Criteria for STEMI in the presence of LBBB and LVH
• Sgarbossa Criteria
• LBBB or pace maker rhythm with concordant or = 5mm ST elevation
LMCA Occlusion
• Seen with occlusion or near-occlusion of the left main artery
• Has been reported in occlusion of the proximal left anterior
descending artery and severe multivessel coronary artery disease
• 12-Lead ECG findings
• ST elevation in aVR ≥ 1mm
• ST elevation in aVR ≥ V1
• ST depression typically seen in lateral leads ( V4-6)
LMCA Occlusion
Criteria for STEMI in the
presence of LBBB and LVH
STEMI in LBBB
Sgarbossa’s Criteria
• Used to identify STEMI in the setting of LBBB or pacemaker
• Original Criteria
≥3 points = 98% probability of STEMI
≥2 is 61–100% specific, 20–79% sensitive
Sgarbossa et al. Electrocardiographic Diagnosis of Evolving Acute Myocardial Infarction in the Presence of Lef
Bundle-Branch Block. N Engl J Med 1996; 334:481-487February 22, 1996
How useful!
Sgarbossa’s Criteria
• ST elevation/depression should be
proportional to the size of the QRS
Sgarbossa’s Criteria
STEMI
Deviations from this suggest MI!
Sgarbossa’s Criteria
Smith’s Modification “Discordant ST elevation ≥.2 (1/5) of terminal S wave”
• Reduces false positives from large QRS
• May reduce false negatives from small QRS (microvoltages)
Make it proportional!
Smith et al. (2012) Diagnosis of ST-Elevation Myocardial Infarction in the Presence of Lef Bundle Branch Block With the ST-Elevation to S-Wave Ratio in a Modified Sgarbossa Rule . Ann Emerg
Med. 2012 Aug 31 Epub
Not STEMI STEMI
STEMI
STEMI in LVH
Left Ventricular Hypertrophy
• Single most common STEMI mimic
• May or may not exhibit ST changes
• Sgarbossa works well when it does
• Can be difficult to determine true size of QRS
(overprinting or clipping)
• Tip: True anterior STEMI almost never present
in setting of profound LVH
• Tip: ST segment may be benignly convex
• Voltage criteria generally irrelevant to question
of MI
No Longer STEMI Equivalents
New LBBB
• New LBBB alone is no longer a reason to activate the cath lab
• However, careful work up for ACS should be taken for symptomatic
patients with LBBB
• 12-Lead ECG findings
• QRS > 0.12 in limb leads
• Leads
• Large and wide R waves — leads I, aVL, V5, and V6
• Small R wave followed by deep S wave —leads II, III, aVF, V1–V3
New LBBB
The Problem: Most STE is not MI
Results
Only 15% of STE patients had MI!
Brady et al., Cause of ST segment abnormality in ED chest pain patients (Am J Emerg Med 2001 Jan;19(1):25-8)
In other words:
• Wrong treatment.
• Nitro? Aspirin? Fibrinolytics? Getting it right affects field and hospital
treatment.
Why?
“… because they have the highest mortality rate
when LBBB is due to extensive AMI”
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 10: Acute Coronary Syndromes
Left Bundle Branch Block
How?
So, if any two of the following are true, it is MI with sensitivity/specificity of 90%:
• R wave in V4 <13mm
• QTc >392
• ST elevation (measured 1.5 boxes after J point) more than 2mm
Smith et al. Electrocardiographic Differentiation of Early Repolarization From Subtle Anterior ST-Segment Elevation Myocardial Infarction. Ann Emerg Med. 2012 Jul;60(1):45-
56.e2. Epub 2012 Apr 19
Benign Early Repolarization
In short, except for ST elevation and big T waves, it shouldn’t look like MI!
Ventricular Rhythms
• Paced ventricular rhythms the only
rhythm other than LBBB with empirical
support for Sgarbossa’s criteria
• Do people with pacemakers have heart
attacks? . . .
• Nothing new here – use the rules – follow
serial ECGs – use your head
• Atypical pacer lead placement (not in
apex of right ventricle – or biventricular)
may not fit this model
Sgarbossa et al. Early Electrocardiographic Diagnosis of Acute Myocardial Infarction in the Presence of
Ventricular Paced Rhythm. Am J Cardiol, 1996; 77: 423–424.
Left Ventricular Aneurysm
• Refers to persistent aftereffects of a previous MI, which often includes
chronically-elevated ST segment
• May or may not actually entail aneurysm (bulging of a weakened section
of myocardium)
• Can present essentially identical to MI since that’s what it was!
• Somewhat more common in anterior leads
• Look into the past: PMH includes prior MI? Old ECG available?
Left Ventricular Aneurysm
Biggest clues:
In other words: compare QS depth to T height. The first should be relatively large,
the second relatively small. Otherwise suspect AMI.
If you want numbers: amplitude of T wave should be no more than .36 (~1/3) of QS
depth in each lead V1–V4. If ratio is greater, suspect AMI.
Smith SW. T/QRS ratio best distinguishes ventricular aneurysm from anterior myocardial infarction. Am J Emerg Med. 2005 May;23(3):279-87.
L V aneurysm
Pericarditis
• Inflammation of the pericardial sac, often infectious
• Clinical signs are suggestive although not specific:
• Chest pain that may be sharp and pleuritic
• Pain is alleviated by sitting up or leaning forward
• May be accompanied signs/symptoms of infection (fever, etc.)
• Friction rub appreciated on auscultation
• No relief with nitro
The disease process produces four distinct stages on the ECG over hrs/days:
• Stage 1: ST elevation
• Stage 2: Normalization
• Stage 3: T wave inversion
• Stage 4: Normalization
Depending on when you show up, you may see any of these.
pericardit
is
Infarct
WARNING! WARNING!
A much more sinister cause can closely resemble
pericarditis: occlusion of the LCA (left main) or
acute three-vessel disease, causing injury to
nearly the entire left ventricle.
If you see widespread ST elevation (or depression) and
start to think pericarditis, consider two things:
Pericarditis
• Clinical context. These patients will usually look terrible and so will their
rhythms.
Despite their acuity, LCA patients need a facility with PCI and CABG –
thrombolysis is not beneficial
Yamaji, et al. Prediction of acute lef main coronary artery obstruction by 12-lead electrocardiography. J Am Coll Cardiol, 2001; 38:1348-1354
less common STEMI mimics
Brugada Syndrome
• Distinct combination of ECG findings found to be a risk factor for sudden
polymorphic VT or VF
• Initially described in 1992, well-studied since and found to have a genetic
factor
• Only confirmed cause of Sudden Unexpected Death Syndrome among
young males in Southeast Asia
• Risk of sudden arrhythmia and possible death is variable (worse if there
is hx of syncope), but may be upward of 8% per year; treatment is EP
study + ICD
Brugada et al. Long-Term Follow-Up of Individuals With the Electrocardiographic Pattern of Right Bundle-Branch
Block and ST-Segment Elevation in Precordial Leads V1 to V3. Circulation. 2002;105:73.
Brugada Syndrome
ECG findings:
• ST elevation in V1–V2, sometimes V3, with particular
morphology
• RBBB or similar appearance
• Appearance may fluctuate over time
• ECG changes may be inducible with certain antiarrhythmics
Brugada is the “evil twin” of BER. . .your 12-lead may be the only chance to
catch a young, asymptomatic Brugada patient early
Brain injury and intracranial hemorrhage
• Head injury (traumatic and non-traumatic) can induce cardiac
dysfunction in 50%–100% of cases
• Some degree of heart failure is the most common result
• Thought to involve myocardial “stunning,” possibly resulting from
neurogenically-mediated vasospasm
• Effects are typically transient, but not necessarily benign
• ECG signs are variable, can include ST changes and giant inverted
“neurogenic” T waves; Osborne wave elevation is possible.
Jain, et al. Management of Patients with Stunned Myocardium Associated with Subarachnoid Hemorrhage. American Journal ofNeuroradiology 25:126-129, January 2004
Brain injury and intracranial hemorrhage
Bottom line:
• Primary point is not to be confused if you see ECG abnormalities
when assessing the brain injury patient. Consider the
circumstances, but the likelihood of concomitant ACS is very low.
• Diagnosing TAD is critical due to its high mortality and potential for rapid
deterioration
• Complicated by its similarity in presentation to AMI, which can include
ECG findings
• Distinguishing the two is critical due to radically different treatment
paths (different destination facilities, surgery vs. thrombolysis, etc.)
• Mechanism for ECG changes is physical impingement on coronary
arteries from retrograde dissection (i.e. it is true ischemia but not ACS)
Thoracic Aortic Dissection
ECG findings:
• May present with LVH baseline due to prevalence of background hypertension in TAD patients
• 8% will show ST elevation
• 42% will show some form of ischemic changes, including ST depression or T wave inversion
• 75% of the time in inferior leads
• 25% of the time in lateral leads
Mattu, A et al. Avoiding Common Errors in the Emergency Department. 2010.
Schubert. Thoracic aortic dissection: Distinguishing it from acute myocardial infarction. Canadian Family Physician.
Available from http://www.cfpc.ca/cfp/2003/May/vol49-may-clinical-3.asp
Bottom line:
• A very difficult and high-stakes diagnosis that still has no good solutions
• Have a high index of suspicion; TAD should be on your differential for all chest pain
patients
• If history and clinical picture leans toward TAD over MI, weigh the risks/benefits and
get to a hospital fast
Prinzmetal (Vasospastic) Angina
• A still-largely-idiopathic disorder involving spontaneous vasoconstriction
of the coronary vessels
• Distinguished from typical angina by its arbitrary onset, unrelated to
exercise
• Often occurs in setting of CAD, but produces symptoms disproportionate
to degree of stenosis
• Typically benign unless very severe, but in combination with CAD can
contribute to poor outcomes
Prinzmetal (Vasospastic) Angina
ECG findings:
• ST elevation, typically slight (1mm or less) but occasionally severe; sometimes with T wave
inversion
• Inverted U waves may be present
• Transient duration, generally relenting within several minutes
• ECG changes normalize with termination of episode, although some T wave inversion may
persist
Bottom line:
• Atypical or not, it’s angina! It will look and smell like angina!
• Nitro will likely be very effective
• It’ll pass – one more reason for serial ECGs. Signs/symptoms 10+ minutes start to point
to AMI.
• May not be distinguishable from aborted or “stuttering” MI (“winking and blinking”),
and those patients do need cardiac care, so play it safe
Miwa et al. Two electrocardiographic patterns with or without transient T-wave inversion during recovery periods of variant anginal attacks. Jpn Circ J. 1983 Dec;47(12):1415-22.
Wolf-Parkinson-White Syndrome
Bottom line:
• Start by recognizing the preexcitation
• Sgarbossa actually works in most cases, but not reliably – each accessory pathway is
different and conduction is unique. Approach it like LVH but keep an open mind.
• If diagnosis of WPW is clear, be skeptical about STEMI; symptoms are much more likely
related to arrhythmia than to MI.
Hypertrophic cardiomyopathy
Hyperkalemia
• Manifests with ECG findings that can resemble ACS
• ECG presentation may correlate unreliably with level of serum potassium
• May require immediate field treatment and management for arrhythmias
• History should be highly suggestive! Renal insufficiency is a major risk factor. Also consider meds
and major soft tissue trauma (crush syndrome, burns) as potential causes.
ECG findings:
• Early sign is hyperacute T waves, which classically appear:
• Fairly symmetric
• Narrow at the base and slim
• With a “sharp” point
• With a concave ST segment
• As it progresses, the QRS and T start to widen and merge, which both can cause apparent ST
elevation (or depression if QRS is positive) and can start to hide the narrowness of the T waves
Potassium 7.1
Potassium 8.5
Potassium 9+
AMI
Hyperkalemia
Bottom line:
• Hyperkalemia should be in your differential for every known dialysis patient with
general complaints or altered mental status
• Most diagnostic early ECG change is T wave morphology: peaked and narrow
• More advanced stages may be less clear, but by then (as QRS begins to resemble
BBB or ventricular rhythm) it should be obvious there is something other than
AMI going on
• Guard against arrhythmias and manage acutely (calcium, bicarb, fluids, etc.)
Tako-Tsubo Cardiomyopathy
Stress Cardiomyopathy
Transient Apical Ballooning
“Ampulla” Cardiomyopathy
or Broken Heart Syndrome
• Clinical correlation.
• Any suspicious ECG findings should be matched against patient presentation
and physical exam.
• Old ECGs.
• Extremely valuable tool when available for establishing baseline.
• Serial ECGs.
• Repeat 12-leads may reveal dynamic changes with time/treatment.
More tools for addressing this
• Expert consultation.
• Upload or interface with medical control, where available.
• Computer interpretation.
• Automatic algorithms provide a “virtual consult,” an always-
available second opinion.
Computer interpretations
Useless?
Infallible?
Massel D et al., Strict reliance on a computer algorithm or measurable ST segment criteria may lead to errors in thrombolytic therapy
eligibility. Am Heart J 2000 Aug; 140(2) 2216
Computer interpretations
• Fooled by SVT – distrust interpretations with HR > 100
But wait!
• No clinical sign/symptoms are completely reliable
• No ECG findings are completely reliable
• H/O regularly fools us
The answer?
Significant ST elevation in contiguous leads, with reciprocal changes, in the setting of clinical
correlation
Brady et al. Electrocardiographic ST-segment elevation: the diagnosis of acute myocardial infarction by morphologic
analysis of the ST segment. Acad Emerg Med. 2001 Oct;8(10):961-7.
More signs that point to MI
• Changes on serial ECGs. ACS is a dynamic process of supply/demand
imbalance; consecutive 12-leads should reveal ongoing changes.
• Mimics are typically electrically stable.
• When possible, obtain an initial ECG prior to treatment; oxygen/nitro may erase
ischemic changes.
• Perform serial recordings and watch for evolution over time; subtle becomes obvious,
NSTEMI becomes STEMI, etc. Any changes are suspicious.
• One of the best tools for distinguishing STEMI vs. mimics!
Early and continuous prehospital ECGs can play a crucial role in eventual care!
Changes from old ECGs. When available (from facility or patient), previous 12-
leads can establish a baseline -- but this only proves changes since the time
of that tracing.
Bringing it all together
• Obtain an early 12-lead, before treatment if possible.
• Are there ST or T-wave changes?
• How profound?
• What is their morphology?
• Are there reciprocal changes?
• What do you think and What does the computer think?
• Does the ECG support an alternate diagnosis?
• Would it explain the chief complaint?
• Is it more or less likely than MI?
• If likely, what is the probability of a comorbid MI?
• Is there any chance of an alternate diagnosis that is as or more pressing than
STEMI? (Aortic dissection, advanced hyperkalemia, etc.)
• Obtain serial ECGs to guide or confirm diagnosis.
Bringing it all together
So how do you make sense of 1,000,00 different mimics?
u r ro m
O i e f l e!
ld D u s c
ho u is M !
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