STEMI MANAGEMENT

 Ischemic heart disease results from an imbalance between myocardial oxygen demand and oxygen supply that
is most often due to coronary atherosclerosis.
 Common clinical manifestations of ischemic heart disease include:
 Chronic stable angina
 The acute coronary syndromes of unstable angina
 Non–ST-segment elevation myocardial infarction, and
 ST Segment elevation myocardial infarction.

DESCRIPTION
 Acute myocardial infarction (AMI) is the rapid development of myocardial necrosis resulting from a sustained
and complete absence of blood flow to a portion of the myocardium.
 ST-segment elevation myocardial infarction (STEMI) occurs when coronary blood flow ceases following
complete thrombotic occlusion of a large coronary artery (usually) affected by atherosclerosis, causing
transmural ischemia.
 This is accompanied by release of serum cardiac biomarkers and ST-segment elevation on an ECG.
ETIOLOGY
Atherosclerotic coronary artery disease (CAD)
 Atherosclerotic lesions can be fibrotic, calcified, or lipid laden.
 Thin-capped atheroma are more likely to rupture and result in thrombotic occlusion.

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Non-atherosclerotic
 Emboli: vegetation, thrombi from left ventricle or atrium
 Mechanical obstruction: chest trauma, dissection of aorta or coronary arteries
 Increased vasomotor tone, variant angina
 Arteritis, others: hematologic (disseminated intravascular coagulation [DIC]), aortic stenosis, cocaine, IV
drug use, severe burns, prolonged hypotension
RISK FACTORS
 Advancing age
 Hypertension
 Tobacco use
 Diabetes mellitus
 Dyslipidemia
 Family history of premature onset of CAD
 Sedentary lifestyle
GENERAL PREVENTION
 Smoking cessation
 Healthy diet, weight control, regular physical activity
 Control of hypertension, hyperlipidemia, and diabetes
ASSOCIATED CONDITIONS
 Abdominal aortic aneurysm,
 Extracranial cerebrovascular (cv) disease,
 Atherosclerotic peripheral vascular disease
Diagnosis
HISTORY
 Classically, sudden onset of chest heaviness/tightness, with or without exertion, lasting minutes to hours
 Pain/discomfort radiating to neck, jaw, interscapular area, upper extremities, and epigastrium
 Previous history of myocardial ischemia (stable or unstable angina, MI, coronary bypass surgery, or
percutaneous coronary intervention [PCI])
 Assess risk factors for CAD, history of bleeding, noncardiac surgery, family history of premature CAD.
 Medications: Ask if recent use of phosphodiesterase type 5 inhibitors (if recent use, avoid concomitant
nitrates).
 Alcohol and drug abuse (especially cocaine)

PHYSICAL-EXAM
 General: restless, agitated, hypothermia, fever
 Neurologic: dizziness, syncope, fatigue, asthenia, disorientation (especially in the elderly)
 CV: dysrhythmia, hypotension, widened pulse pressure, S3 and S4, jugular venous distention (JVD)
 Respiratory: dyspnea, tachypnea, crackles GI: abdominal pain, nausea, vomiting
 Musculoskeletal: pain in neck, back, shoulder, or upper limbs Skin: cool skin, pallor, diaphoresis

TESTS
INITIAL-TESTS
 12-lead ECG: ST-segment elevation in a regional pattern ≥1 mm ST elevation (at least two contiguous
leads), with or without abnormal Q waves.
 ST depression ± tall R wave in V1/V2 may be STEMI of posterior wall.
 Absence of Q waves represents partial or transient occlusion or early infarction.
 New ST- or T-wave changes indicative of myocardial ischemia or injury.
 Consider right-sided and posterior chest leads if inferior MI pattern (examine V3R, V4R, V7–V9).

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ECG with continuous monitoring
 2D and M-mode echocardiographies are useful in evaluating regional wall motion in MI and left ventricular
function.
 Portable echo can clarify diagnosis of STEMI if concomitant LBBB.
 Useful in assessing mechanical complications and mural thrombus
 Once diagnosis suspected, coronary angiography is preferred emergently, with PCI.
TESTS-CONSIDERATIONS
Serum biomarkers
 Troponin I and T (cTnI, cTnT) rise 3 to 6 hours after onset of ischemic symptoms.
 Elevations in cTnI persist for 7 to 10 days, whereas those in cTnT persist for 10 to 14 days after MI.
 Myoglobin fraction of creatine kinase-MB (CK-MB): rises 3 to 4 hours after onset of myocardial injury;
peaks at 12 to 24 hours and remains elevated for 2 to 3 days; CK-MB adds little diagnostic value in
assessment of possible ACS to troponin testing.
 Myoglobin: early marker for myocardial necrosis; rises 2 hours after onset of myocardial necrosis, reaches
peak at 1 to 4 hours and remains elevated for 24 hours; myoglobin adds little diagnostic value in assessment
of possible ACS to troponin testing.
 Fasting lipid profile, CBC with platelets, electrolytes, magnesium,
 BUN, serum creatinine, and glucose; hemoglobin A1C;
 international normalized ratio (INR) if anticoagulation contemplated;
 brain natriuretic peptide (BNP) is elevated in acute MI; may or may not indicate heart failure
PREGNANCY:
 Pregnant patients presenting with STEMI will need discussion of risks and benefits of invasive coronary
angiography with radiation exposure to fetus.
 Management should otherwise be same as in non-pregnant patients, with emergent coronary angiography and
PCI.
GERONTOLOGIC:
 Elderly patients may have an atypical presentation, including silent or unrecognized MI, often with
complaints of syncope, weakness, shortness of breath, unexplained nausea, epigastric pain, altered mental
status, delirium.
 Patients with diabetes mellitus may have fewer and less dramatic chest symptoms.
DIAG-PROCED-SURGERY
 High-quality portable chest x-ray; transthoracic and/or trans-esophageal echocardiography, contrast chest CT
scan may occasionally be of value acutely in equivocal presentations to evaluate for alternative diagnoses
(aortic dissection, PE, ventricular aneurysm).
 Coronary angiography is definitive test. .
ALERT
 Patients with chronic kidney disease need special attention to amount of contrast media used.
 Reduced volume of contrast and use of low or isosmolar contrast media may lower risk of progression of
renal impairment.
Treatment
GENERAL-MEASURES
 Following emergent revascularization, admit to telemetry/coronary care unit (CCU) with continuous ECG
monitoring and bed rest.
 Anxiolytics, if needed; stool softeners
 Antiarrhythmics, as needed, for unstable dysrhythmia; deep vein thrombosis (DVT) prophylaxis
 Continuation of aspirin 81 mg/day and clopidogrel 75 mg/day or prasugrel 10 mg/day or ticagrelor 90 mg
twice daily, β-blocker (BB), ACE inhibitors (or ARB if ACE-intolerant), lipid-lowering therapy, tight BP
control, progressively increased physical activity, smoking cessation
 Assess for depression and treat with an SSRI or psychotherapy if present, as depression is present in 20% of
patients post-MI and is a potent predictor for poor prognosis.
 Although it is unclear yet if treatment improves mortality, it does improve quality of life.
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MEDICATION
Medication recommendations based on 2013 ACC/AHA focused guideline updates and level recommendations
(1)[A,B] and 2017 ESC STEMI guidelines (2)[A,B]
First-Line (While awaiting revascularization)
Supplemental 2 to 4 L/min for patients with oxygen saturation <90% or
oxygen respiratory distress
Nitroglycerin 0.4 mg sublingual q5min for total of 3 doses,
(NTG) followed by nitroglycerin IV if ongoing pain and/or hypertension
sublingual and/or management of pulmonary congestion
if no contraindications exist (systolic <90 mm Hg or >30 mm Hg
below baseline, right ventricle [RV] infarct, use of sildenafil or
vardenafil within 24 hours or within 48 hours of tadalafil)
Morphine 4 to 8 mg IV with 2 to 8 mg IV repeated at 5- to 15-minute
sulfate intervals to relieve pain, anxiety, or pulmonary congestion
Antiplatelet
agents
Aspirin (ASA), initial dose 162 to 325 mg chewed
loading dose of Clopidogrel 300 mg
a P2Y12 Ticagrelor 180 mg Ticagrelor may cause
inhibitor transient dyspnea
Prasugrel 60 mg Do not recommend in
Prasugrel is contraindicated in patients with previous patients aged >75 years or
stroke/transient ischemic attack. lower body weight (<60
kg).
anticoagulation Unfractionated heparin (UFH) usually continued for 48 hours or Monitoring includes aPTT
therapy until PCI or ACT, Hgb/Hct, and Plt.
(1) Intravenous UFH: Initial bolus of 60 units/kg (maximum 4000 Unlike other anticoagulants,
units) UFH is not renally cleared
(2) Initial infusion of 12 units/kg/hour (maximum 1000 units/hour) and can be used safely in
Risks include bleeding, thrombocytopenia, and HIT with or those with renal impairment
without thrombosis.
Enoxaparin 30-mg intravenous bolus given in STEMI (if age
younger than 75)
Bivalirudin 0.75-mg/kg IV bolus and then 1.75-mg/kg/h infusion
for up to 4 hours after procedure
Fondaparinux should not be used as the sole anticoagulant to
support PCI.
An additional 85 units/kg of intravenous UFH is required
immediately before PCI revascularization to reduce the risk of
catheter thrombosis if fondaparinux was initially chosen as the
anticoagulant strategy
Duration of dual antiplatelet therapy (DAPT) is recommended 12 months after PCI.
In patients who are at high risk of severe bleeding complications, a P2Y12 inhibitor may be discontinued after 6
months
PCI (Percutaneous coronary intervention) versus fibrinolysis:
Goal is to keep total ischemic time within 120 minutes.
Door to needle time should be within 30 minutes or door to balloon time within 90 minutes.

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Coronary reperfusion therapy
Primary PCI (balloon angioplasty, coronary stents)
 Symptom onset of ≤12 hours
 Symptom onset of ≤12 hours and contraindication to fibrinolytic therapy irrespective of time delay
 Cardiogenic shock or acute severe HF irrespective of time delay from onset of MI
 Evidence of ongoing ischemia 12 to 24 hours after symptom onset
Radial access is recommended over femoral access.

Procedural considerations
 Routine aspiration thrombectomy no longer recommended prior to PCI as usefulness and safety not fully
established
 PCI of infarct-related artery (IRA) is indicated.
 PCI of a noninfarct artery may be considered in selected patients with STEMI and multivessel disease who
are hemodynamically stable, either at the time of primary PCI or as a planned staged procedure.

Fibrinolysis
 If presenting at a hospital without PCI capability and cannot be transferred to a PCI-capable facility to
undergo PCI within 120 minutes of first medical contact
 If no contraindications, administer within 12 to 24 hours of onset of symptoms if there is evidence of
ongoing ischemia.

Contraindications to Thrombolytic Therapy

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  Long-term Management After ACS
Adjunctive  Aspirin (162- to 325-mg loading dose and then 81 mg daily) indefinitely
antiplatelet  Clopidogrel (300-mg loading dose for patients <75 years of age, 75-mg dose for patients >75
therapy with years of age).
fibrinolysis  Clopidogrel 75 mg daily should be continued for at least 14 days and up to 1 year.
Adjunctive  Use anticoagulants (UFH, enoxaparin, or fondaparinux) as ancillary therapy to reperfusion
anticoagulatio therapy for minimum 48 hours and preferably duration of admission (up to 8 days) or until
n therapy with revascularization, if performed.
fibrinolysis  UFH is preferred for patient who will do PCI, or after fibrinolytic therapy.
 Enoxaparin is preferred for patient not at high risk of bleeding.
 Fondaparinux is preferred for patient at high risk of bleeding. No increased risk of HIT
UFH 60-unit/kg bolus (maximum 4000 units) and 12 units/kg/hour (maximum 1000
units/hour), to obtain an aPTT of 1.5–2.0 times control (about 50–70 seconds)
for at least 48 hours
Enoxaparin 30 mg intravenously (if 75 or older, omit bolus), followed in 15 minutes by a 1-
mg/kg subcutaneous injection (if 75 or older, 0.75 mg/kg) every 12 hours for the
duration of index hospitalization, for up to 8 days, or until revascularization.
Maximum 100 mg for the first two doses.
If 75 or older, maximum 75 mg for the first two doses.
If CrCl is less than 30 mL/minute, extend dosing interval to daily administration
Fondaparinu initial 2.5-mg intravenous dose, followed in 24 hours by 2.5-mg/day
x subcutaneous injections (contraindicated if CrCl is less than 30 mL/minute) for
the duration of the index hospitalization, for up to 8 days, or until
revascularization
Glycoprotein  In general, all patients receive aspirin and P2Y12 receptor antagonists, and a minority of
IIb/IIIa patients may benefit from the addition of GP IIb/IIIa inhibition in the acute management of
receptor ACS.
antagonists  at time of primary PCI in selected patients if there is no reflow or thrombotic complications
(abciximab, eptifibatide, or tirofiban)
 (avoid GPIIb/IIIa inhibitor in case of thrombocytobenia, PT < 100000 and give bivalirudin)
β-blocker  Decrease myocardial ischemia, re-infarction, and frequency of dysrhythmias and increase long-
term survival
 Oral β-blockerc should be initiated within 24 hr in patients who do not have signs of HF,
evidence of low-output state, increased risk of cardiogenic shock, or other contraindications to
β-blockade (e.g., PR interval > 0.24 s, second- or third-degree heart block, active asthma, or
reactive airway disease)
 Reasonable to continue in patients with NSTE-ACS with normal LV function.
 Use metoprolol succinate, carvedilol, or bisoprolol in concomitant stabilized HFrEFc ; add
cautiously in decompensated HF
 Avoid agents with intrinsic sympathomimetic activity (acebutolol, pindolol, penbutolol)
 IV β-blocker is potentially harmful in patients with risk factors for shock (age > 70 yr, HR >
110 beats/min, SBP < 120 mm Hg, and late presentation)
ACE  Should be initiated orally within 24 hours of STEMI in patients with anterior infarction, HF,
inhibitors diabetes, or ejection fraction (EF) ≤0.40 unless contraindicated.
 Contraindications include hypotension, pregnancy, and bilateral renal artery stenosis.
High-intensity  Should be started as early as possible within the first 24 hours.
statin therapy  Atorvastatin 80 mg
 An LDL goal of less than 70 mg/dL is reasonable in patients post-ACS..

(Aldosterone  Is recommended in patients with EF <40% and heart failure or diabetes, who are already
receptor receiving an ACE inhibitor and a BB, if there is no renal failure or hyperkalemia.
blockers)

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Pain control  Pain should be treated with acetaminophen, nonacetylated salicylates, tramadol, or narcotics at
the lowest dose to control symptoms.
 It is reasonable to use nonselective NSAIDs, such as naproxen, if initial therapy is insufficient

Second-Line
 Long-acting non-dihydropyridine calcium channel blocker (CCB) when BB is ineffective or
contraindicated if EF is normal; do not use immediate-release nifedipine.
SURGERY
 Urgent coronary artery bypass graft (CABG) surgery is indicated in patients with STEMI and coronary
anatomy not amenable to PCI who have ongoing or recurrent ischemia, cardiogenic shock, severe HF, or
other high-risk features.

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IN-PATIENT-CONSIDERATIONS
 All patients with STEMI should be admitted to a CCU or intensive cardiac care unit for evaluation and
treatment.
 Transfer high-risk patients who receive fibrinolytic therapy as primary reperfusion therapy at a non–PCI-
capable facility to a PCI-capable facility as soon as possible.
 Right ventricular infarction may need fluid resuscitation for hypotension.

Follow-up Recommendations
 Emphasize medication adherence. Identify high-risk patients for implantable cardioverter defibrillator (ICD)
placement (especially those with EF <30%).
 Consider exercise-based cardiac rehabilitation program and encourage smoking cessation.

DIET
Low-fat diet: reduced intake of saturated fats (to <7% of total calories) (but dairy fats are not likely associated with
CAD), trans fatty acids (to <1% of total calories). Impact of low-cholesterol diet remains uncertain.

COMPLICATIONS Heart failure, myocardial rupture/left ventricular aneurysm, pericarditis, dysrhythmias, acute
mitral regurgitation, and depression (common)

Top 10 Take-Home Messages for the Evaluation and Diagnosis of Chest Pain
1. Chest Pain Means More Than Pain in the Chest. Pain, pressure, tightness, or discomfort in the chest,
shoulders, arms, neck, back, upper abdomen, or jaw, as well as shortness of breath and fatigue should all be
considered anginal equivalents.
2. High-Sensitivity Troponins Preferred. High-sensitivity cardiac troponins are the preferred standard for
establishing a biomarker diagnosis of acute myocardial infarction, allowing for more accurate detection and
exclusion of myocardial injury.
3. Early Care for Acute Symptoms. Patients with acute chest pain or chest pain equivalent symptoms should
seek medical care immediately by calling 9-1-1. Although most patients will not have a cardiac cause, the
evaluation of all patients should focus on the early identification or exclusion of life-threatening causes.
4. Share the Decision-Making. Clinically stable patients presenting with chest pain should be included in
decision-making; information about risk of adverse events, radiation exposure, costs, and alternative options
should be provided to facilitate the discussion.
5. Testing Not Needed Routinely for Low-Risk Patients. For patients with acute or stable chest pain determined
to be low risk, urgent diagnostic testing for suspected coronary artery disease is not needed.
6. Pathways. Clinical decision pathways for chest pain in the emergency department and outpatient settings
should be used routinely.
7. Accompanying Symptoms. Chest pain is the dominant and most frequent symptom for both men and women
ultimately diagnosed with acute coronary syndrome. Women may be more likely to present with accompanying
symptoms such as nausea and shortness of breath.
8. Identify Patients Most Likely to Benefit From Further Testing. Patients with acute or stable chest pain who
are at intermediate risk or intermediate to high pre-test risk of obstructive coronary artery disease, respectively,
will benefit the most from cardiac imaging and testing.
9. Noncardiac Is In. Atypical Is Out. “Noncardiac” should be used if heart disease is not suspected. “Atypical”
is a misleading descriptor of chest pain, and its use is discouraged.
10. Structured Risk Assessment Should Be Used. For patients presenting with acute or stable chest pain, risk
for coronary artery disease and adverse events should be estimated using evidence-based diagnostic protocols.

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References:
Pharmacotherapy principles and practice
UpToDate
Merck manuals
Genebrandex

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