ST-Elevation Myocardial Infarction (STEMI)
Etiology
STEMI results from complete thrombotic occlusion of an epicardial coronary artery, typically developing from rupture of an atherosclerotic plaque. 1
- The underlying atherosclerotic plaque ruptures, exposing thrombogenic material that triggers platelet aggregation and thrombus formation, leading to complete vessel occlusion 1
- Risk factors driving atherosclerotic plaque development include hypertension, diabetes mellitus, dyslipidemia, smoking, and family history 2
- Less common causes include coronary artery dissection (particularly in pregnant women), coronary vasospasm, and embolic phenomena 3
Epidemiology and Risk Factors
STEMI represents the most acute and life-threatening manifestation of coronary artery disease, accounting for approximately 5% of acute myocardial infarction presentations. 1, 4
- Major modifiable risk factors include atherosclerosis, hypertension, diabetes mellitus, hyperlipidemia, smoking, and obesity 2
- Non-modifiable risk factors include advanced age, male gender, and family history of premature coronary disease 2
- Despite advances in treatment, STEMI continues to cause substantial morbidity and mortality worldwide, though in-hospital mortality has decreased from 30% in the 1960s to approximately 5% currently 5
Pathophysiology
The pathophysiologic cascade begins with atherosclerotic plaque rupture, followed by platelet activation, thrombus formation, complete coronary occlusion, myocardial ischemia, and ultimately myocardial necrosis if reperfusion is not achieved. 2, 1
- Plaque rupture exposes subendothelial collagen and tissue factor, triggering the coagulation cascade and platelet aggregation 1
- Complete thrombotic occlusion halts blood flow to the myocardium supplied by the affected coronary artery 1
- Myocardial cell death begins within 20-40 minutes of complete occlusion and progresses in a "wavefront" pattern from endocardium to epicardium 2
- Infarct size correlates directly with duration of ischemia, making time-to-reperfusion the critical determinant of outcomes 1
- Post-infarction complications include ventricular remodeling, heart failure, arrhythmias, mechanical complications (ventricular septal rupture, papillary muscle rupture), and cardiogenic shock 2
Clinical Manifestations
Typical presentation includes acute chest pain or pressure lasting >20 minutes, often radiating to the left arm, neck, or jaw, accompanied by diaphoresis, nausea, and dyspnea. 6
- Chest discomfort is typically described as crushing, squeezing, or pressure-like, not relieved by rest or nitroglycerin 2
- Atypical presentations occur more frequently in women, elderly patients, and diabetics, manifesting as isolated dyspnea, epigastric pain, syncope, or fatigue without chest pain 6
- Physical examination may reveal tachycardia, hypotension, pulmonary rales indicating acute heart failure, or signs of cardiogenic shock (cool extremities, altered mental status, oliguria) 6
- Patients may present with complications including ventricular arrhythmias, heart block, or mechanical complications 7
Diagnostics
STEMI diagnosis requires ST-segment elevation ≥0.1 mV (1 mm) in at least two contiguous precordial or adjacent limb leads on 12-lead ECG, or new/presumed new left bundle branch block. 6, 8
ECG Criteria and Timing
- Obtain 12-lead ECG within 10 minutes of emergency department arrival for all patients with chest discomfort or STEMI-equivalent symptoms 8
- If initial ECG is non-diagnostic but clinical suspicion remains high, perform serial ECGs at 5-10 minute intervals 8
- True posterior MI may present with ST-segment depression in anterior leads (V1-V3) with tall R waves 6
Cardiac Biomarkers
- Troponin elevation confirms myocardial necrosis but should not delay reperfusion therapy, as ECG findings are sufficient for STEMI diagnosis 2
- Peak creatine kinase levels correlate with infarct size and prognosis 4
Imaging
- Routine echocardiography during hospital stay assesses left and right ventricular function, detects mechanical complications, and excludes left ventricular thrombus 8
- Coronary angiography defines coronary anatomy and guides revascularization strategy 1
Management
Immediate Actions (First Medical Contact)
Administer 162-325 mg non-enteric coated aspirin (chewable or IV 250-500 mg) immediately upon first medical contact, followed by urgent reperfusion therapy. 6, 8
- Give aspirin 150-325 mg oral (chewable) or IV 250-500 mg immediately, then maintain with 75-100 mg daily indefinitely 6
- Obtain 12-lead ECG within 10 minutes to confirm STEMI diagnosis 8
- Establish IV access and administer supplemental oxygen only if oxygen saturation <90% 8
Reperfusion Strategy Decision Algorithm
Primary PCI is the preferred reperfusion strategy when performed by an experienced team within 120 minutes of first medical contact-to-device time. 6, 8
Primary PCI (Preferred Strategy)
- Perform primary PCI if first medical contact-to-device time can be achieved within 120 minutes 6, 8
- Goal: balloon inflation within 90-120 minutes of STEMI diagnosis 6, 3
- Primary PCI is superior to fibrinolysis in reducing mortality, reinfarction, and stroke 1
- In cardiogenic shock patients <75 years old, perform emergency angiography and PCI immediately regardless of time from symptom onset 6, 8
- Cardiac arrest patients with ST-elevation on post-resuscitation ECG should undergo primary PCI strategy 6
Fibrinolytic Therapy (Alternative When PCI Unavailable)
- Administer fibrinolytic therapy within 30 minutes of ambulance arrival if primary PCI cannot be performed within 120 minutes 6, 8
- Fibrinolysis is most effective when given within 3 hours of symptom onset, with diminishing benefit up to 12 hours 1
- Immediate PCI after successful fibrinolysis showed no benefit and increased adverse events including bleeding, recurrent ischemia, and death in older trials 7
- Routine PCI might be considered hours to days after successful fibrinolysis as part of an invasive strategy 7
Antiplatelet and Anticoagulant Therapy
Dual antiplatelet therapy with aspirin plus a potent P2Y12 inhibitor (ticagrelor or prasugrel preferred over clopidogrel) should be administered before or at the time of PCI. 6, 8
P2Y12 Inhibitor Selection
Prasugrel 60 mg loading dose, then 10 mg daily (preferred in most patients undergoing PCI) 6, 9
- Consider reducing maintenance dose to 5 mg daily in patients <60 kg due to increased bleeding risk 9
- Contraindicated in patients with prior TIA or stroke 9
- Generally not recommended in patients ≥75 years except in high-risk situations (diabetes or prior MI) 9
- Discontinue at least 7 days prior to CABG when possible 9
Clopidogrel for fibrinolysis strategy or when prasugrel/ticagrelor contraindicated 8
Duration of Therapy
- Continue dual antiplatelet therapy (DAPT) for 12 months after PCI unless contraindications develop 6
- Continue low-dose aspirin 75-100 mg daily indefinitely 6
Post-STEMI Medical Management
Initiate ACE inhibitors within 24 hours in all patients, particularly those with anterior MI, heart failure, or ejection fraction ≤0.40. 8
- Start oral beta-blockers and continue indefinitely in all eligible patients 8
- Initiate high-intensity statin therapy to target LDL-C <70 mg/dL or ≥50% reduction from baseline 6
- Discontinue NSAIDs (except aspirin) due to increased risks of mortality, reinfarction, hypertension, heart failure, and myocardial rupture 3
Emergency CABG Indications
Emergency or urgent CABG should be performed for failed PCI with persistent pain or hemodynamic instability in patients with suitable coronary anatomy. 7
Class I Indications for Emergency CABG
- Failed PCI with persistent pain or hemodynamic instability with suitable anatomy 7
- Persistent or recurrent ischemia refractory to medical therapy with significant myocardium at risk, unsuitable for PCI or fibrinolysis 7
- At time of surgical repair of post-infarction ventricular septal rupture or mitral valve insufficiency 7
- Cardiogenic shock in patients <75 years with severe multivessel or left main disease, revascularization possible within 18 hours of shock onset (within 36 hours of STEMI) 7
- Life-threatening ventricular arrhythmias with ≥50% left main stenosis and/or triple-vessel disease 7
Class IIa Indications
- Emergency CABG as primary reperfusion in patients with suitable anatomy who are not PCI or fibrinolysis candidates, within 6-12 hours of evolving STEMI, especially with severe multivessel or left main disease 7
- Selected patients ≥75 years with cardiogenic shock, good prior functional status, suitable for revascularization within 18 hours of shock 7
Class III (Should Not Perform)
- Persistent angina with small area at risk if hemodynamically stable 7
- Successful epicardial reperfusion but unsuccessful microvascular reperfusion 7
Management of Complications
For cardiogenic shock, perform emergency revascularization (PCI or CABG) regardless of time delay from MI onset. 8
- Intra-aortic balloon counterpulsation for patients not quickly stabilized with pharmacological therapy 8
- Mechanical complications (ventricular septal rupture, papillary muscle rupture) require urgent surgical repair with concomitant CABG 7
Special Population: Pregnancy
Primary PCI is strongly preferred over fibrinolysis in pregnant STEMI patients, as it allows diagnosis of coronary artery dissection (more common than atherosclerosis in pregnancy) while minimizing fetal radiation exposure. 3
- Use bare metal stents rather than drug-eluting stents due to unknown safety and requirement for prolonged DAPT 3
- Low-dose aspirin is relatively safe in pregnancy 3
- Use clopidogrel only when strictly needed and for shortest duration: 14 days for no stent, at least one month for bare-metal stent 3
- Beta-blockers are relatively safe in pregnancy 3
- ACE inhibitors, ARBs, and renin inhibitors are absolutely contraindicated during pregnancy 3
- Consider pre-term delivery in cases of recurrent coronary dissections according to fetal viability 3
Common Pitfalls and Caveats
- Do not delay reperfusion therapy waiting for troponin results—ECG findings are sufficient for STEMI diagnosis 2
- Avoid routine immediate PCI after successful fibrinolysis—this strategy increases bleeding and adverse events without benefit 7
- Do not discontinue antiplatelet therapy prematurely, particularly in the first few weeks after ACS, as this increases risk of subsequent cardiovascular events 9
- Suspect bleeding in any hypotensive patient who has recently undergone coronary angiography, PCI, CABG, or other procedures while on prasugrel 9
- Recognize atypical presentations in women, elderly, and diabetic patients who may present without chest pain 6
- In pregnancy, coronary artery dissection is more common than atherosclerotic disease, affecting management decisions 3