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 becomes unstable and ruptures, exposing thrombogenic material to circulating blood 1
- This triggers platelet aggregation and thrombus formation, leading to complete vessel occlusion 1
- Less commonly, STEMI can result from coronary artery dissection, particularly in younger patients and pregnant women 2
Epidemiology and Risk Factors
STEMI remains a leading cause of cardiovascular morbidity and mortality worldwide, though mortality has decreased dramatically from 30% in the 1960s to approximately 5% currently with modern reperfusion strategies. 3
Major Risk Factors:
- Atherosclerosis is the primary underlying pathology 4
- Hypertension accelerates atherosclerotic plaque development 4
- Diabetes mellitus increases both STEMI risk and severity 4
- Prior myocardial infarction identifies high-risk patients 5
- Age ≥75 years significantly increases bleeding risk and mortality 5
Pathophysiology
The pathophysiologic cascade begins with atherosclerotic plaque rupture, followed by thrombus formation causing complete coronary occlusion, leading to transmural myocardial ischemia and subsequent necrosis. 1
- Plaque rupture exposes subendothelial collagen and tissue factor 1
- Platelet adhesion and activation occur within seconds 1
- Thrombin generation amplifies the coagulation cascade 1
- Complete vessel occlusion prevents oxygen delivery to myocardium 1
- Irreversible myocardial necrosis begins within 20-40 minutes of complete occlusion 4
- Infarct size correlates directly with duration of occlusion, making time-to-reperfusion the critical determinant of outcomes 1
Clinical Manifestations
Typical STEMI presents with severe, crushing chest pain lasting >20 minutes, but atypical presentations including isolated dyspnea, epigastric pain, or syncope occur frequently and require high clinical suspicion. 6
Typical Symptoms:
- Severe chest pain or pressure radiating to left arm, jaw, or back 4
- Diaphoresis and sense of impending doom 4
- Nausea and vomiting, particularly with inferior wall MI 4
Atypical Presentations (require prompt ECG):
- Isolated dyspnea without chest pain 6
- Epigastric pain mimicking gastrointestinal pathology 6
- Syncope as presenting symptom 6
Physical Examination Findings:
- Tachycardia as compensatory response 6
- Hypotension indicating hemodynamic compromise 6
- Pulmonary rales suggesting acute heart failure 6
- Signs of cardiogenic shock (cool extremities, altered mental status, oliguria) 6
Diagnostics
STEMI diagnosis requires ST-segment elevation ≥0.1 mV (1 mm) in at least two contiguous precordial or adjacent limb leads, or new/presumed new left bundle branch block on 12-lead ECG obtained within 10 minutes of presentation. 6, 7
ECG Criteria:
- ST-elevation ≥1 mm in ≥2 contiguous leads is diagnostic 6, 7
- New or presumed new left bundle branch block should be treated as STEMI-equivalent 6
- True posterior MI (ST depression in V1-V3 with tall R waves) requires recognition 7
- Serial ECGs at 5-10 minute intervals if initial ECG non-diagnostic but suspicion remains high 7
Cardiac Biomarkers:
- Troponin elevation confirms myocardial necrosis but should not delay reperfusion therapy 4
- Peak creatine kinase correlates with infarct size 8
Imaging:
- Echocardiography during hospitalization to assess LV/RV function, detect mechanical complications, and exclude LV thrombus 7
- Coronary angiography defines coronary anatomy and guides revascularization 8
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 with goal first medical contact-to-device time <120 minutes. 6, 7
- Obtain 12-lead ECG within 10 minutes of emergency department arrival 7
- Aspirin 162-325 mg (chewable preferred) or IV 250-500 mg immediately 6, 7
- Maintenance aspirin 75-100 mg daily indefinitely 6
Reperfusion Strategy Algorithm
Primary PCI is the preferred reperfusion strategy when performed by an experienced team within 120 minutes of STEMI diagnosis; if this cannot be achieved, administer fibrinolytic therapy within 30 minutes of ambulance arrival. 6, 7
Primary PCI (Preferred):
- Goal: First medical contact-to-device time <120 minutes 6, 7
- Balloon inflation within 90 minutes in optimal circumstances 2
- Immediate angiography and PCI for cardiogenic shock regardless of time from symptom onset 6
- Primary PCI strategy for cardiac arrest patients with ST-elevation on post-resuscitation ECG 6
Fibrinolytic Therapy (Alternative):
- Administer within 30 minutes if primary PCI cannot be achieved within 120 minutes 6, 7
- Contraindicated in pregnancy due to bleeding risk; PCI strongly preferred 2
- Routine immediate PCI after successful fibrinolysis showed no benefit and increased adverse events in older trials 9
- PCI hours to days after successful fibrinolysis is increasingly supported but requires further study 9
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, 7
P2Y12 Inhibitor Selection:
- Prasugrel 60 mg loading dose, then 10 mg daily for patients undergoing PCI 5
- Prasugrel contraindicated in patients with prior TIA/stroke due to increased ICH risk (6.5% vs 1% with clopidogrel) 5
- Prasugrel generally not recommended in patients ≥75 years except high-risk situations (diabetes, prior MI) 5
- Consider 5 mg prasugrel maintenance dose in patients <60 kg due to increased bleeding risk 5
- Ticagrelor preferred alternative to prasugrel 6, 7
- Clopidogrel for fibrinolysis strategy 7
Duration of DAPT:
- Continue DAPT for 12 months after PCI unless contraindications develop 6
- In pregnancy: bare metal stents preferred over drug-eluting stents 2
- Clopidogrel duration in pregnancy: 14 days for no stent, ≥1 month for bare-metal stent 2
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, and continue oral beta-blockers indefinitely in all eligible patients. 7
Mandatory Therapies:
- ACE inhibitors within 24 hours (especially anterior MI, heart failure, LVEF ≤0.40) 7
- Beta-blockers indefinitely in all eligible patients 7
- High-intensity statin therapy targeting LDL-C <70 mg/dL or ≥50% reduction from baseline 6
- Low-dose aspirin 75-100 mg daily continued indefinitely 6
Contraindications in Pregnancy:
- ACE inhibitors, ARBs, and renin inhibitors absolutely contraindicated during pregnancy 2
- NSAIDs (except aspirin) discontinued due to increased mortality, reinfarction, and myocardial rupture risk 2
- Beta-blockers relatively safe in pregnancy 2
Emergency CABG Indications (Class I)
Emergency CABG should be performed for failed PCI with persistent pain/hemodynamic instability, at time of mechanical complication repair, and for cardiogenic shock in patients <75 years with severe multivessel/left main disease when revascularization can be performed within 18 hours of shock onset. 9
Specific Indications:
- Failed PCI with persistent pain or hemodynamic instability in suitable anatomy 9
- Persistent/recurrent ischemia refractory to medical therapy with significant myocardium at risk, unsuitable for PCI/fibrinolysis 9
- Surgical repair of post-infarction ventricular septal rupture or mitral valve insufficiency 9
- Cardiogenic shock in patients <75 years with severe multivessel/left main disease, revascularization within 18 hours of shock 9
- Life-threatening ventricular arrhythmias with ≥50% left main stenosis and/or triple-vessel disease 9
Class IIa (Can Be Useful):
- Primary reperfusion strategy in patients with suitable anatomy, not candidates for fibrinolysis/PCI, within 6-12 hours of evolving STEMI, especially with severe multivessel/left main disease 9
- Selected patients ≥75 years with good prior functional status who agree to invasive care 9
Class III (Should Not Be Performed):
- Persistent angina with small area at risk if hemodynamically stable 9
- Successful epicardial but unsuccessful microvascular reperfusion 9
Management of Complications
Emergency revascularization (PCI or CABG) is indicated for cardiogenic shock regardless of time delay from MI onset, with intra-aortic balloon counterpulsation for patients not quickly stabilized with pharmacological therapy. 7
- Immediate intervention for cardiogenic shock regardless of time from symptom onset 6, 7
- Intra-aortic balloon pump for refractory shock 7
- Suspect bleeding in any hypotensive patient post-procedure on prasugrel 5
- Manage bleeding without discontinuing antiplatelet therapy if possible, as discontinuation increases CV event risk 5
Special Populations
Pregnancy:
- Primary PCI strongly preferred over fibrinolysis to diagnose potential coronary dissection and minimize fetal radiation 2
- Coronary artery dissection more common than atherosclerotic disease in pregnant women 2
- Pre-term delivery considered for recurrent coronary dissections according to fetal viability 2
- Emergency CABG carries high mortality in pregnancy; only when other options fail 2
Elderly (≥75 years):
- Prasugrel generally not recommended except high-risk situations due to increased fatal/intracranial bleeding 5
- Selected patients ≥75 years may benefit from emergency CABG with good prior functional status 9
Critical Pitfalls and Caveats
- Do not delay reperfusion waiting for cardiac biomarkers 4
- Discontinue prasugrel ≥7 days before elective surgery when possible 5
- Do not start prasugrel in patients likely to undergo urgent CABG 5
- Increased bleeding risk with body weight <60 kg, propensity to bleed, concomitant anticoagulants 5
- Timing of prasugrel loading dose: In UA/NSTEMI, consider waiting until coronary anatomy established to avoid bleeding if urgent CABG needed 5
- Transient STEMI (symptoms/ECG changes resolve before reperfusion) requires intense medical therapy with early invasive approach, typically has better outcomes 8
- Discontinuing antiplatelet therapy in first weeks after ACS dramatically increases CV event risk 5