ST-Elevation Myocardial Infarction (STEMI)
Etiology
STEMI results from acute thrombotic occlusion of a coronary artery, typically following rupture or erosion of an atherosclerotic plaque. 1
- The underlying pathophysiology involves atherosclerotic plaque destabilization, leading to platelet aggregation, thrombus formation, and complete vessel occlusion 1
- Less common causes include coronary vasospasm, coronary dissection, or embolic phenomena 1
Epidemiology and Risk Factors
STEMI remains a major cause of cardiovascular morbidity and mortality worldwide, though incidence has declined with improved prevention strategies. 2
Traditional Risk Factors:
- Hypertension - major modifiable risk factor 1
- Diabetes mellitus - significantly increases risk 1
- Dyslipidemia - elevated LDL cholesterol 3
- Tobacco smoking - most important modifiable risk factor 1
- Age and sex - risk increases with age, males at higher baseline risk 1
- Family history of premature coronary disease 1
Pathophysiology
Complete thrombotic occlusion of a coronary artery leads to transmural myocardial necrosis if reperfusion is not achieved within 12 hours. 1
- Plaque rupture exposes thrombogenic material, triggering platelet adhesion and activation 1
- Thrombus propagation causes complete vessel occlusion with cessation of distal blood flow 1
- Myocardial cell death begins within 20-40 minutes of complete occlusion 4
- Infarct size correlates directly with duration of ischemia - time is myocardium 4, 5
- Transmural necrosis produces characteristic ST-segment elevation on ECG 3
Clinical Manifestations
Typical presentation includes severe, crushing chest discomfort lasting >20 minutes, often radiating to the left arm, neck, or jaw, accompanied by diaphoresis, nausea, and dyspnea. 1, 3
Typical Symptoms:
- Chest pain/pressure - substernal, severe, prolonged (>20 minutes) 1, 3
- Radiation to left arm, neck, jaw, or epigastrium 1
- Associated symptoms: diaphoresis, nausea, vomiting, dyspnea 1, 3
Atypical Presentations (especially in elderly, diabetics, women):
- Isolated dyspnea without chest pain 3
- Epigastric pain mimicking gastrointestinal pathology 3
- Syncope as presenting symptom 3
Physical Examination Findings:
- Tachycardia and hypotension suggest extensive infarction 3
- Pulmonary rales indicate left ventricular failure 3
- Signs of cardiogenic shock: cool extremities, altered mental status, oliguria 1, 3
- Jugular venous distension with inferior STEMI suggests right ventricular involvement 1
Diagnostics
A 12-lead ECG must be obtained and interpreted within 10 minutes of first medical contact in all patients with suspected STEMI. 1
ECG Criteria for STEMI:
- ST-segment elevation ≥0.1 mV (1 mm) in at least two contiguous precordial or adjacent limb leads 1, 3
- New or presumed new left bundle branch block 3
- Right-sided ECG leads (V3R, V4R) should be obtained in inferior STEMI to detect right ventricular infarction 1
Serial ECG Monitoring:
- If initial ECG is non-diagnostic but clinical suspicion remains high, repeat ECGs at 5-10 minute intervals or use continuous 12-lead ST-segment monitoring 1
Cardiac Biomarkers:
- Troponin elevation confirms myocardial necrosis but should never delay reperfusion therapy 1
- Biomarkers are useful for diagnosis in unclear cases and for risk stratification 1
Echocardiography:
- Routine echocardiography during hospitalization to assess LV/RV function, detect mechanical complications, and exclude LV thrombus 1, 3
Management
Immediate Pre-Hospital Management
Patients with suspected STEMI should immediately call 9-1-1 for EMS transport rather than self-transport, and should chew 162-325 mg non-enteric-coated aspirin while awaiting EMS arrival. 1, 3
- EMS personnel must perform 12-lead ECG at the site of first medical contact 1
- Pre-hospital ECG transmission to receiving hospital reduces door-to-balloon time and improves outcomes 1
- EMS should be equipped for early defibrillation and staffed with ACLS-trained personnel 1
Reperfusion Strategy Selection
Primary PCI is the preferred reperfusion method when it can be performed by an experienced team within 90 minutes (if presenting to PCI-capable hospital) or 120 minutes (if requiring transfer) from first medical contact. 1
Primary PCI Strategy:
- Direct EMS transport to PCI-capable hospital with goal first medical contact-to-device time ≤90 minutes 1
- Patients at non-PCI-capable hospitals should be immediately transferred with goal first medical contact-to-device time ≤120 minutes 1
- Patients transferred for primary PCI should bypass the emergency department and go directly to catheterization laboratory 1
Fibrinolytic Therapy Strategy:
- Fibrinolytic therapy should be administered within 30 minutes of hospital arrival when anticipated first medical contact-to-device time exceeds 120 minutes 1
- Pre-hospital fibrinolysis is preferred over in-hospital administration when this capability exists 1, 6
- Fibrin-specific agents are recommended: tenecteplase, alteplase, or reteplase 1, 6
Time Windows for Reperfusion
Reperfusion therapy should be administered to all eligible patients with symptom onset within 12 hours. 1
- Class I indication: symptoms <12 hours with persistent ST-elevation 1
- Class IIa indication: symptoms 12-24 hours with ongoing ischemia 1
- Routine PCI of occluded infarct artery >48 hours after symptom onset in asymptomatic patients is NOT indicated (Class III) 1
Antiplatelet Therapy
Aspirin 150-325 mg oral (chewable) or IV 250-500 mg should be administered immediately upon first medical contact, followed by maintenance dose of 75-100 mg daily indefinitely. 1, 3
P2Y12 Inhibitor Selection:
- A potent P2Y12 inhibitor (ticagrelor or prasugrel) should be administered before or at the time of PCI 1, 3
- Ticagrelor 180 mg loading dose, then 90 mg twice daily for 12 months 1, 3
- Prasugrel 60 mg loading dose, then 10 mg daily for 12 months (avoid if prior stroke/TIA, age ≥75 years, or weight <60 kg) 7
- Clopidogrel 300-600 mg loading dose only if ticagrelor or prasugrel unavailable or contraindicated 1
- Dual antiplatelet therapy (DAPT) should be continued for 12 months unless excessive bleeding risk develops 1, 3
Anticoagulation Therapy
For Primary PCI:
- Unfractionated heparin as weight-adjusted IV bolus with activated clotting time monitoring 1
- Bivalirudin has emerged as preferred agent with improved outcomes over UFH plus GP IIb/IIIa inhibitors 8
- Fondaparinux is NOT recommended for primary PCI 1
For Fibrinolytic Therapy:
- Enoxaparin IV followed by subcutaneous (preferred over UFH) 1, 6
- UFH as weight-adjusted IV bolus followed by infusion 1, 6
- Continue anticoagulation until revascularization or for duration of hospital stay up to 8 days 1, 6
Stent Selection in Primary PCI
Placement of either bare-metal stent or drug-eluting stent is recommended in primary PCI for STEMI. 1
- Bare-metal stents should be used in patients with high bleeding risk, inability to comply with 12 months of DAPT, or anticipated invasive/surgical procedures within the next year 1
- Drug-eluting stents should NOT be used in patients unable to tolerate or comply with prolonged DAPT due to increased stent thrombosis risk 1
Post-Fibrinolytic Management (Pharmacoinvasive Strategy)
All patients receiving fibrinolytic therapy should be transferred immediately to a PCI-capable center for angiography. 1, 6
Rescue PCI:
- Rescue PCI is indicated immediately when fibrinolysis has failed (<50% ST-segment resolution at 60-90 minutes) or with hemodynamic/electrical instability 1, 6
Routine Early PCI:
- Angiography and PCI of infarct-related artery should be performed 2-24 hours after successful fibrinolysis 1, 6
- Angiography should NOT be performed within first 2-3 hours after fibrinolytic administration 1
Emergency Angiography:
- Emergency angiography and PCI indicated for cardiogenic shock or acute severe heart failure 1
- Emergency PCI indicated for recurrent ischemia or evidence of reocclusion 1
Special Populations
Cardiogenic Shock:
- Patients with cardiogenic shock should be transferred for cardiac catheterization and revascularization as soon as possible, irrespective of time delay from MI onset 1
- Primary PCI is strongly preferred over fibrinolytic therapy 6
Cardiac Arrest:
- Immediate angiography and PCI should be performed in resuscitated out-of-hospital cardiac arrest patients whose post-resuscitation ECG shows STEMI 1, 3
- Therapeutic hypothermia should be started as soon as possible in comatose patients with STEMI and out-of-hospital cardiac arrest from VF/pulseless VT 1
Secondary Prevention and Long-Term Management
High-intensity statin therapy should be initiated immediately with target LDL-C <70 mg/dL or ≥50% reduction from baseline. 3
Lifestyle Modifications:
- Smoking cessation with repeated counseling, nicotine replacement, varenicline, or bupropion 1
- Cardiac rehabilitation program participation is strongly recommended 1
Medication Regimen:
- Low-dose aspirin 75-100 mg daily indefinitely 1, 3
- DAPT for 12 months (aspirin plus ticagrelor or prasugrel) 1, 3
- High-intensity statin continued long-term 3
- Beta-blockers, ACE inhibitors/ARBs as indicated for LV dysfunction 1
Medication to AVOID:
- NSAIDs (except aspirin) should be discontinued due to increased risks of mortality, reinfarction, hypertension, heart failure, and myocardial rupture 1
Critical Pitfalls to Avoid
- Never delay reperfusion therapy to wait for cardiac biomarkers - ECG diagnosis is sufficient 1
- Never perform PCI of non-infarct artery at time of primary PCI in hemodynamically stable patients (Class III: Harm) 1
- Never perform delayed PCI of totally occluded infarct artery >24 hours after STEMI in asymptomatic stable patients (Class III: No Benefit) 1
- Never use drug-eluting stents in patients unable to comply with 12 months DAPT 1
- Never delay primary PCI to obtain additional imaging or consultations in stable patients 1