Management of ST-Elevation Myocardial Infarction (STEMI)
Etiology
STEMI results from complete thrombotic occlusion of a coronary artery, typically triggered by rupture or erosion of an atherosclerotic plaque with subsequent thrombus formation. 1
- Approximately 88% of patients presenting within 6 hours of symptom onset have a completely occluded coronary artery 2
- The underlying mechanism involves plaque rupture/erosion leading to platelet aggregation, thrombus formation, and distal embolization 2
- Atherosclerotic plaque instability is the primary substrate, with acute thrombosis converting chronic stable disease into acute coronary occlusion 1
Epidemiology and Risk Factors
STEMI remains a leading cause of morbidity and mortality worldwide despite advances in reperfusion therapy. 3, 1
- Multivessel disease is present in approximately 50% of STEMI patients, with residual non-infarct-related artery lesions containing vulnerable plaques 4
- Major risk factors include atherosclerosis, hypertension, diabetes mellitus, hyperlipidemia, and smoking 1
- High-risk subgroups include patients with cardiogenic shock, cardiac arrest, mechanical complications, and multivessel/left main disease 3
Pathophysiology
The pathophysiologic cascade begins with plaque rupture, progresses through thrombotic occlusion, and culminates in a time-dependent wavefront of myocardial necrosis. 2, 1
- Complete coronary occlusion leads to myocardial ischemia within minutes, with irreversible necrosis beginning at 20-40 minutes 1
- The extent of myocardial damage depends on duration of occlusion, collateral circulation, and presence of ischemic preconditioning 2
- Microvascular obstruction ("no-reflow") can occur despite successful epicardial recanalization due to distal embolization and microvascular injury 2
- Complications include pump failure (Killip classification), mechanical complications (free wall rupture, ventricular septal defect, mitral regurgitation), and arrhythmias 5
Clinical Manifestations
STEMI presents with acute chest discomfort, but atypical presentations are common in women, elderly patients, and diabetics. 6
- Typical presentation: substernal chest pressure/pain radiating to left arm, jaw, or back, lasting >20 minutes 1
- Associated symptoms include dyspnea, diaphoresis, nausea, and lightheadedness 1
- Atypical presentations (especially in women, elderly, diabetics) may include isolated dyspnea, epigastric pain, or syncope 6
- Physical examination may reveal tachycardia, hypotension, pulmonary rales (indicating heart failure), or signs of cardiogenic shock 5
- Killip classification stratifies heart failure severity: Class I (no rales/S3), Class II (rales <50% lung fields or S3), Class III (pulmonary edema with rales >50%), Class IV (cardiogenic shock) 5
Diagnostics
Obtain a 12-lead ECG within 10 minutes of first medical contact—this is the cornerstone diagnostic test that drives all subsequent management decisions. 7, 6
ECG Criteria
- ST-segment elevation ≥0.1 mV (1 mm) in at least two contiguous precordial or adjacent limb leads 7
- New or presumed new left bundle branch block 6
- Isolated ST depression in anterior leads (V1-V4) with ST elevation in aVR suggests left main or multivessel disease 6
- True posterior MI: ST depression in V1-V3 with tall R waves 7
Serial Assessment
- If initial ECG is non-diagnostic but clinical suspicion remains high, repeat ECGs at 5-10 minute intervals 7
- Continuous ECG monitoring with defibrillator capacity should be initiated immediately 6
- Follow-up ECGs at 24 hours and hospital discharge assess reperfusion success and infarct extent 7
Cardiac Biomarkers
- Troponin elevation confirms myocardial necrosis but should not delay reperfusion therapy 1
- Biomarkers are useful for risk stratification and diagnosis of reinfarction 1
Echocardiography
- Routine echocardiography must be performed during hospitalization to assess left ventricular and right ventricular function, detect mechanical complications (ventricular septal defect, mitral regurgitation, free wall rupture), and exclude left ventricular thrombus 7, 6
Coronary Angiography
- Emergency angiography is performed as part of primary PCI strategy 6
- In cardiogenic shock, emergency angiography and revascularization are indicated regardless of time from symptom onset 6
Management
Immediate Actions (First 10 Minutes)
Administer 162-325 mg non-enteric coated aspirin (chewable) immediately upon first medical contact—this is a Class I recommendation that should never be delayed. 7, 6
- If patient cannot swallow, give aspirin 150-325 mg IV or 250-500 mg IV 6
- Initiate continuous ECG monitoring with defibrillator capacity 6
- Establish IV access and draw baseline labs (troponin, CBC, metabolic panel, lipid panel within 24 hours) 6
- Administer oxygen only if oxygen saturation <90%—routine oxygen therapy is not recommended 6
- Provide adequate analgesia with IV opioids (morphine) for pain relief 5
Reperfusion Strategy Decision (Critical Time-Dependent Algorithm)
Primary PCI is the preferred reperfusion strategy when performed by an experienced team within 120 minutes of STEMI diagnosis. 7, 6
Choose Primary PCI if:
- First medical contact-to-device time can be achieved within 120 minutes 7
- Patient has cardiogenic shock (regardless of time delay from MI onset) 5, 6
- Patient has contraindications to fibrinolytic therapy 5
- Patient is at especially high risk (severe heart failure, anterior MI) 5
Choose Fibrinolytic Therapy if:
- Primary PCI cannot be performed within 120 minutes of STEMI diagnosis 7, 6
- Pre-hospital setting with trained paramedics and anticipated transport time >60 minutes 5
- Fibrinolytic therapy should be initiated as soon as possible, preferably in the pre-hospital setting 6
Primary PCI Protocol
Transfer patients directly to the catheterization laboratory, bypassing the emergency department and intensive cardiac care unit—every minute of delay increases mortality. 5, 6
Pre-PCI Antiplatelet Therapy
- Aspirin 150-325 mg oral (chewable) or IV 250-500 mg if unable to swallow 6
- Add a potent P2Y12 inhibitor before or at the time of PCI: 7, 6
Anticoagulation During PCI
- Unfractionated heparin IV bolus 100 U/kg (or 60 U/kg if GPIIb/IIIa inhibitors used) 6
- Fondaparinux is contraindicated for primary PCI 6
- Bivalirudin is an alternative anticoagulant option 2
PCI Technique
- Radial access is preferred over femoral access 6
- Drug-eluting stents are standard of care 6
- Routine thrombus aspiration is not recommended (Class IIa evidence) 5
- Routine deferred stenting is contraindicated 6
- For no-reflow phenomenon: consider intracoronary adenosine (30-60 mg bolus) or verapamil (0.5-1 mg bolus), or abciximab 0.25 mg/kg bolus with 0.125 mg/kg/min infusion for 12-24 hours 5
Multivessel Disease Management
- Treat the infarct-related artery immediately with PCI 5
- For stable patients with multivessel disease, evaluate non-infarct-related artery lesions before hospital discharge to achieve complete revascularization 6, 4
- If CABG is predictable in the near future, use bare-metal stents instead of drug-eluting stents to avoid perioperative stent thrombosis 5
Fibrinolytic Therapy Protocol
Administer fibrinolytic therapy within 30 minutes of ambulance arrival if primary PCI cannot be achieved within 120 minutes. 5, 6
Fibrinolytic Agent Selection
- Fibrin-specific agents are recommended: 6
Adjunctive Therapy with Fibrinolysis
- Aspirin 150-325 mg oral or IV 6
- Clopidogrel 300 mg loading dose (75 mg if age ≥75 years), then 75 mg daily 6
- Anticoagulation with unfractionated heparin or enoxaparin for at least 48 hours, preferably for duration of hospitalization (up to 8 days) 6
Post-Fibrinolysis Strategy
- Transfer for routine early catheterization within 3-24 hours after fibrinolytic therapy (not immediate unless rescue PCI needed) 5
- Monitor for successful reperfusion: symptom relief, hemodynamic stability, ≥50% reduction in ST-segment elevation at 60-90 minutes 6
- If reperfusion fails (persistent chest pain, <50% ST resolution), perform rescue PCI immediately 5
Special Populations and High-Risk Scenarios
Cardiogenic Shock
- Emergency angiography and PCI immediately regardless of time from symptom onset 5, 6
- Consider intra-aortic balloon pump for hemodynamic stabilization 6
- Consider alternative left ventricular assist devices for refractory shock 6
- Age <75 years: immediate transfer for PCI/CABG within 18 hours of shock onset (Class I) 5
- Age ≥75 years: consider transfer for PCI/CABG (Class IIa) 5
Cardiac Arrest
- Pursue primary PCI strategy in patients with cardiac arrest and ST-elevation on post-resuscitation ECG 6
Mechanical Complications
- Emergency CABG is indicated for ventricular septal rupture, acute severe mitral regurgitation, or free wall rupture 5
- Echocardiography is the key diagnostic tool for identifying these complications 5
Right Ventricular Infarction
- Characterized by high jugular venous pressure, hypotension, and poor tissue perfusion 5
- Avoid nitrates and diuretics; treat with IV fluid resuscitation 5
In-Hospital Medical Management
Dual Antiplatelet Therapy (DAPT)
- Continue aspirin 75-100 mg daily plus P2Y12 inhibitor for 12 months 7, 6
- Ticagrelor 90 mg twice daily (preferred) 8, 6
- Prasugrel 10 mg daily (5 mg daily if body weight <60 kg; avoid if age ≥75 years unless high-risk features present) 6, 9
- Clopidogrel 75 mg daily (if ticagrelor/prasugrel contraindicated) 6
Statin Therapy
- Initiate high-intensity statin therapy as early as possible 6
- Target LDL-C <70 mg/dL (1.8 mmol/L) or ≥50% reduction from baseline 8, 6
Beta-Blockers
- Start oral beta-blockers in patients with heart failure and/or LVEF <40% unless contraindicated 6
- Continue indefinitely in all eligible patients 7
ACE Inhibitors
- Start within 24 hours in patients with heart failure, LV systolic dysfunction (LVEF ≤0.40), diabetes, or anterior infarction 7, 6
- Continue indefinitely 7
Anticoagulation for Specific Indications
- Atrial fibrillation with CHADS2 score ≥2: vitamin K antagonist targeting INR 2.0-2.5 (lower than usual when combined with DAPT) 6
- Mechanical heart valves: vitamin K antagonist 6
- LV thrombus or anteroapical akinesis/dyskinesis: consider anticoagulation 6
- Minimize duration of triple antithrombotic therapy (vitamin K antagonist + aspirin + P2Y12 inhibitor) to 14 days for fibrinolysis patients, then transition to vitamin K antagonist plus single antiplatelet agent 6
Gastrointestinal Protection
- Proton pump inhibitor should be used in combination with DAPT in patients at high risk of gastrointestinal bleeding 6
Arrhythmia Management
- Implantable cardioverter-defibrillator therapy before discharge for sustained ventricular tachycardia/ventricular fibrillation occurring >48 hours after STEMI (not due to transient/reversible causes) 6
Post-Discharge Management and Secondary Prevention
Long-Term Antiplatelet Therapy
- Low-dose aspirin 75-100 mg daily indefinitely 6
- DAPT for 12 months after PCI unless contraindications develop 6
Lipid Management
- Continue high-intensity statin therapy targeting LDL-C <70 mg/dL or ≥50% reduction 6
Lifestyle Modifications
- Smoking cessation counseling with pharmacological support 6
- Participation in cardiac rehabilitation program is strongly recommended 6
Pre-Discharge Risk Stratification
- Noninvasive testing for ischemia before discharge in patients who have not had coronary angiography and do not have high-risk clinical features 6
Critical Pitfalls to Avoid
- Never delay primary PCI to obtain additional imaging or consultations—time is myocardium 2
- Never withhold aspirin due to concerns about bleeding risk—the mortality benefit far outweighs bleeding risk 7
- Never use prasugrel in patients with prior TIA/stroke (absolute contraindication), age ≥75 years (relative contraindication), or body weight <60 kg without dose reduction 9
- Never discontinue DAPT in the first few weeks after ACS—this dramatically increases risk of stent thrombosis and recurrent MI 9
- Never administer fondaparinux for primary PCI—it is contraindicated in this setting 6
- Never perform routine thrombus aspiration or deferred stenting—these strategies are not beneficial and may cause harm 6
- Never delay reperfusion therapy waiting for troponin results—ECG diagnosis is sufficient to proceed 1
- Never use NSAIDs or glucocorticoids for post-MI pericarditis—these are contraindicated 6
Network and Systems-Based Care
Every community should have a written protocol guiding EMS personnel in determining where to transport STEMI patients. 5
- Target delay times: 10 minutes for ECG transmission, 5 minutes for tele-consultation, 30 minutes for ambulance arrival to fibrinolytic therapy, 120 minutes for ambulance arrival to first balloon inflation 5
- PCI-capable centers should deliver 24/7 service 6
- Patients with cardiogenic shock or contraindications to fibrinolysis should be transferred immediately to PCI-capable facilities (primary-receiving hospital door-to-departure time <30 minutes) 5
- Pre-hospital fibrinolysis is reasonable in settings with physician-staffed ambulances or well-organized EMS systems with trained paramedics, 12-lead ECG transmission capability, and transport times >60 minutes 5