ST-Elevation Myocardial Infarction (STEMI)
Etiology
STEMI results from acute thrombotic occlusion of an epicardial coronary artery, typically following rupture or erosion of an atherosclerotic plaque. 1, 2
- The underlying mechanism involves atherosclerotic plaque destabilization, leading to platelet aggregation, thrombus formation, and complete vessel occlusion 1
- In the majority of cases, approximately 88% of patients presenting within 6 hours have a completely occluded coronary artery 3
- The pathophysiology progresses from plaque rupture/erosion to thrombosis and embolization, with consequences including slow-flow or no-reflow phenomena 3
Epidemiology and Risk Factors
Major modifiable and non-modifiable risk factors must be identified to stratify patient risk. 1
Major Risk Factors:
- Modifiable: Hypertension, diabetes mellitus, dyslipidemia, tobacco smoking 1
- Non-modifiable: Age, sex, family history of premature coronary disease 1
- These traditional risk factors contribute to the development of atherosclerosis, which underlies STEMI pathogenesis 4
Pathophysiology
The pathophysiologic cascade begins with coronary plaque rupture and progresses through a time-dependent "wavefront" of myocardial necrosis. 3, 2
- Complete thrombotic occlusion develops from an atherosclerotic plaque in an epicardial coronary vessel 2
- Myocardial ischemia leads to progressive myocardial necrosis if reperfusion is not achieved rapidly 3
- The concept of "time is muscle" emphasizes that rapidly achieving normal coronary artery flow at both macro and microvascular levels is key to aborting progressive necrosis 3
- STEMI is both a functional and structural issue, with varied consequences of necrosis characterizing the syndrome 3
Clinical Manifestations
Typical presentation includes severe, crushing chest discomfort lasting >20 minutes, often with radiation and associated symptoms. 1
Typical Presentation:
- Severe, crushing chest discomfort lasting >20 minutes 1
- Radiation to left arm, neck, or jaw 1
- Associated symptoms: diaphoresis, nausea, dyspnea 1
Atypical Presentations:
- Isolated dyspnea, epigastric pain, or syncope 5, 1
- More common in elderly patients, diabetics, and women 1
- Physical examination may reveal tachycardia, hypotension, pulmonary rales, or signs of cardiogenic shock 5
Any patient with atypical symptoms should be promptly evaluated with ECG to avoid missing STEMI diagnosis. 5
Diagnostics
A 12-lead ECG must be obtained and interpreted within 10 minutes of first medical contact in all patients with suspected STEMI. 1, 6
ECG Diagnostic Criteria:
- ST-segment elevation ≥0.1 mV (1 mm) in at least two contiguous precordial or adjacent limb leads 7, 5, 1, 6
- New or presumed new left bundle branch block 7, 5, 6
- True posterior MI pattern 7
- Right-sided ECG should be obtained if inferior or RV STEMI is suspected 7
Additional Diagnostic Modalities:
- Cardiac biomarkers (troponin, creatine kinase) confirm myocardial necrosis but should not delay reperfusion therapy 4
- Coronary angiography provides definitive anatomic diagnosis and guides revascularization strategy 3, 4
- Cardiac magnetic resonance imaging and advanced imaging techniques enhance accuracy and risk stratification 4
Pre-hospital Diagnosis:
- Pre-hospital 12-lead ECG by advanced cardiac life support-trained professionals is recommended 7
- Pre-hospital diagnosis with telemedicine or by ambulance physicians reduces treatment delay by 41-81 minutes compared to in-hospital diagnosis 8
Management
Immediate Management (First Medical Contact)
Patients with MI should chew aspirin 162-325 mg immediately unless there is an absolute contraindication. 7, 1, 6
- Aspirin 150-325 mg oral (chewable) or IV 250-500 mg should be administered immediately upon first medical contact 5, 1
- Maintenance dose of 75-100 mg daily should be continued indefinitely 5, 1
- Emergency medical service providers should be trained and equipped to provide early defibrillation 7
Reperfusion Strategy: The Critical Decision
Primary PCI is the preferred reperfusion strategy when performed by an experienced team within 120 minutes of STEMI diagnosis. 5, 1, 6, 2
Primary PCI Preferred When:
- Skilled PCI facility with surgical backup is accessible (operators experience >75 primary PCI cases per year, team experience >36 primary PCI cases per year) 7
- Diagnosis of STEMI is in doubt 7
- High risk from STEMI (cardiogenic shock, Killip class III or greater) 7
- Contraindication to fibrinolysis, including increased risk of bleeding and intracranial hemorrhage 7
- Can be performed within 90 minutes if presenting to PCI-capable hospital, or 120 minutes if requiring transfer from first medical contact 5, 1, 6
Fibrinolytic Therapy Preferred When:
- Early presentation (less than 3 hours from symptom onset) and PCI not readily available 7
- Invasive strategy is not an option (catheterization not available, vascular access difficulties, skilled PCI facility not accessible) 7
- Patient cannot reach PCI facility within required 90-120 minutes 7
- Goal: fibrinolysis to begin less than 30 minutes from first contact with healthcare system 7, 5, 6
The most important point in managing STEMI is minimizing time from symptom onset until initiation of reperfusion therapy. 7
Antiplatelet and Anticoagulant Therapy
Dual antiplatelet therapy with aspirin plus a potent P2Y12 inhibitor should be administered before or at the time of PCI. 5, 1, 6
P2Y12 Inhibitor Selection:
- Ticagrelor or prasugrel preferred over clopidogrel 6
- A potent P2Y12 inhibitor (ticagrelor or prasugrel) should be added to aspirin before or at the time of PCI 5, 1
Duration of Dual Antiplatelet Therapy (DAPT):
- Patients undergoing PCI or stenting should begin clopidogrel therapy 7
- No stent: 14 days 7
- Bare-metal stent: at least one month but ideally one year unless patient is at increased risk of bleeding 7
- Drug-eluting stent: one year 7
- DAPT should be continued for 12 months after PCI unless contraindications develop 5, 1
Glycoprotein IIb/IIIa Inhibitors:
- Abciximab has strong support for added value in STEMI patients 3
- May be considered when patients are at high risk and PCI is not available within 90 minutes, provided bleeding risk is low 7
Special Populations and High-Risk Scenarios
Cardiogenic Shock:
- Patients with cardiogenic shock should be transported to a facility capable of cardiac catheterization and rapid revascularization (PCI and CABG). 7
- Intra-aortic balloon counterpulsation is recommended when cardiogenic shock is not quickly reversed with pharmacological therapy 7, 6
- Early revascularization (PCI or CABG) is recommended for patients <75 years who develop shock within 36 hours of MI and are suitable for revascularization that can be performed within 18 hours of shock 7, 6
- Emergency angiography and PCI should be performed immediately in patients with cardiogenic shock, regardless of time from symptom onset 5
Patients ≥75 Years:
- Prasugrel is generally not recommended in patients ≥75 years except in high-risk situations (patients with diabetes or history of prior MI) due to increased risk of fatal and intracranial bleeding 6, 9
- Early revascularization is reasonable for selected patients ≥75 years with good prior functional status who agree to invasive care 7
Low Body Weight (<60 kg):
- Consider lowering prasugrel maintenance dose to 5 mg in patients <60 kg due to increased exposure to active metabolite and increased bleeding risk 9
Pregnancy:
- Primary PCI is strongly preferred over fibrinolysis to diagnose potential coronary dissection and minimize fetal radiation 6
Cardiac Arrest:
- Cardiac arrest patients with ST-elevation on post-resuscitation ECG should undergo primary PCI strategy 5
Post-PCI Management After Fibrinolysis
Routine immediate PCI after successful fibrinolysis is NOT recommended as it increases bleeding and adverse events without benefit. 5
- Facilitated PCI (full-dose fibrinolysis followed by immediate PCI) may be harmful and is no longer recommended 7
- Routine PCI might be considered hours to days after successful fibrinolysis as part of an invasive strategy 5
- High-risk patients should be transferred for early catheterization (within 24 hours) after fibrinolysis 7
Additional Acute Medical Therapy
ACE Inhibitors:
- Should be initiated within 24 hours of STEMI in patients with no contraindications 7, 6
- Particularly important in patients with anterior MI, heart failure, or ejection fraction ≤0.40 6
Beta-Blockers:
- Oral beta-blockers should be continued indefinitely in all eligible patients 6
Statins:
- High-intensity statin therapy should be initiated immediately with target LDL-C <70 mg/dL or ≥50% reduction from baseline 5, 1
NSAIDs:
- Patients who routinely took NSAIDs (except aspirin) before STEMI should discontinue these agents due to increased risks of mortality, reinfarction, hypertension, heart failure, and myocardial rupture. 7
Management of Recurrent Ischemia
Patients with recurrent ischemic-type chest discomfort and signs of hemodynamic instability, poor LV function, or large area of myocardium at risk should be referred urgently for cardiac catheterization. 7
- Patients considered candidates for revascularization should undergo coronary arteriography and PCI or CABG as dictated by coronary anatomy 7
- Insertion of an IABP should be considered 7
Surgical Revascularization (CABG)
Emergency CABG Indications (Class I):
- Failed PCI with persistent pain or hemodynamic instability in patients with suitable coronary anatomy 5, 6
- Persistent or recurrent ischemia refractory to medical therapy with significant myocardium at risk 5
- At the time of surgical repair of post-infarction ventricular septal rupture or mitral valve insufficiency 5, 6
- Cardiogenic shock in patients <75 years with severe multivessel or left main disease when revascularization can be performed within 18 hours of shock onset 6
Timing Considerations:
- CABG mortality is elevated for the first 3-7 days after infarction 7
- Patients who have been stabilized should have surgery delayed to allow myocardial recovery unless critical anatomy exists 7
- When possible, discontinue prasugrel at least 7 days prior to any surgery 9
Mechanical Complications
Mechanical complications (ventricular septal rupture, papillary muscle rupture) require urgent surgical repair with concomitant CABG. 5
Management of Congestive Heart Failure
- Patients with contraindications to fibrinolysis should be immediately transported to a facility capable of cardiac catheterization, or transferred within 30 minutes 7
- It is reasonable to consider an invasive strategy in patients with severe CHF 7
- Immediate management goals include adequate oxygenation and preload reduction to relieve pulmonary congestion 7
- Nitroglycerin, ACE inhibitors, and inotropic support should be used based on blood pressure and hemodynamic status 7
Long-Term Secondary Prevention
Comprehensive secondary prevention is essential to reduce recurrent cardiovascular events. 1
Pharmacotherapy:
- Low-dose aspirin 75-100 mg daily indefinitely 5, 1
- DAPT for 12 months (aspirin plus ticagrelor or prasugrel) 1
- High-intensity statin continued long-term 5, 1
- ACE inhibitors continued indefinitely 6
- Beta-blockers continued indefinitely 6
Lifestyle Modifications:
- Smoking cessation is strongly recommended 1
- Cardiac rehabilitation program participation 1
- Lifestyle modifications including diet, exercise, and weight management 1
Common Pitfalls and Caveats
- Do not delay reperfusion therapy waiting for cardiac biomarkers - ECG diagnosis is sufficient to initiate treatment 4
- Avoid routine immediate PCI after successful fibrinolysis - this increases bleeding without benefit 5
- Do not use facilitated PCI strategies (full-dose fibrinolysis followed by immediate PCI) as they may be harmful 7
- Suspect bleeding in any hypotensive patient who has recently undergone coronary angiography, PCI, CABG, or other surgical procedures while on prasugrel 9
- If possible, manage bleeding without discontinuing antiplatelet therapy - discontinuing prasugrel, particularly in the first few weeks after ACS, increases risk of subsequent cardiovascular events 9
- Streptokinase should not be readministered to treat recurrent ischemia/infarction in patients who received a non-fibrin-specific fibrinolytic agent more than 5 days previously 7
- Pre-hospital diagnosis significantly reduces treatment delay - systems should be established to enable pre-hospital ECG and direct referral to PCI centers 8