ST-Segment Elevation Myocardial Infarction

Chapter 286 | Part 6: Disorders of the Cardiovascular System

KEY CLINICAL POINTS

• STEMI is characterized by ST-segment elevation on ECG and elevated cardiac biomarkers (troponin).
• Primary reperfusion strategies include primary PCI (preferred) or fibrinolysis (if PCI unavailable).
• TIMI grading system evaluates coronary artery patency post-reperfusion (grade 3 = optimal flow).
• Key risk factors: hypertension, diabetes, hyperlipidemia, smoking, and coronary artery disease.
• Post-MI management includes beta-blockers, ACE inhibitors, and antiplatelet therapy.

3. ETIOLOGY & PATHOPHYSIOLOGY

STEMI results from acute coronary occlusion due to plaque rupture/erosion, leading to thrombosis. Vulnerable plaques have thin fibrous caps, lipid cores, and inflammatory markers. Thrombus formation involves platelet activation, coagulation cascade, and endothelial dysfunction. Myocardial necrosis extent depends on occlusion duration, collateral flow, and reperfusion.

3.1 Plaque Rupture/Erosion

Vulnerable plaques with thin fibrous caps ( ≤ 50 µm) and lipid cores are prone to rupture. Erosion occurs without rupture, often in patients with diabetes. Plaque rupture exposes thrombogenic contents, triggering coagulation and platelet aggregation.

3.2 Thrombus Formation

Platelet activation by collagen/ADP leads to thromboxane A2 release, promoting aggregation. Coagulation cascade (tissue factor, VII/X) generates thrombin, converting fibrinogen to fibrin. Thrombus occludes coronary artery, causing myocardial necrosis.

3.3 Myocardial Necrosis

Necrotic zone (central) is irreversibly damaged; ischemic penumbra may be salvaged with reperfusion. Infarct size depends on occlusion duration, collateral flow, and reperfusion timing. No-reflow phenomenon occurs due to microvascular injury.

4. CLINICAL FEATURES

Classic presentation: chest pain (deep, crushing, radiating to arm/neck), diaphoresis, nausea. Atypical presentations include painless MI (diabetes), sudden hypotension, or syncope. Physical findings: elevated JVP, S3 gallop, murmurs (ventricular septal rupture), or pericardial rub.

4.1 Chest Pain

Typical: deep, crushing, substernal pain. Atypical: burning/stabbing, epigastric, or silent (diabetes). Duration >30 min. Radiates to left arm, jaw, or back. Often associated with diaphoresis, nausea, and anxiety.

4.2 Physical Examination

Elevated JVP, S3 gallop, pericardial rub, or murmurs (ventricular septal rupture, papillary muscle rupture). Hypotension, tachycardia, and signs of heart failure (pulmonary edema) may be present.

4.3 Complications

Cardiogenic shock, ventricular arrhythmias, mechanical complications (ventricular septal rupture, free wall rupture), and thromboembolism. Right ventricular infarction may present with hypotension and jugular venous distension.

5. DIFFERENTIAL DIAGNOSIS

Acute pericarditis, pulmonary embolism, aortic dissection, costochondritis, and gastrointestinal disorders. Key differentiators: ST-segment elevation on ECG, cardiac biomarkers, and response to nitrates (STEMI vs. pericarditis).

5.1 Non-Cardiac Causes

Pericarditis (ST elevation in all leads, pericardial rub), pulmonary embolism (pleuritic chest pain, hypoxia), aortic dissection (sudden severe chest pain, pulse discrepancy).

5.2 Non-ST-Elevation MI

NSTEMI presents with chest discomfort and elevated troponin without ST elevation. Differentiated by biomarker levels and ECG changes.

6. INVESTIGATIONS & DIAGNOSIS

ECG is the first-line test. Cardiac biomarkers (troponin) confirm myocardial injury. Echocardiography assesses wall motion abnormalities. Coronary angiography identifies culprit lesions. TIMI grading evaluates reperfusion success.

6.1 Electrocardiography

ST-segment elevation ≥ 0.1 mV in ≥ 2 contiguous leads. Q-wave development may occur (Q-wave MI) or not (non-Q-wave MI).

6.2 Cardiac Biomarkers

Cardiac troponin I/T (cTnI/T) are preferred. Peak levels correlate with infarct size. Troponin elevation >99th percentile URL confirms myocardial injury.

6.3 Imaging

Echocardiography detects wall motion abnormalities, ventricular dysfunction, and complications (septal rupture). Radionuclide imaging (sestamibi) identifies infarcted myocardium.

7. MANAGEMENT & TREATMENT

Immediate reperfusion (PCI/fibrinolysis) is critical. Antiplatelet agents (aspirin, clopidogrel), anticoagulants (heparin), and beta-blockers are standard. Post-MI management includes ACE inhibitors, statins, and lifestyle modifications.

7.1 Reperfusion Therapy

Primary PCI is preferred (door-to-balloon time <90 min). Fibrinolysis (tPA, streptokinase) is used if PCI unavailable. TIMI grade 3 flow indicates successful reperfusion.

7.2 Pharmacologic Therapy

Aspirin (160–325 mg chewed), P2Y12 inhibitors (clopidogrel, prasugrel, ticagrelor), heparin, beta-blockers, and ACE inhibitors. Bivalirudin is an alternative anticoagulant for PCI.

7.3 Post-MI Care

Cardiac rehabilitation, lifestyle changes (diet, exercise), and long-term antiplatelet/anti-inflammatory therapy. ACE inhibitors reduce remodeling and HF risk.

8. PROGNOSIS & COMPLICATIONS

In-hospital mortality ~5%, long-term mortality ~15%. Complications include cardiogenic shock (10% of cases), ventricular arrhythmias, mechanical complications (septal rupture), and thromboembolism. LV remodeling increases HF risk.

8.1 Mechanical Complications

Ventricular septal rupture (0.2–3%), free wall rupture (0.3–1%), papillary muscle rupture (0.1–1%). Managed with surgical repair or PCI.

8.2 Arrhythmias

Ventricular tachycardia/fibrillation (10–20% mortality), atrial fibrillation, and conduction delays. Beta-blockers reduce arrhythmia risk.

9. SPECIAL CONSIDERATIONS

Pregnancy: STEMI management similar to non-pregnant patients, but avoid certain drugs (e.g., ACE inhibitors). Elderly: higher mortality, cautious use of anticoagulants. Diabetes: increased silent MI risk, need for early reperfusion.

9.1 Pregnancy

Avoid ACE inhibitors/ARBs; use beta-blockers cautiously. Fibrinolytics contraindicated in third trimester. Monitor for fetal distress.

9.2 Elderly Patients

Higher mortality, increased bleeding risk. Use lower heparin doses. Consider renal function when selecting anticoagulants.

10. KEY POINTS & CLINICAL PEARLS

1. STEMI is defined by ST-segment elevation and elevated troponin. 2. Primary PCI is preferred over fibrinolysis. 3. TIMI grade 3 flow indicates successful reperfusion. 4. Beta-blockers reduce reinfarction and arrhythmia risk. 5. ACE inhibitors improve LV remodeling and reduce HF risk.