ST-elevation myocardial infarction (STEMI) is a life-threatening manifestation of acute coronary syndrome caused by acute, complete thrombotic occlusion of an epicardial coronary artery, resulting in transmural myocardial ischaemia and necrosis 1,2. Rapid recognition on a 12-lead ECG within 10 minutes of first medical contact and immediate reperfusion via primary percutaneous coronary intervention (PCI) are critical to reducing mortality 1,2.

Pathophysiology

STEMI most commonly results from rupture or fissuring of an unstable atherosclerotic plaque with subsequent platelet aggregation, fibrin thrombus formation, and complete occlusion of the culprit coronary vessel 1. Myocardial necrosis begins within the subendocardium after 15–20 minutes of occlusion and progresses transmurally toward the epicardium ("wavefront phenomenon") over 3–6 hours 1,2.

Clinical presentation

  • typical ischaemic chest pain: severe, crushing retrosternal chest pain or pressure lasting >20 minutes, radiating to the left arm, neck, or jaw, unimproved by sublingual glyceryl trinitrate (GTN)

  • autonomic features: diaphoresis, nausea, vomiting, and pallor

  • atypical / silent presentation: dyspnoea, epigastric pain, or syncope (particularly in elderly patients, women, and patients with diabetes mellitus) 1

Investigations

ECG

Diagnostic ECG criteria (in the absence of left ventricular hypertrophy or left bundle branch block) require new J-point ST-segment elevation in at least two contiguous leads 1,2:

  • leads V2–V3: ≥2.0 mm in men aged ≥40 years (≥2.5 mm in men <40 years) or ≥1.5 mm in women

  • all other contiguous leads: ≥1.0 mm

  • anatomical localisation:

    • anterior / anteroseptal (V1–V4): left anterior descending (LAD) artery

    • inferior (II, III, aVF): right coronary artery (RCA, 80%) or left circumflex (LCx, 20%); always obtain right-sided leads (V4R) to exclude right ventricular infarction

    • lateral (I, aVL, V5–V6): left circumflex or diagonal branch

    • posterior (tall R waves and horizontal ST depression in V1–V3; ST elevation in V7–V9): posterior descending or LCx artery

  • STEMI equivalents: De Winter T waves, Sgarbossa-positive left bundle branch block, and Wellens syndrome 1,2

Management

  • immediate acute therapy: loading with aspirin (300 mg chewed) plus a potent P2Y12 inhibitor (ticagrelor 180 mg or prasugrel 60 mg), unfractionated heparin, and analgesia; oxygen only if SpO2 <90% 1,2

  • reperfusion strategy:

    • primary PCI: gold standard if achievable within 120 minutes of ECG diagnosis (target door-to-balloon time <60–90 minutes)

    • fibrinolysis (tenecteplase or alteplase): indicated within 12 hours of symptom onset when primary PCI cannot be performed within 120 minutes, followed by transfer for rescue or routine angiography 1,2

  • secondary prevention: dual antiplatelet therapy (DAPT) for 12 months, high-intensity statin, beta-blocker, ACE inhibitor/ARB, and mineralocorticoid receptor antagonist (if LVEF ≤40%) 1

See also