Acute coronary syndromes (STEMI, NSTEMI and unstable angina)

A 62-year-old smoker arrives with crushing central chest pressure radiating to both arms, diaphoretic and nauseous, breathless for the last hour. The ECG shows 3 mm ST elevation in V2 to V4. The cath lab is being called before his troponin comes back — because the ECG, not the biomarker, defines the emergency now.[1]

Two questions decide his next hour, and they decide every ACS: is the artery occluded? (the ECG at first contact) and can I open it in time? (NICE 120 minutes from when fibrinolysis could have been given; DANAMI-2 two-hour transfer). Exclude dissection clinically first, give the bundle, then fork on the ECG — STEMI to reperfusion, NSTE-ACS to risk-stratified timing.[1]

Definition and classification

ACS is classified by the ECG and by troponin. Unstable angina is ischaemia at rest or on minimal exertion without biomarker evidence of necrosis. NSTEMI is ischaemia with a rise or fall in cardiac troponin. STEMI is ischaemia with ST elevation or an ST-elevation equivalent on the ECG. The unstable-angina-versus-NSTEMI line is troponin; the NSTEMI-versus-STEMI line is the ECG. A separate entity, type 2 MI, is myocardial necrosis from a supply-demand mismatch (tachyarrhythmia, hypotension, sepsis, severe anaemia) without plaque rupture, and it must not be confused with the type 1 plaque-rupture ACS that drives the reperfusion pathway. [1]

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