STEMI

ST-elevation myocardial infarction (STEMI) is an acute myocardial infarction caused by sudden and complete occlusion of a coronary artery, most often due to rupture of an atherosclerotic plaque with superimposed thrombosis. The resulting transmural ischemia leads to distinctive changes on the 12-lead electrocardiogram, classically elevation of the ST segment in contiguous leads corresponding to the affected area. Cardiac biomarkers, especially troponin, are typically elevated, reflecting myocardial necrosis. STEMI must be distinguished from non-ST-elevation myocardial infarction (NSTEMI), which involves partial occlusion and does not produce persistent ST elevation.

Diagnosis relies on clinical presentation (classic chest pain or equivalents such as dyspnea, diaphoresis, or syncope), ECG findings of ST-segment elevation, and rising cardiac troponin. Urgent evaluation also includes assessment of hemodynamic stability, electrolyte balance, and contraindications to therapy. Imaging such as echocardiography may assess ventricular function and complications.

Management centers on rapid reperfusion to restore coronary blood flow. Primary percutaneous coronary intervention (PCI) is preferred if it can be performed promptly (commonly within 120 minutes of first medical contact). If PCI is not available within an acceptable time frame, fibrinolytic therapy should be given promptly to achieve reperfusion. Initial pharmacologic treatment includes dual antiplatelet therapy (aspirin plus a P2Y12 inhibitor), anticoagulation, and guideline-directed medical therapy (nitrates for chest pain, beta-blockers if not contraindicated, and high-intensity statin therapy). ACE inhibitors or ARBs are recommended in patients with left ventricular dysfunction or other indications.

Prognosis improves with prompt reperfusion and comprehensive secondary prevention. Complications can include arrhythmias, heart failure, cardiogenic shock, and mechanical events; ongoing monitoring and follow-up care are essential.