ACUTE MYOCARDIAL INFARCTION: PATHOPHYSIOLOGY, CLINICAL FEATURES, AND CONTEMPORARY MANAGEMENT

Abstract

Acute myocardial infarction (AMI) arises from sudden occlusion of a coronary artery, most often following atherosclerotic plaque rupture and superimposed thrombus formation. Within minutes of vessel closure, downstream myocardium experiences ischemic necrosis that, if not promptly reperfused, leads to irreversible injury and loss of contractile function. Clinically, AMI manifests as prolonged chest discomfort – often crushing or constricting – accompanied by diaphoresis, dyspnea, and autonomic features. Electrocardiography differentiates ST-elevation from non-ST-elevation infarctions, while troponin assays confirm myocardial necrosis. Imaging modalities, including echocardiography, cardiac magnetic resonance, and coronary angiography, further delineate infarct extent, guide revascularization decisions, and assess left ventricular function. Early reperfusion via primary percutaneous coronary intervention or fibrinolysis, combined with antiplatelet, anticoagulant, beta-blocker, statin, and renin-angiotensin system inhibitor therapy, markedly reduces infarct size and improves survival. Post-AMI care focuses on prevention of recurrent events through lifestyle modification, pharmacotherapy, and structured cardiac rehabilitation. This review synthesizes current understanding of AMI pathophysiology, clinical presentation, diagnostic strategies, and evidence-based management to optimize patient outcomes.