Clinical meaning
Myocardial infarction (MI) occurs when coronary artery blood flow is abruptly reduced or ceased, most often due to rupture of an atherosclerotic plaque with superimposed thrombus formation. The ischemic cascade begins within seconds: ATP depletion halts the Na+/K+-ATPase pump, causing intracellular sodium and water accumulation (cellular edema). Anaerobic glycolysis produces lactate, lowering intracellular pH and impairing enzyme function. Within 20-40 minutes of sustained ischemia, irreversible injury begins with mitochondrial swelling, membrane disruption, and release of intracellular contents including troponin, CK-MB, and myoglobin into the bloodstream. The wavefront phenomenon describes necrosis progressing from the subendocardium (most vulnerable due to highest oxygen demand and lowest perfusion pressure) outward toward the epicardium. ST-elevation MI (STEMI) indicates transmural ischemia with complete occlusion, while non-ST-elevation MI (NSTEMI) reflects partial occlusion with subendocardial injury. Reperfusion injury can paradoxically worsen damage through reactive oxygen species, calcium overload, and inflammatory cell infiltration.