Myocardial infarction (MI) occurs when prolonged myocardial ischemia results in irreversible cardiomyocyte death (necrosis). MI is classified as STEMI (ST-elevation MI) or NSTEMI (non-ST-elevation MI) based on ECG findings. In STEMI, complete thrombotic occlusion of a coronary artery causes transmural ischemia affecting the full thickness of the ventricular wall, producing ST-segment elevation on ECG in the leads corresponding to the affected territory. In NSTEMI, partial or intermittent occlusion causes subendocardial necrosis (affecting the inner layer of the ventricle which is most susceptible to ischemia), producing ST depression, T-wave inversion, or sometimes no ECG changes. Both types result in elevated cardiac troponin due to release of intracellular proteins from necrotic myocytes. The subendocardium is most vulnerable because it has the highest oxygen demand, receives blood flow only during diastole, and experiences the greatest wall stress during systolic contraction. Cell death begins within 20 minutes of complete occlusion and progresses as a wavefront from subendocardium to epicardium over 3-6 hours. Irreversible injury is characterized by mitochondrial swelling, sarcolemmal disruption, and release of intracellular contents (troponin, CK-MB, myoglobin, LDH) into the bloodstream. The...