Acute Coronary Syndrome (ACS)

Acute myocardial infarction (MI) results from the rupture or erosion of a vulnerable atherosclerotic plaque within a coronary artery, which exposes the lipid-rich necrotic core and thrombogenic subendothelial matrix to circulating blood. This exposure triggers thrombus formation, leading to ischemia and subsequent myocardial injury. Both types of acute coronary syndrome cause elevated cardiac troponin levels due to the release of intracellular proteins from necrotic myocytes. Irreversible myocardial injury is characterized by mitochondrial swelling, sarcolemmal disruption, and the release of intracellular contents such as troponin, CK-MB, myoglobin, and LDH into the bloodstream. Diagnosis of acute MI requires evidence of a rise and/or fall in cardiac troponin with at least one value above the assay's 99th-percentile upper reference limit, combined with clinical evidence of ischemia, including symptoms, new ischemic ECG changes, pathological Q waves, new regional wall-motion abnormalities or loss of viable myocardium, or identification of a coronary thrombus. In cases of cardiogenic shock, emergency revascularization of the culprit lesion is essential regardless of symptom duration; however, routine immediate percutaneous coronary intervention (PCI) of non-culprit vessels during the shock-producing procedure is not...