Myocardial Infarction: Diagnosis and Thrombolytics

Myocardial infarction occurs when an atherosclerotic plaque ruptures, forming a thrombus that occludes coronary blood flow and causes severe oxygen deprivation. The heart, an aerobic organ with limited anaerobic capacity, responds to ischemia through contractile dysfunction, which may manifest as stunned or hibernating myocardium. Diagnosis relies on a constellation of patient symptoms, EKG changes—specifically ST-segment elevation or new left bundle branch blocks—and biochemical markers like troponins and CPK isoenzymes. While thrombolytic therapy, including agents like TPA and tenecteplase, effectively reduces mortality in STEMI patients by dissolving clots and restoring patency, it is contraindicated in cases of active bleeding, recent surgery, or intracranial pathology. Because fibrinolysis can trigger platelet activation and reocclusion, these interventions require careful management alongside appropriate anticoagulant or antiplatelet therapy to prevent further cardiac damage.