A Double Threat: Concurrent Non-ST-Elevation Myocardial Infarction and Transient Ischemic Attack Symptoms Revealing Triple-Vessel Coronary Artery Disease

Impaired ventricular wall motion and reduced ejection fraction after an acute myocardial infarction promote blood stasis - especially in hypokinetic or akinetic segments - activating coagulation pathways, platelet aggregation, and thrombus formation. Concurrent endothelial injury from ischemia further exposes thrombogenic surfaces, and if the thrombus embolizes, it can trigger serious neurologic events such as stroke or transient ischemic attack (TIA). We describe the case of a 56-year-old man with hypertension and methamphetamine use who presented with chest pain, dyspnea, and transient left-sided weakness. Work-up revealed elevated troponin, severely calcified triple-vessel coronary disease, and an apical mural thrombus with an ejection fraction of 45%, confirmed on transthoracic echocardiography, with subsequent paroxysmal atrial flutter. Methamphetamine use, known to accelerate atherosclerosis and heighten thromboembolic risk, likely compounded his coronary disease. The patient was anticoagulated with enoxaparin, bridging to warfarin, and discharged for follow-up imaging and surgical evaluation. This case highlights the need for heightened vigilance, prompt anticoagulation, and thorough cardiac evaluation for mural thrombus and embolic complications in methamphetamine-associated myocardial injury, even when initial cerebrovascular imaging is negative.