Ischemic cardiomyopathy in a 43-year-old male with stroke during admission: the role of chronic amphetamine-dextroamphetamine use.

Cardiomyopathy associated with amphetamine-dextroamphetamine (Adderall) use is an emerging and under-recognized clinical concern, particularly in the context of chronic stimulant exposure. While most reported cases involve non-ischemic myocardial dysfunction, the potential for Adderall to accelerate atherosclerosis and contribute to ischemic cardiomyopathy remains unexplored. This case report aims to document the potential severity of Adderall-induced cardiomyopathy with concomitant coronary artery disease (CAD), examine the pathophysiological link between chronic stimulant exposure and accelerated atherosclerosis, and emphasize the need for vigilant cardiovascular monitoring in patients on long-term stimulant therapy. We report the case of a 43-year-old man with no known cardiovascular history who presented with progressive dyspnea and signs of heart failure. He disclosed a five-year history of high-dose Adderall use (45-65 mg daily) and tobacco consumption but had no prior history of hypertension, diabetes, or known CAD. Evaluation revealed a severely reduced left ventricular ejection fraction (10-15%), consistent with dilated cardiomyopathy. Coronary angiography unexpectedly revealed severe three-vessel CAD, necessitating urgent coronary artery bypass grafting (CABG). Postoperative recovery was uneventful, and the patient was initiated on guideline-directed heart failure therapy, with structured follow-up and strict recommendations for stimulant cessation and lifestyle modification. This case illustrates the multifactorial cardiotoxicity of chronic Adderall use, including direct myocardial injury, fibrotic remodeling, vasospasm, and accelerated coronary atherosclerosis. Unlike prior reports of reversible non-ischemic cardiomyopathy, this case required surgical revascularization, underscoring the irreversible nature of the damage in some patients. It uniquely highlights the synergistic contribution of stimulant-induced toxicity and underlying CAD to the development of severe cardiac dysfunction.