Key result
Chronic anabolic steroid use is linked to anterior STEMI, coronary thrombosis, and severe LV dysfunction.
Why the study?
Myocardial infarction before age 40 is uncommon and chronic nonmedical anabolic-androgenic steroid use may contribute to premature coronary artery disease but requires further evaluation.
Case Report (n=1)
Highlights the potential for accelerated atherosclerosis, atherogenic dyslipidemia, and premature STEMI in young patients associated with chronic nonmedical use of anabolic-androgenic steroids.
Alerts clinicians to inquire about anabolic-androgenic steroid use in young men with STEMI; leaves open causality and need for controlled studies.
Myocardial infarction (MI) before the age of 40 years is uncommon and warrants a comprehensive evaluation of potential etiologies. Chronic nonmedical anabolic-androgenic steroid (AAS) use has been associated with endothelial dysfunction, accelerated atherosclerosis, and a prothrombotic state, all of which may contribute to premature coronary artery disease. A 29-year-old man with no known medical history and approximately two years of nonmedical testosterone and stanozolol use presented with acute chest pain. Electrocardiography revealed an anterior ST-segment elevation myocardial infarction (STEMI). Emergency coronary angiography demonstrated a thrombotic total occlusion of the mid-left anterior descending coronary artery. Primary percutaneous coronary intervention restored coronary blood flow. The patient presented with Killip class II acute heart failure requiring temporary continuous positive airway pressure (CPAP) and inotropic support. Transthoracic echocardiography (TTE) revealed a left ventricular ejection fraction (LVEF) of 30-35%, with anterior and apical hypokinesia. Admission laboratory tests revealed marked atherogenic dyslipidemia (total cholesterol, 302 mg/dL; low-density lipoprotein cholesterol, 250 mg/dL; high-density lipoprotein cholesterol, 29 mg/dL; triglycerides, 113 mg/dL; and non-high-density lipoprotein cholesterol, 273 mg/dL). In addition to the culprit lesion, nonobstructive atherosclerotic plaques were identified in other coronary segments. At the one-month follow-up, low-density lipoprotein cholesterol had decreased to 85 mg/dL following statin therapy and the reported discontinuation of AAS use. At three months, the patient remained clinically stable, although LVEF remained at 30%. AAS exposure may have contributed to accelerated atherosclerosis and coronary thrombosis in a susceptible young individual. However, alternative causes of MI at a very young age should be systematically considered.
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Boladan et al. (2026) conducted a case report in ST-Segment Elevation Myocardial Infarction (STEMI) (n=1). Chronic nonmedical anabolic-androgenic steroid (testosterone and stanozolol) use was evaluated. Chronic nonmedical anabolic-androgenic steroid use in a 29-year-old man was associated with an anterior ST-segment elevation myocardial infarction, coronary thrombosis, and severe LV dysfunction.
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