Very Young ST-Segment Elevation Myocardial Infarction Associated With Chronic Nonmedical Anabolic-Androgenic Steroid Use: A Case Report.

IF 0.6
Ayşe İrem Boladan, Oktay Şeker, Göktuğ Savaş, Semih Eren
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Abstract

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.

非常年轻的st段抬高型心肌梗死与慢性非药物性使用合成代谢雄激素类固醇相关:一例报告。
心肌梗死(MI)在40岁之前是罕见的,需要对潜在的病因进行全面的评估。慢性非药物合成代谢雄激素类固醇(AAS)的使用与内皮功能障碍、动脉粥样硬化加速和血栓形成前状态有关,所有这些都可能导致过早的冠状动脉疾病。29岁男性,无已知病史,约2年非药物性睾酮和司他诺唑尔使用,急性胸痛。心电图显示前st段抬高型心肌梗死(STEMI)。急诊冠状动脉造影显示血栓性全闭塞左中冠状动脉前降支。初步经皮冠状动脉介入治疗可恢复冠状动脉血流。患者表现为Killip II级急性心力衰竭,需要暂时持续气道正压通气(CPAP)和肌力支持。经胸超声心动图(TTE)显示左心室射血分数(LVEF)为30-35%,伴有前叶和根尖运动减退。入院实验室检查显示明显的动脉粥样硬化性血脂异常(总胆固醇,302 mg/dL;低密度脂蛋白胆固醇,250 mg/dL;高密度脂蛋白胆固醇,29 mg/dL;甘油三酯,113 mg/dL;非高密度脂蛋白胆固醇,273 mg/dL)。除了罪魁祸首病变外,在其他冠状动脉节段也发现了非阻塞性动脉粥样硬化斑块。在一个月的随访中,低密度脂蛋白胆固醇在他汀类药物治疗和停止使用AAS后降至85 mg/dL。3个月时,患者保持临床稳定,尽管LVEF保持在30%。在易感的年轻人中,暴露于AAS可能会加速动脉粥样硬化和冠状动脉血栓形成。然而,在非常年轻的时候,应该系统地考虑心肌梗死的其他原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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