Iliakis Panagiotis, Stamou Eleftheria, Kasiakogias Alexandros, Manta Eleni, Sakalidis Athanasios, Vakka Angeliki, Theofilis Panagiotis, Kourti Freideriki Eleni, Konstantinidis Dimitrios, Dimitriadis Kyriakos, Vlachopoulos Charalambos, Tsioufis Costas
First Department of Cardiology, School of Medicine, National and Kapodistrian University of Athens, Hippokration General Hospital, 115 27 Athens, Greece.
Biomedicines. 2025 Sep 7;13(9):2190. doi: 10.3390/biomedicines13092190.
Anabolic-androgenic steroids (AASs) are synthetic derivatives of testosterone and are increasingly misused to enhance muscle growth and physical performance, particularly among athletes and recreational bodybuilders. Although AASs affect multiple organ systems, their severe and potentially life-threatening complications involve the cardiovascular system. This review summarizes current knowledge on the pathophysiological mechanisms and clinical manifestations of AAS-induced cardiomyopathy. Chronic supraphysiologic AAS use promotes cardiac injury and adverse cardiac remodeling via oxidative stress, androgen receptor overactivation, RAAS dysregulation, and pro-apoptotic signaling. These changes could lead to hypertension, dyslipidemia and atherosclerosis, myocardial fibrosis and hypertrophy, arrhythmias, heart failure, and kidney injury. Vascular dysfunction, increased arterial stiffness, and a prothrombotic state further compound the cardiovascular risks. Diagnostic approaches involve biomarker evaluation, echocardiography, and cardiac magnetic resonance imaging, revealing structural and functional cardiac abnormalities such as reduced ejection fraction, concentric hypertrophy, myocardial fibrosis, and impaired diastolic function. Although cessation of AAS use may lead to partial or complete reversal of cardiac dysfunction in some individuals, others may experience irreversible myocardial damage. The reversibility appears to depend on dosage, duration of exposure, and early intervention. This review explores the cardiovascular consequences of AAS use, with a focus on the mechanisms, diagnosis, and management of AAS-induced cardiomyopathy, and underlines the importance of education and early detection.
合成代谢雄激素类固醇(AASs)是睾酮的合成衍生物,正被越来越多地滥用,以促进肌肉生长和提高体能,尤其是在运动员和业余健美爱好者中。尽管AASs会影响多个器官系统,但其严重且可能危及生命的并发症累及心血管系统。本综述总结了目前关于AAS诱导的心肌病的病理生理机制和临床表现的知识。长期超生理剂量使用AASs会通过氧化应激、雄激素受体过度激活、肾素-血管紧张素-醛固酮系统(RAAS)失调和促凋亡信号传导促进心脏损伤和不良心脏重塑。这些变化可能导致高血压、血脂异常和动脉粥样硬化、心肌纤维化和肥大、心律失常、心力衰竭以及肾损伤。血管功能障碍、动脉僵硬度增加和血栓前状态进一步加重了心血管风险。诊断方法包括生物标志物评估、超声心动图和心脏磁共振成像,可揭示心脏结构和功能异常,如射血分数降低、向心性肥大、心肌纤维化和舒张功能受损。尽管停用AASs可能会使一些人的心脏功能障碍部分或完全逆转,但其他人可能会出现不可逆的心肌损伤。其可逆性似乎取决于剂量、暴露持续时间和早期干预。本综述探讨了使用AASs的心血管后果,重点关注AAS诱导的心肌病的机制、诊断和管理,并强调了教育和早期检测的重要性。