Department of Medicine and Surgery, Via Gramsci 14, 43126, Parma, Italy.
Department of anatomical, histological, medico-legal and orthopedic sciences, Section of Histology, Sapienza University of Rome, Rome, Italy.
Int J Legal Med. 2017 Nov;131(6):1589-1595. doi: 10.1007/s00414-017-1589-3. Epub 2017 Apr 21.
Several fatal cases of bodybuilders, following a myocardial infarction after long exposure to androgenic-anabolic steroids (AAS), are reported. In recent years, evidence has emerged of cases of heart failure related to AAS consumption, with no signs of coronary or aorta atherosclerosis. This study aims to further investigate the pathogenesis of the ventricular AAS-related remodeling performing immunohistochemistry (IHC).
In order to examine innate immunity activity and myocytes and endothelial cell apoptosis, IHC analyses were performed on heart tissue of two cases of bodybuilders who died after years of supratherapeutic use of metelonone and nandrolone and where no atherosclerosis or thrombosis were found, using the following antibodies: anti-CD68, anti-iNOS, anti-CD163, anti-CD 15, anti-CD8, anti-CD4, anti-HIF1 α, and in situ TUNEL staining.
Results confirm the experimental findings of recent research that, in the absence of other pathological factors, if intensive training is combined with AAS abuse, myocytes and endothelial cells undergo apoptotic alterations. The absence of inflammatory reactions and the presence of an increased number of M2 macrophages in the areas of fibrotic remodeling confirm that the fibrotic changes in the heart are apoptosis-related and not necrosis-related.
In conclusion, the study indicates that, in very young subjects with chronic hypoxia-related alterations of the heart, signs of a heart failure in the other organs and a history of AAS abuse, death can be ascribed to progressive heart failure due to the direct apoptotic cardiac and endothelial changes produced by AAS.
有报道称,一些健美运动员在长期接触雄激素-合成代谢类固醇(AAS)后,发生心肌梗死而死亡。近年来,有证据表明 AAS 消费与心力衰竭有关,而没有冠状动脉或主动脉粥样硬化的迹象。本研究旨在通过免疫组织化学(IHC)进一步研究心室 AAS 相关重构的发病机制。
为了检查固有免疫活性和心肌细胞和内皮细胞凋亡,我们对两名健美运动员的心脏组织进行了免疫组织化学分析,他们在多年超治疗剂量使用美替诺龙和诺龙后死亡,并且没有发现动脉粥样硬化或血栓形成,使用以下抗体:抗 CD68、抗 iNOS、抗 CD163、抗 CD15、抗 CD8、抗 CD4、抗 HIF1α 和原位 TUNEL 染色。
结果证实了最近研究的实验发现,在没有其他病理因素的情况下,如果与 AAS 滥用相结合的高强度训练,心肌细胞和内皮细胞会发生凋亡改变。炎症反应的缺失和纤维化重构区域中 M2 巨噬细胞数量的增加,证实了心脏纤维化变化与凋亡相关,而与坏死无关。
总之,该研究表明,在慢性低氧相关心脏改变的年轻患者中,其他器官心力衰竭的迹象和 AAS 滥用的病史,死亡可能归因于 AAS 直接引起的心肌和内皮细胞凋亡导致的进行性心力衰竭。