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Old 08-10-2018, 05:54 AM
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rss Ventricular androgenic-anabolic steroid-related remodeling: an immunohistochemical st

Related Articles Ventricular androgenic-anabolic steroid-related remodeling: an immunohistochemical study.

Int J Legal Med. 2017 Nov;131(6):1589-1595

Authors: Cecchi R, Muciaccia B, Ciallella C, Di Luca NM, Kimura A, Sestili C, Nosaka M, Kondo T

Abstract
BACKGROUND: 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).
METHOD: 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 ?, and in situ TUNEL staining.
RESULTS: 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.
CONCLUSIONS: 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.


PMID: 28432434 [PubMed - indexed for MEDLINE]



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