Androgen Abuse and Increased Cardiac Risk

Higgins, Julian P T; Heshmat, Alireza; Higgins, Christopher L.

doi:10.1097/smj.0b013e3182749269

Cited by 20 publications

(7 citation statements)

References 44 publications

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“…Similar observations have been reported in autopsies of young men engaging in androgen abuse (79). The aetiologies of this fibrosis is beyond the scope of this study and are discussed elsewhere (80). Although the mechanisms remain unclear, the fibrotic response to androgen treatment may be driven by localized disruption to redox homeostasis in the cardiac myocyte (81).…”

Section: Effects Of Androgens On LV Masssupporting

confidence: 50%

Trenbolone Improves Cardiometabolic Risk Factors and Myocardial Tolerance to Ischemia-Reperfusion in Male Rats With Testosterone-Deficient Metabolic Syndrome

et al. 2016

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The increasing prevalence of obesity adds another dimension to the pathophysiology of testosterone (TEST) deficiency (TD) and potentially impairs the therapeutic efficacy of classical TEST replacement therapy. We investigated the therapeutic effects of selective androgen receptor modulation with trenbolone (TREN) in a model of TD with the metabolic syndrome (MetS). Male Wistar rats (n=50) were fed either a control standard rat chow (CTRL) or a high-fat/high-sucrose (HF/HS) diet. After 8 weeks of feeding, rats underwent sham surgery or an orchiectomy (ORX). Alzet miniosmotic pumps containing either vehicle, 2-mg/kg·d TEST or 2-mg/kg·d TREN were implanted in HF/HS+ORX rats. Body composition, fat distribution, lipid profile, and insulin sensitivity were assessed. Infarct size was quantified to assess myocardial damage after in vivo ischaemia reperfusion, before cardiac and prostate histology was performed. The HF/HS+ORX animals had increased sc and visceral adiposity; circulating triglycerides, cholesterol, and insulin; and myocardial damage, with low circulating TEST compared with CTRLs. Both TEST and TREN protected HF/HS+ORX animals against sc fat accumulation, hypercholesterolaemia, and myocardial damage. However, only TREN protected against visceral fat accumulation, hypertriglyceridaemia, and hyperinsulinaemia and reduced myocardial damage relative to CTRLs. TEST caused widespread cardiac fibrosis and prostate hyperplasia, which were less pronounced with TREN. We propose that TEST replacement therapy may have contraindications for males with TD and obesity-related MetS. TREN treatment may be more effective in restoring androgen status and reducing cardiovascular risk in males with TD and MetS.

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Section: Effects Of Androgens On LV Masssupporting

confidence: 50%

Trenbolone Improves Cardiometabolic Risk Factors and Myocardial Tolerance to Ischemia-Reperfusion in Male Rats With Testosterone-Deficient Metabolic Syndrome

et al. 2016

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“…Changes in lipid profile were observed in this patient a few days before his AMI. The high LDL and low HDL cholesterol levels (204 mg/dL and 30 mg/dL, respectively) suggest hormonal action on lipid metabolism, which increases cardiovascular risk [ 5 , 24 – 27 ]. High levels of CRP (3.54 mg/L) have been associated with AAS misuse.…”

Section: Discussionmentioning

confidence: 99%

Acute Myocardial Infarction in a Young Bodybuilder: A Case Report and Review of the Literature

Junior

Araujo

et al. 2020

Am J Case Rep

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“…However, the studies that have been mentioned either excluded toxicological confounders as a cause for SCD, or had such a small percentage of cases that they were not addressed [ 1 , 2 , 6 – 8 ]. Androgen abuse has been shown to have the direct effects of cardiac hypertrophy and myocardial fibrosis, and indirect effects of hypertension, dyslipidemia, arrhythmia, and myocardial infarction [ 42 ]. One study reviewing the autopsy findings of four body builders who experienced SCD found cardiac hypertrophy and fibrosis in the myocytes of these subjects [ 43 ].…”

Section: Causes Of Sudden Cardiac Death In Soccer Playersmentioning

confidence: 99%

Soccer and Sudden Cardiac Death in Young Competitive Athletes: A Review

Higgins

Andino

2013

Journal of Sports Medicine

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Sudden cardiac death (SCD) in young competitive athletes (<35 years old) is a tragic event that has been brought to public attention in the past few decades. The incidence of SCD is reported to be 1-2/100,000 per year, with athletes at a 2.5 times higher risk. Soccer is the most popular sport in the world, played by people of all ages. However, unfortunately it is cardiovascular diseases such as hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy that have subtly missed screening and claimed the lives of soccer stars such as Marc Vivien Foe and Antonio Puerta during live action on the field and on an internationally televised stage. This paper covers the physiological demands of soccer and the relationship between soccer and SCD. It also reviews the most common causes of SCD in young athletes, discusses the current guidelines in place by The Fédération Internationale de Football Association (FIFA) for screening among professional soccer players, and the precautions that have been put in place to prevent SCD on the field in professional soccer.

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Androgen Abuse and Increased Cardiac Risk

Cited by 20 publications

References 44 publications

Trenbolone Improves Cardiometabolic Risk Factors and Myocardial Tolerance to Ischemia-Reperfusion in Male Rats With Testosterone-Deficient Metabolic Syndrome

Trenbolone Improves Cardiometabolic Risk Factors and Myocardial Tolerance to Ischemia-Reperfusion in Male Rats With Testosterone-Deficient Metabolic Syndrome

Acute Myocardial Infarction in a Young Bodybuilder: A Case Report and Review of the Literature

Soccer and Sudden Cardiac Death in Young Competitive Athletes: A Review

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