The effects of anabolic steroids on myocardial structure and cardiovascular fitness

Sachtleben, Thomas R.; Berg, Kris; Elias, Barbara; Cheatham, John P.; Felix, Gary L.; Hofschire, Philip J.

doi:10.1249/00005768-199311000-00006

Cited by 74 publications

(42 citation statements)

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“…This is supported by data from human weight lifters with anabolic androgenic steroid use, who were shown to develop cardiac hypertrophy, and systolic and diastolic dysfunction. 28,29 The blockade of androgen action by castration (gonadectomy) in male mice prevented pathological hypertrophy, left ventricular dysfunction, fibrosis, and dilation in response to TACinduced pressure overload, myocardial infarction, transgenic β 2 -adrenergic receptor overexpression, and lack of the guanylyl cyclase-A. 12,[30][31][32] Furthermore, finasteride exerted protective effects on the myocardium in the setting of ischemia/reperfusion injury.…”

Section: Discussionmentioning

confidence: 99%

Antiandrogenic Therapy With Finasteride Attenuates Cardiac Hypertrophy and Left Ventricular Dysfunction

et al. 2015

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A pproximately 5 million Americans have chronic heart failure. 1 The most common causes for the development of chronic heart failure are chronic arterial hypertension, myocardial hypertrophy, and previous myocardial infarction. 1 The progression of heart failure is driven by pathological ventricular remodeling processes, which mainly involve cardiomyocyte hypertrophy, myocardial fibrosis, and profound changes in gene expression that together lead to left ventricular dilation and systolic, and diastolic dysfunction over time. [2][3][4] Despite recent therapeutic advances, the mortality of chronic heart failure remains high, and, a fact that is somewhat neglected, strikingly different between women and men. Women with heart failure have a lower mortality than men and also a better prognosis when experiencing hypertension, aortic valve stenosis, or hypertrophic cardiomyopathy.1,5 Sex hormones might account for these differences, and, indeed, the expression of androgen, and estrogen receptors was found in male and female hearts, implying that estrogen and androgens could directly act on the myocardium. 6,7 Although, in general, estrogen has been deemed cardioprotective, large randomized and controlled studies have failed to demonstrate the beneficial effects of estrogen therapy in postmenopausal women. 8,9 As a consequence, it is now proposed that the rise in cardiovascular mortality in women after the onset of menopause might be caused by an increased ovarian production of testosterone. 10 Clinical Perspective on p 1081Testosterone and its highly active metabolite dihydrotestosterone (DHT) operate by binding to the androgen receptor, Background-In comparison with men, women have a better prognosis when experiencing aortic valve stenosis, hypertrophic cardiomyopathy, or heart failure. Recent data suggest that androgens like testosterone or the more potent dihydrotestosterone contribute to the development of cardiac hypertrophy and failure. Therefore, we analyzed whether antiandrogenic therapy with finasteride, which inhibits the generation of dihydrotestosterone by the enzyme 5-α-reductase, improves pathological ventricular remodeling and heart failure. Methods and Results-We found a strongly induced expression of all 3 isoforms of the 5-α-reductase (Srd5a1 to Srd5a3) in human and mouse hearts with pathological hypertrophy, which was associated with increased myocardial accumulation of dihydrotestosterone. Starting 1 week after the induction of pressure overload by transaortic constriction, mice were treated with finasteride for 2 weeks. Cardiac function, hypertrophy, dilation, and fibrosis were markedly improved in response to finasteride treatment in not only male, but also in female mice. In addition, finasteride also very effectively improved cardiac function and mortality after long-term pressure overload and prevented disease progression in cardiomyopathic mice with myocardial Gαq overexpression. Mechanistically, finasteride, by decreasing dihydrotestosterone, potently inhibited hypertrophy and Akt-dependent p...

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Section: Discussionmentioning

confidence: 99%

Antiandrogenic Therapy With Finasteride Attenuates Cardiac Hypertrophy and Left Ventricular Dysfunction

et al. 2015

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“…Upon autopsy as well as in living persons, a dose-dependent left-ventricular hypertrophy has been observed (De Piccoli et al 1991;Dickerman et al 1997;Karila 2003;Karila et al 2003;Krieg et al 2007;McKillop et al 1986;Nottin et al 2006;Sachtleben et al 1993;Sader et al 2001;Thiblin et al 2000;Urhausen et al 2004;Yeater et al 1996; own observation). Similar findings have been described for the cardiac ventricular septum (Sader et al 2001).…”

Section: Pathological Findingsmentioning

confidence: 92%

Side Effects of Anabolic Androgenic Steroids: Pathological Findings and Structure–Activity Relationships

Büttner

Thieme²

2009

Handbook of Experimental Pharmacology

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Side effects of anabolic steroids with relevance in forensic medicine are mainly due to life-threatening health risks with potential fatal outcome and cases of uncertain limitations of criminal liability after steroid administration. Both problems are typically associated with long-term abuse and excessive overdose of anabolic steroids. Side effects may be due to direct genomic or nongenomic activities (myotrophic, hepatotoxic), can result from down-regulation of endogenous biosynthesis (antiandrogenic) or be indirect consequence of steroid biotransformation (estrogenic).Logically, there are no systematic clinical studies available and the number of causally determined fatalities is fairly limited. The following compilation reviews typical abundant observations in cases where nonnatural deaths (mostly liver failure and sudden cardiac death) were concurrent with steroid abuse. Moreover, frequent associations between structural characteristics and typical side effects are summarized.

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“…Several studies demonstrated an increase in left ventricular end diastolic volume, left ventricular mass and/or worsening diastolic function [11][12][13], while other studies demonstrated no cardiovascular changes with anabolic steroid use [14][15][16]. However, in bodybuilding, the doses used are often 10-100 times the therapeutic dose; in one report involving 24 weight lifters, the lowest dose was 350% of the usual therapeutic dose [17].…”

Section: Discussionmentioning

confidence: 99%

“…Poor visualization of the right ventricle, a poorly defined endocardial surface, irregular right ventricular geometry, and limited reproducibility of exercise studies are important limitations of echocardiography in evaluating the left and right ventricle [26]. Cardiac exercise CT has been shown to have excellent sensitivity and specificity for detecting coronary disease and for assessing changes in both right and left ventricles [11][12][13][14][15]27,34]. CT also allows clear apical delineation, and breast shadows, obesity, the diaphragm or bowel do not cause attenuation, and excellent reproducibility has been demonstrated, with interstudy, intraobserver and interobserver variations were 0.01±1.4, 0.06±2.0 and 0.28±2.1% respectively [14,28,29,36].…”

Section: Discussionmentioning

confidence: 99%

“…Ejection fraction, end-systolic and end-diastolic volumes were calculated at each tomographic level. Using a computer summation program, global ejection fraction was obtained at rest and exercise as described previously [10,12,15]. Stroke volume was also calculated on every level, as well as the end-diastolic volume, end-systolic volume and myocardial mass.…”

Section: Left and Right Ventricular Ejection Fraction Assessment By Ctmentioning

confidence: 99%

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Effect of Testosterone and Resistance Training on Cardiac Mass and Contractility in Men with COPD

Budoff¹,

Mao²,

Rambod³

et al. 2011

J Allergy Ther

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Introduction: Testosterone therapy and resistance training have been demonstrated to improve muscle mass and strength in patients with testosterone deficiency. However the effects on cardiac mass and contractility of these interventions have not been identified in prospective placebo-controlled trials. The hypothesis of this trial was that resistance training and testosterone replacement would improve cardiac mass and contractility in male COPD patients with low testosterone levels. Methods:We conducted a 10 week trial in a 2 by 2 factorial design, randomizing 53 patients to replacement doses of testosterone enanthate (100 mg weekly) or placebo, as well as to a program of lower extremity resistance training or no exercise. We performed rest and exercise cardiac computed tomography (CCT) studies before and after 10 weeks of therapy to evaluate right and left heart function. Patients were injected with 40-50 ml of non-ionic, iodinated contrast and cine CCT images were obtained at rest. Patients were exercised to 60% of their maximal work rate on a semi-supine ergometer, then re-injected with another bolus of 40-50 ml of contrast and re-imaged. We evaluated cardiac output and left ventricular (LV) and right ventricular (RV) mass, LV and RV stroke volume, ejection fractions and end-diastolic volumes at rest and exercise, before and after therapy.Results: 42 men with COPD (mean FEV 1 =40%pred. pre-bronchodilator) and low testosterone levels (mean=320ng/dl) completed the 10 week protocol. Factorial analysis demonstrated that testosterone, but not resistance training increased LV and RV mass (by 4.9% and 8.3%, respectively). Resistance training, but not testosterone, was associated with increased LV ejection fraction at rest and during exercise (by 5.5% and 4.4%, respectively). In the entire study group, increases in both left and right ventricular mass were correlated with increases in lean body mass (assessed by DEXA) (r=0.49 and r=0.65, respectively). Conclusions:In men with COPD, testosterone replacement and strength training are associated with distinct alterations in cardiac structure and function. Specifically, resistance training improved ejection fraction, while testosterone increased lean body mass and LV mass.

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The effects of anabolic steroids on myocardial structure and cardiovascular fitness

Cited by 74 publications

References 0 publications

Antiandrogenic Therapy With Finasteride Attenuates Cardiac Hypertrophy and Left Ventricular Dysfunction

Antiandrogenic Therapy With Finasteride Attenuates Cardiac Hypertrophy and Left Ventricular Dysfunction

Side Effects of Anabolic Androgenic Steroids: Pathological Findings and Structure–Activity Relationships

Effect of Testosterone and Resistance Training on Cardiac Mass and Contractility in Men with COPD

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