Androgenic Anabolic Steroid Abuse and the Cardiovascular System

Abstract

Abuse of anabolic androgenic steroids (AAS) has been linked to a variety of different cardiovascular side effects. In case reports, acute myocardial infarction is the most common event presented, but other adverse cardiovascular effects such as left ventricular hypertrophy, reduced left ventricular function, arterial thrombosis, pulmonary embolism and several cases of sudden cardiac death have also been reported. However, to date there are no prospective, randomized, interventional studies on the long-term cardiovascular effects of abuse of AAS. In this review we have studied the relevant literature regarding several risk factors for cardiovascular disease where the effects of AAS have been scrutinized:(1) Echocardiographic studies show that supraphysiologic doses of AAS lead to both morphologic and functional changes of the heart. These include a tendency to produce myocardial hypertrophy (Fig. 3), a possible increase of heart chamber diameters, unequivocal alterations of diastolic function and ventricular relaxation, and most likely a subclinically compromised left ventricular contractile function. (2) AAS induce a mild, but transient increase of blood pressure. However, the clinical significance of this effect remains modest. (3) Furthermore, AAS confer an enhanced pro-thrombotic state, most prominently through an activation of platelet aggregability. The concomitant effects on the humoral coagulation cascade are more complex and include activation of both pro-coagulatory and fibrinolytic pathways. (4) Users of AAS often demonstrate unfavorable measurements of vascular reactivity involving endothelial-dependent or endothelial-independent vasodilatation. A degree of reversibility seems to be consistent, though. (5) There is a comprehensive body of evidence documenting that AAS induce various alterations of lipid metabolism. The most prominent changes are concomitant elevations of LDL and decreases of HDL, effects that increase the risk of coronary artery disease. And finally, (6) the use of AAS appears to confer an increased risk of life-threatening arrhythmia leading to sudden death, although the underlying mechanisms are still far from being elucidated. Taken together, various lines of evidence involving a variety of pathophysiologic mechanisms suggest an increased risk for cardiovascular disease in users of anabolic androgenic steroids.

Anabolic steroids and cardiovascular risk: A national population-based cohort study

“…This notion is motivated by our findings that the difference remained after adjusting for the possible identified confounders (keeping in mind that smoking was not controlled for) and is also in line with a large body of scientific literature describing various adverse cardiac effects of illicit AAS use (Vanberg and Atar, 2010). Also the fact that the cardiovascular events appeared to be represented by cardiac diseases previously associated with use of AAS (e.g., sudden cardiac death and heart failure (Montisci et al, 2012;Sullivan et al, 1998;Thiblin et al, 2000) to a higher degree among the AAS-positive subjects than was the case for the AAS-negative subjects seems to support a causal connection.…”

Enfermedad de riesgo vital de origen respiratorio o alérgico en el deporte

“…Se debe sospechar un TEP siempre, y hay que descartarlo en pacientes con antecedentes de trombofilia genética, o en aquellos que experimentan disnea súbita, sobre todo si no hay otros signos o síntomas y, sin duda, si se instaura y revierte de forma rápida con el ejercicio. Debe considerarse mantener una alerta específica en aquellos sujetos con trastornos de la coagulación o con una predisposición a la trombosis venosa profunda, con el retorno venoso comprometido, después de viajes largos, en posibles estados de deshidratación, cirugía reciente, o si mantienen un tratamiento anovulatorio o, por alguna razón, toman esteroides anabolizantes 61 . Por otro lado, en los individuos que padecen procesos inflamatorios sistémicos existe una modulación del sistema de coagulación que facilita la activación del factor tisular mediado por la trombina, y se reduce la respuesta de los mecanismos anticoagulantes fisiológicos y se inhibe, de alguna manera, la fibrinólisis 62 , lo que promociona la aparición de un TEP.…”

“Normative Content” and Health Inequity Enculturation

“…Testosterone also has been implicated in higher resting blood pressure, which can predispose males to stroke (Vanberg & Atar, 2010). The vast majority of issues affecting male health outcomes, however, are socially based and not biological in nature .…”