[Cardiovascular side effects of anabolic-androgenic steroids].
The intake of anabolic-androgenic steroids (AAS) leads to an increase in skeletal muscle mass and is prohibited as a doping measure in sport. AAS abuse is not limited to competitive athletes. It is also prevalent in subjects who do body building or resistance training for cosmetic reasons only. Out of the numerous and partly serious side effects, the cardiovascular ones are presented here. An increase in left ventricular muscle mass is well documented, and some researchers have even reported concentric hypertrophy. By contrast, resistance training without AAS intake does not lead to increased ventricular wall thickness. AAS do not affect the systolic function of the left ventricle, whereas diastolic function might be impaired. Different ultrastructural myocardial alterations have been documented in animal studies. In addition, AAS can induce arterial hypertension. Blood clotting and fibrinolysis are negatively affected, and several case studies of thrombi exist in young strength athletes. Changes in the concentration of blood lipoproteins, particularly a reduction in vessel-protective HDL cholesterol, can lead to early atherosclerosis. Many case reports exist about cardiac deaths in seemingly healthy subjects-most often body builders and other strength athletes. In fatal and nonfatal myocardial infarctions patent coronary arteries were proven frequently. Besides the prothrombotic effects of AAS, an impaired endothelial function and vasospasms are discussed hypothetically as pathomechanisms. Also, cardiomyopathies can occur due to AAS abuse. On the basis of the described possible cardiovascular side effects, it can be concluded that in cases of sudden cardiac deaths in young athletes, a misuse of AS should be excluded.
Kindermann
Wilfried
W
Institut für Sport- und Präventivmedizin der Universität des Saarlandes, Saarbrücken. w.kindermann@mx.uni-saarland.de
D000328:Adult; D045930:Anabolic Agents / Q000009:adverse effects*; D000818:Animals; D050197:Atherosclerosis / Q000139:chemically induced; D009202:Cardiomyopathies / Q000139:chemically induced; D002318:Cardiovascular Diseases / Q000139:chemically induced* / Q000401:mortality; D008076:Cholesterol, HDL / Q000097:blood; D002986:Clinical Trials as Topic; D003327:Coronary Disease / Q000139:chemically induced; D016757:Death, Sudden, Cardiac / Q000209:etiology*; D003971:Diastole / Q000187:drug effects; D004300:Doping in Sports; D006801:Humans; D006973:Hypertension / Q000139:chemically induced; D017379:Hypertrophy, Left Ventricular / Q000139:chemically induced; D008074:Lipoproteins / Q000097:blood; D009203:Myocardial Infarction / Q000139:chemically induced / Q000401:mortality; D012307:Risk Factors; D013927:Thrombosis / Q000175:diagnosis; D013997:Time Factors; D016277:Ventricular Function, Left / Q000187:drug effects
D045930:Anabolic Agents; D008076:Cholesterol, HDL; D008074:Lipoproteins