Cardiovascular effects of androgenic-anabolic steroids

Med Sci Sports Exerc. 1995 Sep;27(9):1252-62.


Evidence has accumulated over the pst several years which associates androgenic-anabolic steroid (AAS) use with sudden cardiac death, myocardial infarction, altered serum lipoproteins, and cardiac hypertrophy in humans who habitually use these drugs. Even though some experimental data obtained from animals correlate well with the human findings, the adverse cardiovascular effects of AAS use are poorly understood. The evidence presented in this review suggests that there are at least four hypothetical models of AAS-induced adverse cardiovascular effects: 1) an atherogenic model involving the effects of AAS on lipoprotein concentrations; 2) a thrombosis model involving the effects of AAS on clotting factors and platelets; 3) a vasospasm model involving the effects of AAS on the vascular nitric oxide system; and 4) a direct myocardial injury model involving the effects of AAS on individual myocardial cells. Future studies should be directed at determining the exact mechanisms responsible for AAS-induced adverse cardiovascular effects, at determining the relative contribution of each of these models, and at identifying other possible contributing factors such as metabolism of these steroids and the effects of potential metabolites on various target organs.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Anabolic Agents / adverse effects
  • Anabolic Agents / pharmacology*
  • Animals
  • Cardiomegaly / chemically induced
  • Cardiomegaly / physiopathology
  • Cardiovascular System / drug effects*
  • Cardiovascular System / physiopathology
  • Coronary Thrombosis / chemically induced
  • Coronary Thrombosis / physiopathology
  • Coronary Vessels / drug effects
  • Coronary Vessels / physiopathology
  • Exercise / physiology
  • Heart Diseases / chemically induced*
  • Humans
  • Lipase / blood
  • Liver / enzymology
  • Myocardial Infarction / chemically induced
  • Myocardial Infarction / physiopathology


  • Anabolic Agents
  • Lipase