Cardiovascular System and AAS

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Serum Lipoproteins and the Cardiovascular System

AS also affect the cardiovascular system and the serum lipid profile. Relatively few studies have been done to investigate the effect of anabolic steroids on the cardiovascular system. No longitudinal studies have been conducted on the effect of anabolic steroids on cardiovascular morbidity and mortality.

Most of the investigations have been focused on risk factors for cardiovascular diseases, and in particular the effect of anabolic steroids on blood pressure and on plasma lipoproteins. In most cross-sectional studies serum cholesterol and triglycerides between drug-free users and non-users is not different. However, during anabolic steroid use total cholesterol tends to increase, while HDL-cholesterol demonstrates a marked decline, well below the normal range. Serum LDL-cholesterol shows a variable response: a slight increase or no change. The response of total cholesterol seems to be influenced by the type of training that is done by the athlete. When a great deal of the exercise consists of aerobic exercise, the increasing effect of AS is counterbalanced by an exercise-induced increasing effect, which may result in a net decline in total cholesterol. Aerobic training does not seem to be able to offset the steroid-induced decline in HDL-cholesterol and its subfractions HDL-2, and HDL-3.

The precise effect of anabolic steroids on LDL-cholesterol is unknown yet. It appears that anabolic steroids influence hepatic triglyceride lipase (HTL) and lipoprotein lipase (LPL). Males usually have higher levels of HTL, while females have higher LPL activity. HTL is primarily responsible for the clearance of HDL-cholesterol, while LPL takes care of cellular uptake of free fatty acids and glycerol. Androgens and anabolic steroids stimulate HTL, presumably resulting in decreased serum levels of HDL-cholesterol.

The effect of anabolic steroids on triglycerides is not well known. It is suggested that relatively low doses do not affect the serum triglyceride levels, while it cannot be excluded that higher doses elicit an increase.

No unanimity exists about the influence of anabolic steroids on arterial blood pressure. The response is most probably dose dependent. There is some data suggesting that high doses increase diastolic blood pressure, whereas low doses fail to have a significant effect on diastolic blood pressure. Increases in diastolic blood pressure normalize within 6-8 weeks after abstinence from anabolic steroids. It appears that repeated intermittent use of anabolic steroids does not affect diastolic blood pressure during drug free periods.

There is evidence that the use of anabolic steroids does elicit structural changes in the heart and that the ischemic tolerance is decreased after steroid use. Echocardiographic studies in bodybuilders, using anabolic steroids, reported a mild hypertrophy of the left ventricle, with a decreased diastolic relaxation, resulting in a decreased diastolic filling. Some investigators have associated cardiomyopathy, myocardial infarction, and cerebro-vascular accidents with abuse of anabolic steroids. However, a possible causal relationship could not been proved, because longitudinal studies that are necessary to prove such a relationship, have not been conducted yet. There is convincing evidence that oral administration of anabolic steroids has stronger adverse effects on the mentioned variables than parenteral administration.

Although the effects of anabolic steroids have an unfavorable influence on the risk factors for cardiovascular disease, no data are available about the long term effects. Most of the mentioned effects appear to reverse within 6-8 weeks after abstention. It is unknown, however, whether the structural changes as reported in the heart, are reversible as well.