Supraphysiological doses of testosterone esters administered to normal men suppressed serum HDL cholesterol levels by 13%, but LDL-cholesterol (LDL-C) and triglyceride levels were unchanged (52). On the other hand, in hypogonadal men administered transdermal testosterone in patches or gels, serum HDL-cholesterol (HDL-C) levels were not significantly changed (17,53-55). The decrease in serum HDL-C was dependent on the dose of testosterone administered and serum testosterone achieved (43). Thus, in androgen replacement of hypogonadal men with near physiological doses of testosterone, significant changes of serum lipid levels are uncommon.
As discussed more thoroughly in Chapter 17, epidemiological studies have shown that men with lower serum total testosterone levels are at higher risk for cardiovascular events (56,57). In men undergoing coronary angiograms, those with evidence for coronary artery disease had significantly lower serum free androgen index and bioavailable testosterone levels than did those without apparent coronary artery disease (58,59). Older studies described a lessening of ST segment depression and reduced anginal symptoms in men with coronary artery disease after testosterone treatment (60,61). Acute administration of testosterone in men with exercise-induced myocardial ischemia reduced ST segment depression and increase exercise testing time compared to placebo (62,63). Because of this acute action of testosterone, the effect may be ascribed to a direct coronary vasodilatory effect of the steroid. A subsequent study confirmed this hypothesis by showing that acute testosterone infusion increased coronary artery diameter coronary blood flow in men with established coronary artery disease compared to vehicle administration (64). Others failed to demonstrate a beneficial effect on acute stress-induced myocardial ischemia (65). In summary, these studies indicate that testosterone administration does not have an adverse effect on coronary artery disease. Whether testosterone administration has beneficial effects on coronary artery disease needs to be addressed in randomized controlled clinical studies.
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