T he use of anabolic-androgenic steroids (AAS) among athletes is not new, nor is concern about their potential cardiac effects, but it has been difficult to definitively document deleterious cardiovascular effects from these drugs. There are case reports of unexpected myocardial infarctions 1 and even sudden cardiac death 2 in AAS users, but such reports are relatively rare given the reported widespread use of AAS. Moreover, their effects on cardiovascular risk factors are confusing. Oral synthetic steroids, such as stanozolol, reduce high-density lipoprotein and increase low-density lipoprotein cholesterol more than parenterally administered testosterone at similar androgenic doses, 3 suggesting that oral AAS are more atherogenic, but both stanozolol 4 and testosterone 5 decrease lipoprotein (a), an important atherosclerotic risk factor. There is also concern that AAS increase blood pressure, but even the literature on this topic is equivocal, 6 and some of the purported increase in blood pressure with AAS may be due to the use of undersized sphygmomanometer cuffs in subjects with increased arm circumference. 7 Consequently, the overall clinical effect of AAS use on atherosclerotic risk and events is not clear.
Article see p 472AAS have more consistently been shown to impair left ventricular (LV) diastolic function, 8 -10 and these clinical studies are supported by pathological evidence of increased myocardial collagen content after exposure to AAS. 11 Evidence of LV systolic dysfunction with AAS use has been evasive, 12 but recent studies using measures of myocardial strain 8,9 suggest that AAS also subtly impair cardiac systolic performance.In contrast to these subtle effects of AAS on systolic function, Baggish et al 13 in this issue of Circulation: Heart Failure present evidence that chronic, high-dose AAS use produces a dramatic impairment of LV systolic function. These authors recruited 19 male weightlifters, including 12 with prolonged AAS use. Recruitment was designed to minimize selection biases. Standardized questionnaires were used to determine participants' lifetime AAS exposure as well as their use of illicit drugs and other ergogenic drugs including growth hormone.The AAS users were remarkable for both their steroid dose and duration of use. For comparison, subjects in prior studies generally reported weekly AAS doses equivalent to 200 to 250 mg of testosterone, 3,7 whereas subjects in the present study reported a median weekly dose equivalent to 675 mg of testosterone. The present subjects also reported a median of almost 9 years of steroid use.These investigators confirmed the decreased early, and increased late, diastolic filling in the AAS users noted previously. LV hypertrophy did not differ between AAS users and control subjects. Both radial and longitudinal strain, measures of myocardial systolic function, were decreased in the AAS users, but more impressive was the decrease in LV ejection fraction (LVEF). Median LVEF was 51% in AAS users versus 59% in control subjects, and half of the AAS...