Body-Building Steroids May Promote CAD, Ventricular Dysfunction

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BOSTON, MA — Long-term illicit use of anabolic-androgenic steroids (AAS) by recreational weightlifters may lead to reduced ventricular function, which may persist even after the drugs are stopped, warn US researchers based on their cross-sectional cohort study[heartwire from Medscape.

"The type of people that we studied are going to end up being sent to cardiologists because of lower ejection fractions or premature coronary disease," he said.


"I think the paradigm shift that we'd like to see occur is that cardiovascular practitioners recognize that steroid use is a possible explanation for some of these [signs] in otherwise-healthy young men," Baggish said.

"They won't know unless they ask, so the first place to start is really by encouraging doctors to ask their patients about drug abuse."

The issue of illicit steroid use is not confined to elite competitive athletes, Baggish observed, and "there's a misconception in the general population, as well as in the medical world, that the people you read about in the newspapers" are the ones who are the primary users of AAS.

"In fact, it's much more of a mainstream, general-population problem," he said.

"Some work that we did prior to this study, which was more epidemiologic in focus, suggested that approximately a million US men have a steroid dependence problem, which means that this is something that's affecting people in every community."

The researchers measured LV systolic and diastolic function and coronary artery plaque volume in 140 experienced male weightlifters aged 34 to 54 years. The group consisted of 54 nonusers of AAS and 86 users, of whom 58 were using the drugs at the time and 28 had used them a median of 15 months before the evaluation.

There were few significant baseline differences between users and nonusers of AAS, although users had a significantly higher mean body mass index and fat-free mass index, which is consistent with AAS use.

Overall, AAS users had significantly reduced LV systolic function compared with nonusers, at 52% vs 63% respectively (P<0.001). Their LV relaxation velocity as a reflection of diastolic function was also down at 9.3 cm/s vs 11.1 cm/s (P<0.001).


Users of AAS also showed significant greater plaque volume, with an estimated mean difference of 0.46 mm3 (P=0.012).


The analyses were adjusted for age, race/ethnicity, history of tobacco use, cocaine and/or alcohol dependence, weekly hours of aerobic activity in the past 10 years, and reported family history of coronary artery disease.


The team found that there was a significant difference in the estimated mean difference of LV systolic function between AAS users who were still taking the drugs and those who had stopped before the study, at -9.5% (95% CI -13.8 to -5.2; P<0.001).


There was also a still significant but less pronounced difference in the LV diastolic function between current and former AAS users, at an estimated mean difference of -1.1 cm/second (P=0.035).


Lifetime AAS dose was strongly linked to coronary atherosclerotic burden, with each 10-year increase in the cumulative duration of AAS use elevating the standardized rank plaque volume by 0.60 SD units (P=0.008).


"The hypothesis that some cardiovascular phenotypes associated with AAS use may wax and wane with drug exposure," such as LV systolic dysfunction, "while others may be more permanent, perhaps irreversible," such as LV diastolic dysfunction and coronary atherosclerosis, "deserves rigorous assessment."


Baggish received grant support from the National Institute on Drug Abuse; disclosures for the coauthors are listed in the paper.

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