The human heart is a muscle. It possesses functional androgen receptors, and is growthresponsive to male steroid hormones. This fact partly accounts for men having a larger heart mass on average than women. Physical activity can also have a strong effect on the growth of the heart. Resistance exercise (anaerobic) tends to increase heart size by a thickening of the ventricular wall, usually without an equal expansion of the internal cavity. This is known as concentric remodeling. Endurance (aerobic) athletes, on the other hand, tend to increase heart size via expansion of the internal cavity, without significant thickening of the ventricles (eccentric remodeling). Even with concentric or eccentric remodeling, diastolic function usually remains normal in the athletic heart. The heart muscle is also dynamic. When regular training is removed from a conditioned athlete, the wall thickening and cavity expansion tend to reduce.
Anabolic steroid abusers are at risk for thickening of the left and right ventricular walls, known as ventricular hypertrophy. Hypertrophy of the left ventricle (the main pumping chamber) in particular is extensively documented in anabolic/androgenic steroid abusers. While left ventricular hypertrophy is, again, also found in natural power athletes, substanceabusing athletes tend to have a much more profound wall thickening. They also tend to develop pathological issues related to this thickening, including impaired diastolic function, and ultimately reduced heart efficiency. The level of impairment is closely associated with the dose and duration of steroid abuse. A left ventricle wall exceeding 13mm in thickness is rare naturally, and may be indicative of steroid-abuse or other causes. It may further suggest that pathological left ventricular hypertrophy has developed. Additional testing of such patients is recommended.
Left ventricular hypertrophy (LVH) is an independent predictor of mortality in overweight individuals with high blood pressure. It has also been linked to atrial fibrillation, ventricular arrhythmia, and sudden collapse and death. While LVH in non-steroid-using athletes tends to be without clinical significance, pathological increases in QT dispersion are noticed in steroid abusers with LVH. These changes tend to be similar to the increases in QT dispersion noted in hypertensive patients with LVH. Among other things, this could leave a steroid abusing individual more susceptible to a serious adverse event, including arrhythmia or heart attack. Isolated medical case studies of longtime steroid abusers support an association between LVH and related pathologies including ventricular tachycardia (arrhythmia originating in the left ventricle), left ventricular hypokinesis (weakened contraction of the left ventricle), and decreased ejection fraction (reduced pumping volume and efficiency).
Heart mass can increase or decrease in relation to the current state of anabolic/steroid use, the average dosage, and duration of intake. Likewise, the heart usually begins to reduce in size once anabolic/androgenic steroids are no longer being used. This effect is similar to the way the heart will reduce in size once an athlete no longer follows a rigorous training schedule. Even with this effect, however, some changes in heart muscle size and function caused by the drugs may persist. Studies examining the effects of steroid use and withdrawal on left ventricular hypertrophy noted that athletic subjects who abstained from steroid abuse for at least several years still had a slightly greater degree of concentric left ventricular hypertrophy compared to non-steroid-using athletic controls. The disposition of pathological left ventricular hypertrophy following long-term steroid abuse and then abstinence remains the subject of investigation and debate.
Wlliam Llewellyn (2011) - Anabolics