Enlarged Heart

The human heart is a muscle that contains functional androgen receptors and responds to anabolic steroid hormones with growth. This fact partly explains why male hearts are, on average, larger than female hearts. Physical activity also significantly affects heart growth. Resistance training (anaerobic) increases heart size by thickening the ventricular walls, usually without an equal expansion of the internal cavity. This is known as concentric remodeling. On the other hand, endurance (aerobic) athletes tend to increase heart size through cavity expansion without significantly thickening the ventricular walls (eccentric remodeling). Despite concentric or eccentric remodeling, diastolic function usually remains normal in athletic hearts. The myocardium is also dynamic; when regular training is removed from conditioned athletes, wall thickening and cavity expansion often decrease.

Anabolic steroid abusers risk thickening of both the left and right ventricular walls, a condition known as ventricular hypertrophy. Left ventricular hypertrophy (LVH) is particularly well-documented among anabolic-androgenic steroid (AAS) abusers. While LVH can also be found in natural athletes, steroid-abusing athletes often exhibit more pronounced wall thickening. This can slowly develop into pathological issues associated with this thickening, including impaired diastolic function and eventually reduced cardiac function. The level of damage is closely related to the dosage and duration of steroid abuse. Naturally, a left ventricular wall thickness exceeding 13mm is rare and likely indicates steroid abuse or other causes, potentially further suggesting the development of pathological LVH. Additional testing is recommended for these patients.

LVH is an independent predictor of mortality in hypertensive overweight patients. It is also associated with atrial fibrillation, ventricular arrhythmias, sudden collapse, and death. While LVH in athletes not using steroids may have no clinical significance, pathological increases in QT dispersion have been observed in steroid-abusing athletes with LVH. These changes are similar to those seen in hypertensive patients with LVH. Such changes may lead to serious adverse events for steroid abusers, including arrhythmias or heart attacks. Long-term case studies of isolated steroid abusers support the association between LVH and related pathologies, including ventricular tachycardia (arrhythmias originating from the left ventricle), hypokinesis of the left ventricle (reduced left ventricular contraction), and decreased ejection fraction (reduced blood output and efficiency).

The current status of anabolic steroid use, average dosage, and duration of intake can all influence increases or decreases in heart mass. Similarly, once anabolic-androgenic steroids are no longer used, the heart typically begins to shrink. This effect is similar to what happens when athletes stop following a rigorous training regimen—the size of the heart decreases. However, despite this effect, some changes in heart muscle size and function caused by drug use may persist. Studies observing the effects of steroid use and withdrawal on LVH indicate that, compared to athletes who have not used steroids, steroid-abusing athletes retain slightly higher levels of concentric LVH for several years after discontinuing the drugs. The treatment of steroid-induced LVH remains a subject of ongoing investigation and debate.