The use of anabolic-androgenic steroids (AAS), synthetic derivatives of the male hormone testosterone, is associated with adverse effects on the cardiovascular system. These compounds are used in high doses to enhance muscle development and athletic performance, but they carry a risk of heart damage. The heart is susceptible to the direct and indirect actions of AAS, leading to complications from electrical instability to structural remodeling. AAS use can increase the risk of heart attack, stroke, and sudden cardiac death, even in young, otherwise healthy individuals.
Mechanisms Behind Increased Heart Rate and Arrhythmia Risk
AAS directly influence the heart’s electrical system, increasing the risk of abnormal heart rhythms. Elevated hormonal levels can potentiate oxidative stress within the heart muscle cells, which lowers the threshold for electrical instability. This increased excitability can manifest as tachycardia, or an elevated resting heart rate, by altering the heart muscle’s sensitivity to natural stimulants.
Research suggests that high levels of male sex hormones can disrupt the function of specialized ion channels, such as sodium channels, that are responsible for generating and conducting the heart’s electrical impulse. Impaired electrical conduction, particularly in the heart’s upper chambers (atria), raises the likelihood of developing conditions like atrial fibrillation. Atrial fibrillation is a chaotic and rapid heart rhythm that increases the risk of blood clot formation and stroke. The direct action of AAS on the heart muscle’s structure can also lead to issues with electrical signaling, which increases the risk of life-threatening ventricular arrhythmias and sudden cardiac death.
Physical Remodeling of the Heart Muscle
Chronic AAS use promotes changes in the heart’s physical structure, known as adverse cardiac remodeling. The most prominent structural change is Left Ventricular Hypertrophy (LVH), a thickening of the wall of the heart’s main pumping chamber. This hypertrophy is caused by the heart working harder against increased systemic resistance and the direct binding of AAS to androgen receptors on the heart muscle cells.
The resulting muscle growth is often disorganized, leading to a condition called concentric LVH, where the muscle wall thickens inward. This inward thickening reduces the volume of the left ventricle and impairs its ability to fully relax and fill with blood between beats, known as diastolic dysfunction. Diastolic dysfunction is a precursor to heart failure and can be less reversible than other changes.
Over time, this structural damage can progress to steroid-induced cardiomyopathy, where the heart muscle becomes weakened and less efficient at pumping blood. Studies have shown that long-term AAS users may exhibit reduced left ventricular systolic function, meaning the heart’s ability to contract forcefully is compromised. Furthermore, AAS use can promote the deposition of collagen and scar tissue, or fibrosis, within the heart muscle, inhibiting proper function.
Systemic Vascular and Blood Pressure Consequences
Beyond the heart muscle, AAS affect the entire circulatory system, contributing to the risk of heart attack and stroke. One consequence is the induction of hypertension, or high blood pressure, which links directly to the duration of AAS use. This elevated pressure results from increased fluid retention and vasoconstriction, the narrowing of blood vessels.
AAS use disrupts the lipid profile. Users frequently experience a lowering of high-density lipoprotein (HDL) cholesterol by as much as 20% to 70%. Simultaneously, AAS can increase levels of low-density lipoprotein (LDL) cholesterol, which contributes to plaque buildup.
These changes accelerate atherosclerosis, the hardening and narrowing of the arteries due to plaque accumulation. The combination of hypertension, adverse lipid changes, and direct damage to the arterial walls increases the risk of acute coronary events. AAS can also promote a pro-thrombotic state by altering the blood’s coagulation factors, making the blood more prone to clotting, increasing the risk of heart attack or stroke from a blocked artery.
Long-Term Outlook and Reversibility of Damage
The prognosis for individuals who have used AAS depends on the duration of use, the dosage levels, and the extent of pre-existing cardiovascular damage. Upon cessation of AAS use, some adverse effects, such as changes to the lipid profile and mild hypertension, are reversible, with levels returning toward normal within weeks to months.
In cases of mild LVH, heart muscle thickness may decrease after the drugs are stopped. However, the reversibility of structural damage, such as extensive myocardial fibrosis or advanced cardiomyopathy, can be incomplete. While some individuals with severe systolic dysfunction have reported significant recovery following cessation and medical treatment, diastolic dysfunction and LVH can persist for years after the drugs are discontinued. Long-term users are also more likely to have a higher burden of coronary artery plaque, a change associated with the lifetime cumulative dose of AAS and often irreversible.