Most discussions of steroids and heart health focus on risk factors such as blood pressure and cholesterol. But research using heart imaging suggests that anabolic-androgenic steroids (AAS) can also affect the heart directly, changing the size of the heart muscle, how well it pumps and relaxes, and the condition of the arteries that supply it.
This article focuses on those structural and functional changes: what studies have found, how these changes differ from the normal effects of training, whether they reverse after use stops, and why they often go unnoticed. The related effects on blood pressure and cholesterol are covered in separate articles.
How can steroids affect the heart?
The heart is a muscle, and it contains androgen receptors. AAS can therefore influence heart tissue directly, in addition to affecting the heart indirectly through blood pressure, blood lipids, and red blood cell production.
Research has identified several types of change associated with AAS use:
Structure: thickening of the walls of the left ventricle, the heart’s main pumping chamber.
Systolic function: a reduction in how effectively the heart pumps blood out with each beat.
Diastolic function: increased stiffness, meaning the heart relaxes and fills less efficiently between beats.
Arteries: a greater amount of plaque in the coronary arteries, which supply the heart muscle with blood.
Can steroids make the heart bigger?
Evidence indicates that they can. In the HAARLEM study, a subset of men underwent detailed heart imaging before and after an AAS cycle. During the cycle, left ventricular mass increased, due to thickening of both the wall between the heart’s chambers and the back wall of the left ventricle (Smit et al., 2021).
A cross-sectional study of experienced male weightlifters found a similar pattern. Men with at least two years of cumulative AAS use had substantially greater left ventricular mass than weightlifters who had never used AAS (Baggish et al., 2017).
Is this the same as an “athlete’s heart”?
No, and this is an important distinction. Regular training, especially endurance training, can lead to a larger heart as a normal adaptation. This “athlete’s heart” typically comes with normal or even improved heart function.
The changes associated with AAS differ because the increase in heart muscle mass has been accompanied by reduced pumping function and increased stiffness. In the Baggish study, both groups were experienced weightlifters, so training alone does not explain the differences between them. A larger heart in an AAS user therefore should not be assumed to be a harmless training adaptation.
Can steroids weaken how the heart pumps?
Research suggests they can. Ejection fraction is the percentage of blood the left ventricle pumps out with each beat, and it is a standard measure of heart function.
In the Baggish study, AAS users had an average ejection fraction of 52%, compared with 63% in weightlifters who did not use AAS. They also showed reduced diastolic function, meaning the heart relaxed less effectively between beats. Men who were using AAS at the time of testing had lower ejection fractions than men who had stopped (Baggish et al., 2017).
The HAARLEM study found that a single cycle, with a median duration of 16 weeks, reduced ejection fraction by about 5% and made the left ventricle stiffer (Smit et al., 2021).
A more recent study of men and women who used AAS found that nearly all participants with more than five years of cumulative use had left ventricular mass above, and ejection fraction below, the middle of the normal range.
What these numbers mean
Many AAS users in these studies still had ejection fractions within or near the normal range, and the changes were averages across groups. However, a reduction in heart function that occurs without symptoms can still be clinically meaningful, and some case reports have described severe heart muscle disease (cardiomyopathy) in AAS users.
Can steroids affect the coronary arteries?
Evidence suggests that long-term use may accelerate atherosclerosis, the build-up of plaque in the arteries.
In the Baggish study, AAS users had a higher coronary plaque volume than non-users, and a longer cumulative duration of AAS use was associated with a greater plaque burden (Baggish et al., 2017). The study of men and women similarly found that a longer cumulative duration of use was associated with higher odds of coronary artery calcium and non-calcified plaque.
This is consistent with the known effects of AAS on risk factors. Lower HDL cholesterol, higher LDL cholesterol, and raised blood pressure can all contribute to plaque formation over time.
Do steroids increase the risk of heart events?
Studies of structure and function do not directly measure heart attacks, strokes, or deaths, and those outcomes are harder to study. However, registry research supports concern. A Danish registry study of men sanctioned for AAS use found a markedly higher rate of cardiovascular events than in matched controls over about 11 years of follow-up (as summarized in a 2025 review).
These studies are observational, so they cannot fully separate the effects of AAS from other factors, such as the use of other substances. Even so, the overall pattern across imaging, risk-factor, and registry studies points in the same direction.
Are heart changes from steroids reversible?
Some appear to be, at least after limited use. In the HAARLEM study, heart size and function returned to their baseline values after a median recovery period of about eight months following a single cycle (Smit et al., 2021).
The picture is less clear for long-term or repeated use. In the Baggish study, men who had stopped AAS had better heart function than current users, which suggests some recovery, but long-term users as a group still differed from non-users. Whether coronary plaque that develops over years of use can reverse is much less certain.
Recovery after one cycle therefore should not be assumed to apply to every pattern of use.
Why heart changes often go unnoticed
Thickening of the heart muscle, a modest decline in pumping function, and early plaque build-up usually cause no symptoms. A person can feel well, train hard, and perform at a high level while these changes are developing.
Symptoms that may indicate a heart problem include shortness of breath, chest pain or pressure, palpitations or an irregular heartbeat, fainting, and swelling in the legs or ankles. These symptoms require prompt medical evaluation, and chest pain or fainting requires urgent care.
How is heart health evaluated?
A healthcare professional may use tests such as an electrocardiogram (ECG), echocardiography (an ultrasound of the heart), and blood tests, and in some cases imaging of the coronary arteries. Which tests are appropriate depends on the individual’s history, symptoms, and risk factors.
Anyone who has used or is using AAS can benefit from telling their doctor, because that history affects how heart test results are interpreted. Our guide to the key facts about steroids provides broader background on how AAS affect the body.
The bottom line
Research on steroids and heart health indicates that AAS can do more than change risk factors. Imaging studies have found that AAS use is associated with thicker heart muscle, reduced pumping function, a stiffer left ventricle, and greater coronary plaque, with plaque burden increasing with longer use.
Some of these changes appear to reverse after a single cycle, but the effects of long-term or repeated use are less certain, and plaque build-up may not reverse in the same way. Because these changes usually cause no symptoms, a fit appearance and good training performance do not indicate a healthy heart. Anyone with concerns should speak with a qualified healthcare professional.
References
Baggish AL, Weiner RB, Kanayama G, et al. Cardiovascular toxicity of illicit anabolic-androgenic steroid use. Circulation. 2017;135(21):1991–2002.
Illicit anabolic steroid use and cardiovascular status in men and women. 2025 study. Available at PubMed Central: PMC12397887.
Impact of anabolic–androgenic steroid abuse on the cardiovascular system: molecular mechanisms and clinical implications. 2025 review. Available at PubMed Central: PMC12652398.
