Metabolic & Cardiometabolic
anabolic-androgenic steroids increases cardiovascular disease risk
In plain terms: Do anabolic steroids increase cardiovascular disease risk?
Part of: 💊 anabolic-androgenic steroids
Yes — a nationwide cohort and imaging studies show steroid users have more coronary plaque, worse heart function and adverse lipids; long-term cardiovascular risk is clearly raised (short courses may not show acute changes).
📅 Last reviewed: 2026-07-14 ⓘ
Evidence ladder
How far up the ladder this claim has climbed. A high consensus on a low rung means "consistent so far," not "proven in people."
Top evidence so far: ()
How the studies fall
The evidence (30)
| Source | Grade | Stance | Quality | Finding |
|---|---|---|---|---|
| de Souza 2022 · Int J Sports Med | observational | supports | moderate | Strength-trained AAS users showed impaired myocardial contractility (reduced strain) and higher LV mass by cardiac MRI versus non-users. |
| Vasilaki 2016 · Toxicol Lett | animal | supports | moderate | Long-term nandrolone in rabbits caused focal myocardial fibrosis, oxidative stress and diastolic impairment. |
| Di Fazio 2025 · Front Cardiovasc Med | observational | supports | low | Systematic review of AAS-related deaths found LV hypertrophy, myocardial fibrosis and sudden cardiac death even without coronary disease. |
| Fyksen TS et al 2025 · study_type: observational | observational | supports | moderate | Prospective cohort of 32 AAS users vs 13 strength-trained non-users followed a median of 16 vs 13 years: users had larger LV mass (266g vs 215g, p<0.01) and lower LVEF (49% vs 53%, p=0.05) at baseline; LVEF remained impaired in continued us |
| Ahmed AE et al 2026 · study_type: observational | n-of-1 | supports | low | Single case report: 29-year-old man with long-term AAS abuse developed cerebral venous sinus thrombosis with polycythemia; thrombophilia workup unremarkable, improved with anticoagulation and steroid cessation. |
| Hartgens 2003 · Int J Sports Med | RCT | tested-null | high | Short-term (up to 16 weeks) AAS/nandrolone administration produced no detectable echocardiographic changes in heart structure or function. |
| Baggish 2017 · Circulation | observational | supports | high | AAS users had reduced LV systolic/diastolic function and markedly higher coronary atherosclerotic plaque volume than non-using weightlifters. |
| Vecchiato M et al 2026 · study_type: mechanism | observational | supports | moderate | Review of performance-enhancing drug classes noting AAS (with ESAs) show the strongest ergogenic signals but are also associated with myocardial remodeling, arrhythmia, and thrombotic events; states current PED-CV evidence derives mainly fr |
| Celik 2024 · Medicina | observational | mixed | low | Bodybuilders showed altered paraoxonase/arylesterase activity and lipid profiles associated with a pro-atherosclerotic pattern. |
| Abdelsamie AH et al 2025 · study_type: observational | observational | supports | low | Single case report: 30-year-old male with AAS abuse history presented with NSTEMI; OCT-confirmed intimal hyperplasia, plaque erosion, and thrombus in the LAD, attributed by authors to AAS-related atherogenic/thrombogenic/vasospastic mechani |
| Iliakis P et al 2025 · study_type: mechanism | observational | supports | moderate | Narrative review summarizing pathophysiological mechanisms (oxidative stress, androgen receptor overactivation, RAAS dysregulation) by which chronic supraphysiologic AAS use causes hypertension, dyslipidemia, atherosclerosis, myocardial fib |
| D'Andrea 2022 · Eur J Prev Cardiol | observational | supports | moderate | AAS-abusing athletes showed biventricular dysfunction and lung congestion on speckle-tracking and stress echocardiography. |
| de Carvalho Vilarinho M et al 2025 · study_type: observational | observational | supports | low | Case report: 30-year-old male with chronic AAS abuse found to have dyslipidemia and hypertension attributed to AAS use, alongside gynecomastia and testicular atrophy. |
| Vanberg 2010 · Handb Exp Pharmacol | observational | supports | moderate | Review concludes AAS raise LDL and lower HDL, induce a prothrombotic state and hypertrophy, increasing cardiovascular disease risk. |
| Place F et al 2026 · study_type: observational | observational | supports | moderate | Cross-sectional study of 141 resistance-trained individuals: current AAS users (n=95) had higher calibrated integrated backscatter than non-users (n=46) (-19.54±4.63 vs -20.88±3.94, p=0.047), correlating with LV mass index and LA stiffness |
| Poyorena C et al 2025 · study_type: observational | n-of-1 | supports | low | Single case report: 45-year-old with anabolic steroid and pre-workout use presented with hyperacute T waves progressing to ventricular fibrillation and cardiac arrest, meeting STEMI criteria after ROSC. |
| Ilic 2014 · Hellenic J Cardiol | observational | supports | moderate | AAS-using athletes showed adverse LV remodeling and diastolic function changes versus non-using athletes. |
| Davies A. 2026 · study_type: observational | n-of-1 | supports | low | Single case report: AAS-using patient presented with pulmonary oedema from suspected steroid-induced cardiomyopathy, confirmed by MRI showing hypertrophied LV with systolic dysfunction. |
| Windfeld-Mathiasen 2025 · Circulation | observational | supports | high | Nationwide cohort of male AAS users showed substantially higher incidence of cardiovascular disease than age/sex-matched general-population controls. |
| Gurumurthy G et al 2025 · study_type: mechanism | observational | supports | low | Review describing AAS use as predisposing to venous and arterial thromboses via androgen-induced polycythemia, platelet hyperaggregability, procoagulant shifts, and vascular injury; notes current evidence is largely observational/pharmacolo |
| Magnolini R et al 2025 · study_type: in-vitro | n-of-1 | supports | low | Case report: 38-year-old recreational bodybuilder with years of supraphysiologic androgen use developed anabolic steroid-induced cardiomyopathy (ASIC) and polycythemia; despite ASIC normalizing and >1 year of abstinence, he ultimately died |
| Udd-Garnica K et al 2026 · study_type: observational | n-of-1 | supports | low | Single case report: 34-year-old on testosterone developed nonischemic cardiomyopathy with LVEF 16% and global LV hypokinesis/dilation; discussion cites AAS users having significantly higher incidence of MI, coronary intervention, VTE, arrhy |
| Barbosa Neto 2018 · Clin Auton Res | observational | supports | moderate | Male bodybuilder AAS users had higher blood pressure, altered cardiac dimensions and cardiac autonomic dysfunction. |
| Buhl LF et al 2025 · study_type: observational | observational | supports | high | Cross-sectional study of 164 Danish recreational athletes (80 active AAS users, 26 former users, 58 non-users): longer cumulative AAS use was associated with higher odds of positive coronary artery calcium score (OR 1.23, 95% CI 1.09-1.39) |
| Borowiec A et al 2025 · study_type: mechanism | observational | supports | low | Narrative review (not a formal SR/MA) synthesizing mechanistic and clinical literature on AAS-induced endothelial injury, oxidative stress, fibrosis, and arrhythmogenesis, describing AAS abuse as a modifiable cardiovascular risk factor. |
| Vauhkonen PK et al 2026 · study_type: observational | observational | mixed | low | Forensic autopsy comparative study of 16 AAS-positive vs 30 AAS-negative male decedents: overall arteriolosclerosis, hypertrophy, disarray, and fibrosis frequencies were similar between groups, though AAS-positive cases showed more diffuse/ |
| Buhl LF et al 2026 · study_type: observational | observational | supports | moderate | Cross-sectional study of 80 active AAS users, 26 former users, and 58 non-users found active users had altered IGF-2/IGFBP-3/STC2 levels; higher STC2 associated with adverse cardiac outcomes and lower IGF-2/IGFBP-3 with lower LV mass and be |
| Makarem NN et al 2025 · study_type: observational | n-of-1 | supports | low | Single case report: 35-year-old bodybuilder on trenbolone/testosterone/nandrolone for six weeks suffered acute MI with 80% coronary lesion. |
| Urhausen 2004 · J Sports Med Phys Fitness | observational | mixed | moderate | Some adverse cardiac effects (hypertrophy, diastolic changes) persisted while others partly reversed after AAS cessation in strength athletes. |
| Meagher S et al 2025 · study_type: mechanism | mechanism | supports | moderate | Review of recreational-athlete AAS use reporting elevated blood pressure, adverse lipid profiles, accelerated atherosclerosis, subclinical cardiomyopathy, and increased MI/sudden cardiac death risk, with some structural changes persisting a |
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