Can anabolic steroid use cause premature ventricular contractions?

Anabolic Steroid Use and Premature Ventricular Contractions

Yes, anabolic steroid use can cause premature ventricular contractions (PVCs) and is associated with serious ventricular arrhythmias, including ventricular tachycardia and ventricular fibrillation, which can lead to sudden cardiac death.

Direct Cardiac Effects of Anabolic Steroids

Anabolic-androgenic steroids (AAS) have well-documented cardiotoxic effects that create an arrhythmogenic substrate through multiple mechanisms 1:

• Cardiac hypertrophy and structural remodeling that increases susceptibility to ventricular arrhythmias 1
• Electrical remodeling of the myocardium that predisposes to arrhythmias 1
• Myocardial fibrosis documented on endomyocardial biopsy in chronic users 2
• Impaired ventricular function with worse left and right ventricular global longitudinal strain associated with cumulative AAS exposure 3

Clinical Evidence of Arrhythmias

The literature contains multiple documented cases of life-threatening arrhythmias directly attributed to AAS use:

• Ventricular fibrillation during exercise requiring resuscitation in a weightlifter 2
• Sudden cardiac arrest from ventricular fibrillation in an adolescent attributed to AAS use 4
• Ventricular tachycardia in a 73-year-old former Olympic athlete with 20 years of AAS use, presenting with non-ischemic cardiomyopathy 5
• Fulminant heart failure with severe biventricular dysfunction (LVEF 15%) in a 39-year-old weightlifter using testosterone and boldenone 6

Risk Assessment When PVCs Are Detected

When evaluating a patient with PVCs and suspected or confirmed AAS use, the 2017 AHA/ACC guidelines recommend a comprehensive medication history that specifically includes supplements including anabolic steroids 7. The evaluation should proceed as follows:

Initial workup for any patient with ≥2 PVCs on ECG 7:

• Ambulatory Holter monitor to quantify PVC burden over 24 hours
• Echocardiogram to assess for structural heart disease and ventricular function
• Exercise stress test to evaluate PVC behavior with exertion

Risk stratification based on PVC burden 7:

• ≥2,000 PVCs per 24 hours: Up to 30% have underlying structural heart disease
• <2,000 PVCs per 24 hours: 3% have structural heart disease
• <100 PVCs per 24 hours: 0% have structural heart disease

Additional testing if high-risk features present 7:

• Contrast-enhanced cardiac MRI if ≥2,000 PVCs/24h or episodes of non-sustained VT
• Electrophysiology study if increasing ectopy burden during incremental exercise testing
• Cardiac MRI is particularly valuable for detecting myocardial fibrosis, a hallmark of AAS-induced cardiomyopathy 7

Critical Pitfalls to Avoid

Do not assume PVCs are benign simply because they have right ventricular outflow tract (RVOT) morphology (left bundle branch block pattern with inferior axis). While RVOT-origin PVCs are generally benign in structurally normal hearts, this same morphology can occur in early arrhythmogenic right ventricular cardiomyopathy, particularly when QRS duration exceeds 160 ms 7. AAS use can cause structural changes that mimic or coexist with cardiomyopathy 7.

Do not rely on detraining as a diagnostic or therapeutic measure. Although some studies suggested regression of PVC burden with detraining indicates good prognosis, other studies have not confirmed this, and detraining is not recommended as a diagnostic tool 7.

Do not dismiss symptoms in young, athletic individuals. The 2025 study of 164 recreational athletes found that cumulative AAS exposure exceeding 5 years was associated with coronary artery calcification, non-calcified plaques, and impaired biventricular function, with nearly all athletes (35 of 36) showing ventricular mass above and ejection fraction below the median normal range 3.

Long-Term Cardiovascular Consequences

The cardiovascular effects of AAS can persist long after cessation:

• Delayed presentation of cardiomyopathy decades after AAS use, as demonstrated in the 73-year-old former Olympic athlete who remained asymptomatic until developing ventricular tachycardia 5
• Cumulative dose-dependent effects with longer AAS exposure associated with higher odds of coronary artery calcification (OR 1.23 per year) and coronary non-calcified plaques (OR 1.17 per year) 3
• Atrial fibrillation can also occur as a consequence of AAS-induced structural remodeling 8

Management Approach

Immediate cessation of AAS use is essential when arrhythmias are detected. One case demonstrated rapid improvement in cardiac function after stopping AAS, with left ventricular wall thickness reducing from 12 to 10.5 mm and fractional shortening increasing from 14% to 27% 2.

For patients with frequent symptomatic PVCs or non-sustained VT in the setting of left ventricular dysfunction, amiodarone or catheter ablation should be considered 7. However, the underlying structural substrate from AAS use must be addressed, as this represents the fundamental problem rather than just the arrhythmia manifestation.

Hospitalization is warranted for patients presenting with syncope when ventricular arrhythmia is documented or thought to be the likely cause 7.