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A TEST OF THE HEART: TESTOSTERONE-INDUCED CARDIOMYOPATHY
Abstract   Open access   Peer reviewed

A TEST OF THE HEART: TESTOSTERONE-INDUCED CARDIOMYOPATHY

Madiha Rasool, Ravneet Randhawa, Amjad Basheer, Hina Amin and Jeffrey Kluger
Journal of the American College of Cardiology, Vol.77(18 Suppl 1), pp.2204-2204
05/11/2021
DOI: 10.1016/S0735-1097(21)03559-2
url
https://doi.org/10.1016/S0735-1097(21)03559-2View
Published (Version of record) Open Access

Abstract

Background A few case reports describe the phenomenon of anabolic steroid-induced cardiomyopathy. Early initiation of guideline-directed medical therapy may result in a recovery of cardiac function. Case A 57-year-old male with hypogonadism presented with exertional dyspnea and leg swelling for three months. He also complained of orthopnea and abdominal fullness. He had been receiving 200 mg weekly intramuscular testosterone enanthate injections for the past 18 months for hypogonadism. On exam, oxygen saturation was 86%, which improved to 97% on 2 L. A cardiac exam revealed a regular heart rate and rhythm without an appreciable murmur; however, JVD was notable. Lung exam revealed coarse bibasilar crackles. Abdomen was soft, distended, and nontender. He had 2+ bilateral pitting edema extending up to the abdomen. Abnormal labs included Hgb 17.9, BUN 27, Cr 1.8 from a baseline of 1.2, proBNP 671. Total testosterone level was 1500. Thyroid studies, iron panel, and viral panel were normal. EKG showed normal sinus rhythm, incomplete right bundle branch block, and left atrial enlargement. Troponin was negative. Echocardiogram showed an ejection fraction (EF) of 16%, global hypokinesis without regional variation, and echodensities in the apex of the left ventricle suggestive of thrombus. CTA chest showed a filling defect in the right branch of the pulmonary artery. Decision-making He underwent vasodilator myocardial perfusion testing, which showed no evidence of ischemia. Cardiac catheterization was deferred, given his poor renal function. The patient was diagnosed with testosterone-induced cardiomyopathy, given he was receiving 200 mg weekly injections instead of the recommended dose of 100 mg weekly. He also had thrombosis, likely due to testosterone use. The patient was started on Warfarin for his thrombi. He was started on diuretics and guideline-directed medical therapy. Testosterone was discontinued with plans for a repeat echocardiogram in three months. Conclusion A thorough evaluation of the causes of cardiomyopathy is crucial, and a high index of suspicion should be applied to supplement use. There is also an associated thrombosis risk with testosterone-induced cardiomyopathy.

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