Strong muscles, weak heart: testosterone-induced cardiomyopathy

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madman

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Abstract
Exogenous anabolic androgen steroid use is associated with adverse cardiovascular outcomes.
A 53-year-old bodybuilder presented with 3 months of exertional dyspnoea. Physical examination showed tachycardia and pan-systolic murmur; an echocardiogram showed a left ventricular ejection fraction (EF) of 15%. Evaluations included normal coronary angiogram, iron panel and thyroid studies, a negative viral panel (human immunodeficiency virus, Lyme disease, and hepatitis), and urine toxicology. He admitted to intramuscular anabolic steroid use; his testosterone level was 30 160.0 ng/dL (normal 280–1100 ng/dL). In addition to discontinuation of anabolic steroid use, he was treated with guideline-directed heart failure medical therapy. Repeat echocardiogram at 6 months showed an EF of 54% and normalized testosterone level of 603.7 ng/dL. Anabolic steroid use is a rare, reversible cause of cardiomyopathy in young, otherwise healthy athletes; a high index of suspicion is required to prevent potentially fatal side effects.







Discussion
Normal male physiologic levels of testosterone have been documented to be between 280 and 1100 ng/dL and may vary on the basis of age, race, physiologic or emotional stress, incurrent illness, and even time of day. Experimental and indirect human evidence presumes that testosterone is beneficial for cardiovascular health, as several studies have shown an inverse association of endogenous testosterone level and cardiovascular outcome independent of the traditional risk factors. Amid growing public concern and after the US Food and Drug Administration’s release of a warning statement about testosterone therapy, a published literature review showed that the normal physiologic testosterone level is beneficial to the cardiovascular health in men and that its deficiency is associated with unfavourable metabolic profile and increased cardiovascular disease events.

Exogenous AAS use is a growing public health concern among young athletes; estimates indicate that 3–4 million Americans use AAS, some of which include testosterone preparations. Access to various AAS formulations is unregulated, and these formulations can have active metabolites that are 5–15 times more potent than standard testosterone replacement therapies. Animal studies have demonstrated that exogenous AAS administration has deleterious cardiovascular effects including indirect neurohormonal activation and direct androgenic receptor stimulation resulting in hypertension, myocyte hypertrophy and extracellular fibrosis, apoptotic cell death, premature coronary artery disease, and arrhythmogenesis. Multiple reports of exogenous AAS have been linked with adverse cardiovascular outcome in humans, and long-term testosterone use may lead to hypertension and stroke, cardiac diastolic and systolic dysfunction, coronary artery disease, arrhythmias, and sudden death.

The diagnosis of AAS-induced cardiomyopathy requires a thorough history and physical, and exclusion of other common causes of cardiomyopathy. Finally, a high index of suspicion regarding conditioned athletes with cardiovascular disease should prompt questions about exogenous AAS use, and the measurement of blood levels may be diagnostic. Discontinuation of AAS use and the initiation of GDMT are advocated and, as demonstrated in our case, may normalize cardiac structure and function. Further studies are warranted to fully investigate the long-term use of AAS and its cardiovascular adverse effects. We advocate medical societies to raise public awareness of the detrimental cardiovascular effects of AAS use.
 

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Figure 1 (A) Parasternal long-axis view shows the dilated left ventricle (6.9 cm) and severe global hypokinesis with a left ventricular ejection fraction of 15%. (B) Colour Doppler apical four-chamber view demonstrates severe functional mitral regurgitation.
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Figure 2 Myocardial strain assessed with two-dimensional speckle-tracking echocardiography shows severe peak systolic longitudinal strain abnormality (-6.7%).
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Figure 3 (A) Parasternal long-axis view shows normal left ventricular size (4.5 cm) and normal left ventricular ejection fraction of 53%. (B) Colour Doppler apical four-chamber view demonstrates trace mitral regurgitation
Screenshot (379).png
 
Figure 4 Myocardial strain assessed with two-dimensional speckle-tracking echocardiography shows persistent mild peak systolic longitudinal strain abnormality (-13.9%).
Screenshot (380).png
 
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