Session: SUN 176-202-Male Reproductive Endocrinology and Male Reproductive Tract (posters)
Bench to Bedside
Poster Board SUN 195
A 49-year old Caucasian male with a past medical history of hypertension and testosterone abuse 250mg/week (intramuscular injection) over the last 2 years, presented with 1-2 weeks of progressive shortness of breath with exertion, orthopnea, and epigastric pain.
Initial laboratory tests on admission revealed: Hemoglobin 18.0 g/dL(Ref 14-17 g/dl), hematocrit 52.5%, total testosterone 1988 ng/dL (Ref 250-1100 ng/dl), free testosterone 485 pg/dL(Ref 35-155 pg/dl), ProBNP 1149 pg/ml (Ref <125 pg/ml), troponin T 0.03 ng/ml( Ref <0.01 ng/ml), ferritin 72ng/ml( Ref 30-400ng/ml), ANA negative. Echocardiogram (ECHO) revealed patient to be in acute systolic heart failure with an ejection fraction of 10-20%, diffuse enlargement of both atria and ventricles, left ventricular thrombus, and mild pulmonary hypertension. Right heart catheterization revealed severely elevated right heart pressures: Pulmonary artery-45/27mmHg, PCWP- 29mmHg, Right atrium- 17/15mmHg, Right ventricle- 38/15mmHg, with depressed cardiac output. Diagnostic cardiac catheterization revealed no occlusive coronary artery disease. No suspicious markers for myocarditis, infiltrative disorders such as sarcoidosis or amyloidosis were found based on ECHO findings.
Review of the past medical records since 2013 revealed total testosterone levels in the range of 1300-2000 ng/dL (Ref 250-1100ng/dl), and free testosterone level in the range of 400-700 pg/mL (Ref 35-155pg/dl).
The patient was started on a dobutamine infusion and then transitioned to milrinone infusion post right heart catheterization and aggressively diuresed with furosemide. He was stablized and sent home on medical therapy.
DISCUSSION: Chronic abuse of androgenic anabolic steroids (AAS) and their deleterious effects on the heart are well established. Although the association between dilated cardiomyopathy and AAS use has not been proven unequivocally, evidence in humans indicates severe reductions in left ventricular ejection fraction, which may be secondary to myocardial fibrosis . Additionally, pathological studies have implicated that androgen abuse often leads to left ventricular hypertrophy, which can progress in some patients to systolic dysfunction and ultimately dilated cardiomyopathy.
CONCLUSION: This is a rare case of androgen abuse causing dilated non- ischemic cardiomyopathy, and the underlying mechanisms are still under investigation in literature.
Nothing to Disclose: ST, PK, NA, IA
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