ORF04-02 - When Testosterone GAHT Meets Valvular Heart Disease: A Case of Accelerated Mitral Regurgitation in a Transgender Man

Background
Testosterone-based gender-affirming hormone therapy (GAHT) is essential for many transgender men. While metabolic and blood pressure effects are known, the effects of long-term testosterone on heart valves are not well described. Sex hormones can influence collagen and extracellular matrix remodeling, which are important in mitral valve prolapse (MVP) and mitral regurgitation (MR). We present a case of rapid worsening of mitral valve disease in a transgender man receiving long-term testosterone.

Case
A 39-year-old transgender man on weekly testosterone GAHT for 7 years presented with worsening shortness of breath and leg swelling. Before starting GAHT, he had mild MVP and heart failure with preserved ejection fraction (HFpEF). Pre-GAHT echocardiography showed LVEF 55%, mild MR, and trace tricuspid regurgitation (TR). On presentation, he was tachycardic with borderline low blood pressure. Labs showed leukocytosis and elevated BNP. Repeat echocardiography showed new reduced systolic function (LVEF 30–35%) and severe MR due to posterior leaflet prolapse with partial flail (P2) with pulmonary venous systolic flow reversal. He also had moderate TR. He underwent mitral and tricuspid valve repair with annuloplasty rings. His post-operative course was complicated by cardiogenic shock and atrial flutter requiring cardioversion. Guideline-directed medical therapy was restarted, but beta-blocker use was limited by bradycardia. Symptoms improved and LVEF recovered on follow-up.

Discussion
This patient progressed from mild MVP/MR to severe valve disease and reduced LVEF over several years while receiving testosterone GAHT. A single case cannot prove cause and effect. However, long-term testosterone exposure may shift sex hormone signaling and could affect valve tissue remodeling through changes in collagen structure and metalloproteinase activity. Testosterone may also worsen blood pressure and ventricular remodeling, which can increase valve stress. This case highlights a possible gap in cardiovascular monitoring for transgender patients with pre-existing valvular disease receiving GAHT.

Conclusion
For transgender men with known MVP or valvular disease, testosterone GAHT may require baseline and follow-up echocardiography, optimization of cardiometabolic risk, and shared care between endocrinology and cardiology. Larger studies are needed to define whether testosterone dose, duration, and hormone levels influence valve remodeling and heart failure risk.