LAUSR

Sex hormones influence the prevalence and the outcome of heart diseases. The conversion of testosterone to its more active metabolite dihydrotestosterone drives cardiac growth and dysfunction, while inhibition of this step by the anti-androgenic drug finasteride counteracts these pathological processes in preclinical models. In this retrospective, observational study, we aim to investigate whether finasteride, which is in clinical use mainly for prostate disease, might ameliorate cardiac hypertrophy and heart failure in patients. Retrospective chart review of 1041 medical cases with heart failure between 1995 and 2015 was conducted. Stratification was performed by concomitant prostate treatment status (tamsulosin versus finasteride). A propensity score analysis yielded a total of 328 matched medical cases without residual differences in the baseline patient characteristics. In this propensity score matched samples, anti-androgenic therapy with finasteride was associated with significantly reduced left ventricular hypertrophy (interventricular septal thickness 13.3 ± 2.4 mm control vs. 12.6 ± 2.1 mm finasteride group (p = 0.029); estimated average treatment effects on the treated: −0.7 mm, 95% CI mean difference −1.3 to −0.1). In this retrospective analysis anti-androgenic therapy with finasteride for prostate disease was associated with attenuated cardiac hypertrophy in patients with heart failure. Therefore, our data encourage further analysis of this approach in larger heart failure patient cohorts.