Relaxin Suppresses Atrial Fibrillation by Reversing Fibrosis and Myocyte Hypertrophy and Increasing Conduction Velocity and Sodium Current in Spontaneously Hypertensive Rat Hearts

Abstract

RLX treatment suppressed AF in SHR hearts by increasing CV from a combination of reversal of fibrosis and hypertrophy and by increasing INa. The study provides compelling evidence that RLX may provide a novel therapy to manage AF in humans by reversing fibrosis and hypertrophy and by modulating cardiac ionic currents.