Male sex aggravates the phenotype in mouse models of hypertrophic cardiomyopathy.

Abstract

The authors have created transgenic mouse models of hypertrophic cardiomyopathy with mutations in either cardiac troponin T or myosin heavy chain. Mice mutant in myosin heavy chain develop significant cardiac hypertrophy at young adult age. Female mice keep that hypertrophic state, whereas male mice undergo progressive dilatation and exhibit systolic dysfunction at older age. Mice mutant in troponin, however, exhibit no baseline hypertrophy. When put under chronic adrenergic stress, all male mice die suddenly, whereas female mice show no mortality. These examples highlight the aggravated phenotype in male mice modeling hypertrophic cardiomyopathy and are a starting point to new mechanistic experiments.