Mechanical Environment and Cardiac Hypertrophy
Hypertension, valve disease, myocardial infarction, and even pregnancy cause cardiac hypertrophy, defined as an increase in cardiomyocyte mass. The risk of progression to heart failure in these conditions, however, depends primarily on changes in myocyte shape. In patients with pressure overload (PO) states such as chronic hypertension, individual cardiomyocytes and the left ventricular wall become thicker, and heart failure typically develops only after decades. In volume overload (VO) states such as mitral regurgitation, myocytes become longer, the left ventricle dilates, and heart failure develops much faster. Our lab uses a combination of multiscale models and experiments to understand this regulation and develop predictive models of hypertrophy following myocardial infarction, reverse remodeling in response to cardiac resynchronization therapy (CRT), and heart growth in children with congenital heart disease.