This is a past event.

Dr. Robert Larson, Assistant Professor

Department of Biological Sciences, Michigan Technological University

Abstract:

Familial hypertrophic cardiomyopathy (HCM) is the most common genetic heart disease with an estimated prevalence of 1:500 individuals in the general population. Sarcomere gene mutations result in the characteristic features of HCM include left ventricular (LV) hypertrophy, myocyte disarray, interstitial fibrosis, diastolic dysfunction, and high risk of cardiac arrhythmias and sudden death. Hypercontractile sarcomeres in the heart accompanied by metabolic dysfunction, energy depletion, and inflammation are considered causal mechanisms in HCM. We demonstrate that metabolic and inflammatory signals produced in HCM hearts are detected by cardiac sensory nerves, resulting in abnormal autonomic reflexes that contribute to acute cardiovascular instability, chronic and selective increases in sympathetic nerve activity to the heart and decreased parasympathetic nerve activity. We will discuss mechanisms contributing to the increased activity of excitatory cardiac spinal afferent nerves and the impact of chronic elevations in cardiac sympathetic tone on disease progression in a mouse model of HCM.