Metabolism of the right ventricle and the response to hypertrophy and failure

Abstract

Profound transcriptional, translational and energetic derangements develop in the right ventricle (RV) in response to physiologic and pathophysiologic stress. The transition from pressure and volume overload to cardiac hypertrophy and subsequent failure is accompanied by a distinct switch from preferential fatty acid to glucose utilization for ATP generation. The failing RV is characterized by an energy-starved state with insufficient ATP levels. Modern non-invasive imaging using positron emission tomography using specific radioactive tracers allows a detailed spatial and temporal characterization of RV metabolism. While the current role for pharmacologic interventions on RV metabolic abnormalities is unclear, several potentially promising molecular targets have been identified and clinical trials targeting molecular dysfunction in RV hypertrophy and failure have been designed.