Can the Right Ventricle Support the Failing Left Ventricle?

Abstract

Ventricular failure, from cardiomyopathy or adverse loading, is the leading cause of cardiac death in children. In severe pediatric dilated cardiomyopathy of the left ventricle, heart transplant is the only life-saving option, but is limited by donor availability, cost and relatively poor survival. Alternatives are clearly needed. We have made a series of observations regarding therapeutic modification of ventricular afterload to improve contra-lateral ventricular function. These findings demonstrate novel mechanisms of ventricular–ventricular interactions (VVI), the potential to harness them for therapeutic benefit, and may constitute a paradigm shift in the treatment of pediatric heart failure. The pathophysiological rationale is that although left (LV) and right (RV) ventricular function are usually considered separately, they are inextricably linked through a common septum, shared myofibers and pericardium. Using the Anrep effect induced by banding of the pulmonary artery, LV function can be enhanced via VVI. Thus, VVI may hold great potential for treatment of LV failure. Future studies are needed to further delineate the geometrical, temporal and molecular mechanisms of PA-banding-induced ventricular crosstalk; and to examine their potential modulation through mechanical, electrophysiological and pharmacological interventions.