Abstract
For many patients with severe pulmonary arterial hypertension, heart failure-and, in particular, right heart failure-is the final chapter of their chronic illness. Targeted therapy for pulmonary hypertension is effective only if the right ventricular ejection fraction is maintained or improved. Because improvement of right heart function and reversal of right heart failure are treatment goals, it is important to investigate the cellular and molecular mechanisms that cause right heart failure. Here, we propose that right ventricular capillary rarefaction is an important hallmark of right heart failure and consider that the "sick lung circulation" and the pressure-overloaded right ventricle constitute a functional unit.