526R ight ventricular (RV) dysfunction is the principal predictor of adverse outcome in pulmonary hypertension (PH).1,2 For those PH patients requiring inpatient intensive care because of acutely decompensated heart failure, mortality estimates can range as high as 30% to 48%. [3][4][5] Hyponatremia, renal insufficiency, systemic hypotension, and severe tricuspid regurgitation are worrisome clinical characteristics that prognosticate poor outcome in this PH patient subpopulation. 3,5,6 Effective strategies to optimize cardiopulmonary hemodynamics and support RV function are paramount; clinical responsiveness to pulmonary vascular/RV-specific treatment is likely to decrease the probability of requiring surgical intervention and, ultimately, improve outcome. This review will discuss existing evidence pertaining to the timing and utility of mechanical support in patients with RV failure attributable to pulmonary vascular disease.
Pathophysiology of RV Failure in PHConstrictive pericardial disease, selected forms of congenital heart disease, inflow obstruction, primary myocardial disease, and pressure or volume overload are each well-described causes of adverse RV remodeling, RV systolic dysfunction, and cor pulmonale.7 Among patients with RV dysfunction as a result of pressure overload, precapillary PH and left-sided heart failure are the most common etiologies.The first adaptive response of the RV to pressure overload is hypertrophy. If untreated, the RV dilates to compensate for increased RV preload and, according to the Frank-Starling principle, to maintain stroke volume. When further increases in RV end-diastolic filling volume do not offset progressive RV contractile dysfunction, clinically evident RV failure ensues. In advanced stages, RV cavitary dilation may also impair left ventricular (LV) diastolic filling kinetics and contribute further to global pump dysfunction and, consequently, to the congestive heart failure syndrome.Mechanical support in the setting of RV dysfunction aims to stabilize and therapeutically improve several key mechanisms underpinning RV decompensation and heart failure by reducing RV preload and afterload, and by improving RV cardiac output, as well. As a consequence of achieving these goals, a number of additional beneficial effects may occur to stabilize RV performance, including (1) decreased pulmonary artery (PA) diameter and prevention of left-sided coronary artery compression 8 ; (2) decreased tricuspid regurgitation attributable to attenuated RV cavitary dilation 9 and improved interventricular septal bowing; and (3) decreased free-wall stress that maintains favorable RV myocardial oxygen demand/perfusion dynamics.10 Addressing the aforementioned contributors to RV failure is conceptually important in the management of RV failure, because, although the RV is less adaptable to pressure overload, it carries a substantial potential of recovery once its afterload is normalized.
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Mechanical Circulatory Support for the Failing RV: Patient SelectionIf pharmacological therapies a...