Prognostic Role of Pulmonary Arterial Capacitance in Advanced Heart Failure

Author:

Dupont Matthias1,Mullens Wilfried1,Skouri Hadi N.1,Abrahams Zuheir1,Wu Yuping1,Taylor David O.1,Starling Randall C.1,Tang W. H. Wilson1

Affiliation:

1. From the Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH (M.D., Z.A., D.O.T., R.C.S., W.H.W.T.); Department of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium and Doctoral School for Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium (W.M.); Department of Internal Medicine, American University of Beirut Medical Center, Beirut, Lebanon (H.N.S.); and Department of Mathematics, Cleveland State University, Cleveland, OH (Y.W.).

Abstract

Background— Right ventricular (RV) dysfunction frequently occurs and independently prognosticates in left-sided heart failure. It is not clear which RV afterload measure has the greatest impact on RV function and prognosis. We examined the determinants, prognostic role, and response to treatment of pulmonary arterial capacitance (PAC, ratio of stroke volume over pulmonary pulse pressure), in relation to pulmonary vascular resistance (PVR) in heart failure. Methods and Results— We reviewed 724 consecutive patients with heart failure who underwent right heart catheterization between 2000 and 2005. Changes in PAC were explored in an independent cohort of 75 subjects treated for acute decompensated heart failure. PAC showed a strong inverse relation with PVR ( r =−0.64) and wedge pressure ( r =−0.73), and provides stronger prediction of significant RV failure than PVR (area under the curve ROC 0.74 versus 0.67, respectively, P =0.003). During a mean follow-up of 3.2±2.2 years, both lower PAC ( P <0.0001) and higher PVR ( P <0.0001) portend more adverse clinical events (all-cause mortality and cardiac transplantation). In multivariate analysis, PAC (but not PVR) remains an independent predictor (Hazard ratio=0.92 [95% CI: 0.84–1.0, P =0.037]). Treatment of heart failure resulted in a decrease in PVR (270±165 to 211±88 dynes·s –1 ·cm –5 , P =0.002), a larger increase in PAC (1.65±0.64 to 2.61±1.42 mL/mm Hg, P <0.0001), leading to an increase in pulmonary arterial time constant (PVR×PAC) (0.29±0.12 to 0.37±0.15 second, P <0.0001). Conclusions— PAC bundles the effects of PVR and left-sided filling pressures on RV afterload, explaining its strong relation with RV dysfunction, poor long-term prognosis, and response to therapy.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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