Right ventricular pressure-volume loop shape and systolic pressure change in pulmonary hypertension

Author:

Richter Manuel J.1,Hsu Steven2,Yogeswaran Athiththan1ORCID,Husain-Syed Faeq1,Vadász István1ORCID,Ghofrani Hossein A.134,Naeije Robert5,Harth Sebastian6,Grimminger Friedrich17,Seeger Werner7,Gall Henning1,Tedford Ryan J.8,Tello Khodr1

Affiliation:

1. Department of Internal Medicine, Justus-Liebig-University Giessen, Universities of Giessen and Marburg Lung Center (UGMLC), German Center for Lung Research (DZL), Giessen, Germany

2. Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland

3. Department of Pneumology, Kerckhoff Heart, Rheuma and Thoracic Center, Bad Nauheim, Germany

4. Department of Medicine, Imperial College London, London, United Kingdom

5. Erasme University Hospital, Brussels, Belgium

6. Department of Radiology, Justus-Liebig-University Giessen, Universities of Giessen and Marburg Lung Center (UGMLC), German Center for Lung Research (DZL), Giessen, Germany

7. Institute for Lung Health, Justus-Liebig-University Giessen, Universities of Giessen and Marburg Lung Center (UGMLC), German Center for Lung Research (DZL), Giessen, Germany

8. Division of Cardiology, Department of Medicine, Medical University of South Carolina, Charleston, South Carolina

Abstract

Right ventricular (RV) function determines outcome in pulmonary arterial hypertension (PAH). RV pressure-volume loops, the gold standard for measuring RV function, are difficult to analyze. Our aim was to investigate whether simple assessments of RV pressure-volume loop morphology and RV systolic pressure differential reflect PAH severity and RV function. We analyzed multibeat RV pressure-volume loops (obtained by conductance catheterization with preload reduction) in 77 patients with PAH and 15 patients without pulmonary hypertension in two centers. Patients were categorized according to their pressure-volume loop shape (triangular, quadratic, trapezoid, or notched). RV systolic pressure differential was defined as end-systolic minus beginning-systolic pressure (ESP − BSP), augmentation index as ESP − BSP/pulse pressure, pulmonary arterial capacitance (PAC) as stroke volume/pulse pressure, and RV-arterial coupling as end-systolic/arterial elastance (Ees/Ea). Trapezoid and notched pressure-volume loops were associated with the highest afterload (Ea), augmentation index, pulmonary vascular resistance (PVR), mean pulmonary arterial pressure, stroke work, B-type natriuretic peptide, and the lowest Ees/Ea and PAC. Multivariate linear regression identified Ea, PVR, and stroke work as the main determinants of ESP − BSP. ESP − BSP also significantly correlated with multibeat Ees/Ea (Spearman’s ρ: −0.518, P < 0.001). A separate retrospective analysis of 113 patients with PAH showed that ESP − BSP obtained by routine right heart catheterization significantly correlated with a noninvasive surrogate of RV-arterial coupling (tricuspid annular plane systolic excursion/pulmonary arterial systolic pressure ratio; ρ: −0.376, P < 0.001). In conclusion, pressure-volume loop shape and RV systolic pressure differential predominately depend on afterload and PAH severity and reflect RV-arterial coupling in PAH.

Funder

HHS | NIH | National Heart, Lung, and Blood Institute

Publisher

American Physiological Society

Subject

Cell Biology,Physiology (medical),Pulmonary and Respiratory Medicine,Physiology

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