TY - JOUR
T1 - Right ventricular pressure-volume loop shape and systolic pressure change in pulmonary hypertension
AU - Richter, Manuel J.
AU - Hsu, Steven
AU - Yogeswaran, Athiththan
AU - Husain-Syed, Faeq
AU - Vadász, István
AU - Ghofrani, Hossein A.
AU - Naeije, Robert
AU - Harth, Sebastian
AU - Grimminger, Friedrich
AU - Seeger, Werner
AU - Gall, Henning
AU - Tedford, Ryan J.
AU - Tello, Khodr
N1 - Funding Information:
This work was supported by the Excellence Cluster CardioPulmonary System (ECCPS) and the Collaborative Research Center (SFB) 1213 – Pulmonary Hypertension and Cor Pulmonale, Grant number SFB1213/1, project B08 (German Research Foundation, Bonn, Germany). This work was also supported by the National Heart, Lung, and Blood Institute of the National Institutes of Health Grants K23-HL146889 (to S. Hsu) and R01-HL114910 (to P. M. Hassoun, R. S. Tedford, D. A. Kass), and the Jerome Greene Scholarship (to S. Hsu).
Funding Information:
We thank Claire Mulligan, PhD (Beacon Medical Communications Ltd, Brighton, UK) for editorial support, funded by the University of Giessen. We also thank Prof. David A. Kass and Prof. Paul M. Hassoun (Johns Hopkins University School of Medicine) for funding and patient enrollment.
Funding Information:
M. J. Richter has received support from United Therapeutics and Bayer; speaker fees from Bayer, Actelion, Mundipharma, Roche, and OMT; and consultancy fees from Bayer. H. A. Ghofrani has received consultancy fees from Bayer, Actelion, Pfizer, Merck, GSK, and Novartis; fees for participation in advisory boards from Bayer, Pfizer, GSK, Actelion, and Takeda; lecture fees from Bayer HealthCare, GSK, Actelion, and Encysive/Pfizer; industry-sponsored grants from Bayer HealthCare, Aires, Encysive/Pfizer, and Novartis; and sponsored grants from the German Research Foundation, Excellence Cluster Cardiopulmonary Research, and the German Ministry for Education and Research. R. Naeije has relationships with drug companies including AOPOrphan Pharmaceuticals, Actelion, Bayer, Reata, Lung Biotechnology Corporation, and United Therapeutics. In addition to being an investigator in trials involving these companies, relationships include consultancy service, research grants, and membership of scientific advisory boards. W. Seeger has received speaker/consultancy fees from Pfizer and Bayer Pharma AG. H. Gall has received fees from Actelion, AstraZeneca, Bayer, BMS, GSK, Janssen-Cilag, Lilly, MSD, Novartis, OMT, Pfizer, and United Therapeutics. R. J. Tedford reports no direct conflicts pertinent to the development of this manuscript. Other general conflicts include consulting relationships with Medtronic, Arena Pharmaceuticals, Aria CV, and United Therapeutics. R. J. Tedford is on a steering committee for Medtronic and the research advisory board for Abiomed. He also does hemodynamic core laboratory work for Actelion and Merck. K. Tello has received speaking fees from Actelion and Bayer. None of the other authors has any conflicts of interest, financial or otherwise, to disclose.
Publisher Copyright:
Copyright © 2021 the American Physiological Society
PY - 2021/5
Y1 - 2021/5
N2 - 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 r: -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; r: -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.
AB - 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 r: -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; r: -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.
KW - Pressure-volume relationship
KW - Pulmonary arterial hypertension
KW - Right ventricle
KW - Right ventricle-pulmonary arterial
KW - Systolic function coupling
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U2 - 10.1152/ajplung.00583.2020
DO - 10.1152/ajplung.00583.2020
M3 - Article
C2 - 33655769
AN - SCOPUS:85105107781
SN - 1040-0605
VL - 320
SP - L715-L725
JO - American Journal of Physiology
JF - American Journal of Physiology
IS - 5
ER -