How to incorporate tricuspid regurgitation in right ventricular-pulmonary arterial coupling.

Autor: Yoshida K; Department of Pulmonary Medicine, Amsterdam University Medical Centre, Vrije Universiteit, Amsterdam, The Netherlands., Axelsen JB; Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark., Saku K; Department of Cardiovascular Dynamics, National Cerebral and Cardiovascular Center, Suita, Japan., Andersen A; Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark., de Man FS; Department of Pulmonary Medicine, Amsterdam University Medical Centre, Vrije Universiteit, Amsterdam, The Netherlands., Sunagawa K; Circulatory System Research Foundation, Kyushu University, Fukuoka, Japan., Vonk Noordegraaf A; Department of Pulmonary Medicine, Amsterdam University Medical Centre, Vrije Universiteit, Amsterdam, The Netherlands., Bogaard HJ; Department of Pulmonary Medicine, Amsterdam University Medical Centre, Vrije Universiteit, Amsterdam, The Netherlands.
Jazyk: angličtina
Zdroj: Journal of applied physiology (Bethesda, Md. : 1985) [J Appl Physiol (1985)] 2023 Jul 01; Vol. 135 (1), pp. 53-59. Date of Electronic Publication: 2023 May 25.
DOI: 10.1152/japplphysiol.00081.2023
Abstrakt: Adaptation of the right ventricle (RV) to a progressively increasing afterload is one of the hallmarks of pulmonary arterial hypertension (PAH). Pressure-volume loop analysis provides measures of load-independent RV contractility, i.e., end-systolic elastance, and pulmonary vascular properties, i.e., effective arterial elastance (E a ). However, PAH-induced RV overload potentially results in tricuspid regurgitation (TR). TR makes RV eject to both PA and right atrium; thereby, a ratio of RV end-systolic pressure (P es ) to RV stroke volume (SV) could not correctly define E a . To overcome this limitation, we introduced a two-parallel compliance model, i.e., E a = 1/(1/E pa + 1/E TR ), while effective pulmonary arterial elastance (E pa = P es /PASV) represents pulmonary vascular properties and effective tricuspid regurgitant elastance (E TR ) represents TR. We conducted animal experiments to validate this framework. First, we performed SV analysis with a pressure-volume catheter in the RV and a flow probe at the aorta in rats with and without pressure-overloaded RV to determine the effect of inferior vena cava (IVC) occlusion on TR. A discordance between the two techniques was found in rats with pressure-overloaded RV, not in sham. This discordance diminished after IVC occlusion, suggesting that TR in pressure-overloaded RV was diminished by IVC occlusion. Next, we performed pressure-volume loop analysis in rats with pressure-overloaded RVs, calibrating RV volume by cardiac magnetic resonance. We found that IVC occlusion increased E a , suggesting that a reduction of TR increased E a . Using the proposed framework, E pa was indistinguishable to E a post-IVC occlusion. We conclude that the proposed framework helps better understanding of the pathophysiology of PAH and associated right heart failure. NEW & NOTEWORTHY This study reveals the impact of tricuspid regurgitation on pressure-volume loop analysis in right ventricle pressure overload. By introducing a novel concept of parallel compliances in the pressure-volume loop analysis, a better description is provided for the right ventricular forward afterload in the presence of tricuspid regurgitation.
Databáze: MEDLINE