How to Incorporate Tricuspid Regurgitation in Right Ventricular-Pulmonary Arterial Coupling

Keimei Yoshida; Julie Birkmosse Axelsen; Keita Saku; Asger Andersen; Frances S de Man; Kenji Sunagawa; Anton Vonk Noordegraaf; Harm Jan Bogaard

doi:10.1152/japplphysiol.00081.2023

How to Incorporate Tricuspid Regurgitation in Right Ventricular-Pulmonary Arterial Coupling

Keimei Yoshida, Julie Birkmosse Axelsen, Keita Saku, Asger Andersen, Frances S de Man, Kenji Sunagawa, Anton Vonk Noordegraaf, Harm Jan Bogaard

Institut for Klinisk Medicin - Hjertesygdomme

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avis › Tidsskriftartikel › Forskning › peer review

Abstract

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 (Ea). 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 (Pes) to RV stroke volume (SV) could not correctly define Ea. To overcome this limitation, we introduced a two-parallel compliance model, i.e., Ea = 1/(1/Epa 1/ETR), while effective pulmonary arterial elastance (Epa = Pes/PASV) represents pulmonary vascular properties and effective tricuspid regurgitant elastance (ETR) 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 Ea, suggesting that a reduction of TR increased Ea. Using the proposed framework, Epa was indistinguishable to Ea post-IVC occlusion. We conclude that the proposed framework helps better understanding of the pathophysiology of PAH and associated right heart failure.

Originalsprog	Engelsk
Tidsskrift	Journal of Applied Physiology
Vol/bind	135
Nummer	1
Sider (fra-til)	53-59
Antal sider	7
ISSN	8750-7587
DOI	https://doi.org/10.1152/japplphysiol.00081.2023
Status	Udgivet - jul. 2023

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title = "How to Incorporate Tricuspid Regurgitation in Right Ventricular-Pulmonary Arterial Coupling",

abstract = "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 (Ea). 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 (Pes) to RV stroke volume (SV) could not correctly define Ea. To overcome this limitation, we introduced a two-parallel compliance model, i.e., Ea = 1/(1/Epa 1/ETR), while effective pulmonary arterial elastance (Epa = Pes/PASV) represents pulmonary vascular properties and effective tricuspid regurgitant elastance (ETR) 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 Ea, suggesting that a reduction of TR increased Ea. Using the proposed framework, Epa was indistinguishable to Ea post-IVC occlusion. We conclude that the proposed framework helps better understanding of the pathophysiology of PAH and associated right heart failure.",

keywords = "Animals, Cardiac Catheterization, Heart Ventricles, Hypertension, Pulmonary, Pulmonary Artery, Rats, Stroke Volume, Tricuspid Valve Insufficiency, Ventricular Dysfunction, Right, Ventricular Function, Right",

author = "Keimei Yoshida and Axelsen, {Julie Birkmosse} and Keita Saku and Asger Andersen and {de Man}, {Frances S} and Kenji Sunagawa and Noordegraaf, {Anton Vonk} and Bogaard, {Harm Jan}",

year = "2023",

month = jul,

doi = "10.1152/japplphysiol.00081.2023",

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volume = "135",

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journal = "Journal of Applied Physiology",

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T1 - How to Incorporate Tricuspid Regurgitation in Right Ventricular-Pulmonary Arterial Coupling

AU - Yoshida, Keimei

AU - Axelsen, Julie Birkmosse

AU - Saku, Keita

AU - Andersen, Asger

AU - de Man, Frances S

AU - Sunagawa, Kenji

AU - Noordegraaf, Anton Vonk

AU - Bogaard, Harm Jan

PY - 2023/7

Y1 - 2023/7

N2 - 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 (Ea). 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 (Pes) to RV stroke volume (SV) could not correctly define Ea. To overcome this limitation, we introduced a two-parallel compliance model, i.e., Ea = 1/(1/Epa 1/ETR), while effective pulmonary arterial elastance (Epa = Pes/PASV) represents pulmonary vascular properties and effective tricuspid regurgitant elastance (ETR) 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 Ea, suggesting that a reduction of TR increased Ea. Using the proposed framework, Epa was indistinguishable to Ea post-IVC occlusion. We conclude that the proposed framework helps better understanding of the pathophysiology of PAH and associated right heart failure.

AB - 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 (Ea). 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 (Pes) to RV stroke volume (SV) could not correctly define Ea. To overcome this limitation, we introduced a two-parallel compliance model, i.e., Ea = 1/(1/Epa 1/ETR), while effective pulmonary arterial elastance (Epa = Pes/PASV) represents pulmonary vascular properties and effective tricuspid regurgitant elastance (ETR) 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 Ea, suggesting that a reduction of TR increased Ea. Using the proposed framework, Epa was indistinguishable to Ea post-IVC occlusion. We conclude that the proposed framework helps better understanding of the pathophysiology of PAH and associated right heart failure.

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KW - Heart Ventricles

KW - Hypertension, Pulmonary

KW - Pulmonary Artery

KW - Rats

KW - Stroke Volume

KW - Tricuspid Valve Insufficiency

KW - Ventricular Dysfunction, Right

KW - Ventricular Function, Right

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U2 - 10.1152/japplphysiol.00081.2023

DO - 10.1152/japplphysiol.00081.2023

M3 - Journal article

C2 - 37227183

SN - 8750-7587

VL - 135

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EP - 59

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

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ER -

How to Incorporate Tricuspid Regurgitation in Right Ventricular-Pulmonary Arterial Coupling

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