Impact of Right Ventricle-Pulmonary Artery Coupling on Clinical Outcomes in the PARTNER 3 Trial.
coupling
right ventricle
surgical aortic valve replacement
transcatheter aortic valve replacement
Journal
JACC. Cardiovascular interventions
ISSN: 1876-7605
Titre abrégé: JACC Cardiovasc Interv
Pays: United States
ID NLM: 101467004
Informations de publication
Date de publication:
26 09 2022
26 09 2022
Historique:
received:
17
02
2022
revised:
16
06
2022
accepted:
05
07
2022
entrez:
22
9
2022
pubmed:
23
9
2022
medline:
28
9
2022
Statut:
ppublish
Résumé
Physiologic right ventricle-pulmonary artery (RV-PA) coupling may be impaired in patients with aortic stenosis (AS). This study aimed to assess the incidence and prognostic significance of impaired RV-PA coupling in low-risk patients with symptomatic severe AS undergoing transcatheter aortic valve replacement or surgical aortic valve replacement. RV-PA coupling was measured by transthoracic echocardiography as the ratio of tricuspid annular plane systolic excursion (TAPSE) to pulmonary artery systolic pressure (PASP) in patients in the PARTNER (Placement of Aortic Transcatheter Valve) 3 trial. The primary endpoint was the composite of all-cause mortality, stroke, and rehospitalization at the 2-year follow-up. Among 570 low-risk patients included in the analysis, RV-PA uncoupling was defined by a TAPSE/PASP ratio ≤ 0.55 mm/mm Hg. At baseline, 222 of 570 (38.9%) patients had RV-PA uncoupling. At 2 years, patients with baseline RV-PA uncoupling had an increased incidence of the primary endpoint (19.1% vs 9.9%, P = 0.002), all-cause mortality (5.9% vs 0.6%, P < 0.001), cardiovascular mortality (4.1% vs 0.6%, P = 0.003), and rehospitalization (13.5% vs 7.3%, P = 0.018). On multivariable analysis, baseline RV-PA uncoupling remained an independent predictor of the primary endpoint at 2 years (HR: 1.92; 95% CI: 1.04-3.57; P = 0.038). In patients with symptomatic severe AS at low surgical risk undergoing transcatheter aortic valve replacement or surgical aortic valve replacement, baseline RV-PA uncoupling defined by TAPSE/PASP ≤ 0.55 mm Hg was associated with adverse clinical outcomes at 2 years, including all-cause mortality, cardiovascular mortality, and rehospitalization.
Sections du résumé
BACKGROUND
Physiologic right ventricle-pulmonary artery (RV-PA) coupling may be impaired in patients with aortic stenosis (AS).
OBJECTIVES
This study aimed to assess the incidence and prognostic significance of impaired RV-PA coupling in low-risk patients with symptomatic severe AS undergoing transcatheter aortic valve replacement or surgical aortic valve replacement.
METHODS
RV-PA coupling was measured by transthoracic echocardiography as the ratio of tricuspid annular plane systolic excursion (TAPSE) to pulmonary artery systolic pressure (PASP) in patients in the PARTNER (Placement of Aortic Transcatheter Valve) 3 trial. The primary endpoint was the composite of all-cause mortality, stroke, and rehospitalization at the 2-year follow-up.
RESULTS
Among 570 low-risk patients included in the analysis, RV-PA uncoupling was defined by a TAPSE/PASP ratio ≤ 0.55 mm/mm Hg. At baseline, 222 of 570 (38.9%) patients had RV-PA uncoupling. At 2 years, patients with baseline RV-PA uncoupling had an increased incidence of the primary endpoint (19.1% vs 9.9%, P = 0.002), all-cause mortality (5.9% vs 0.6%, P < 0.001), cardiovascular mortality (4.1% vs 0.6%, P = 0.003), and rehospitalization (13.5% vs 7.3%, P = 0.018). On multivariable analysis, baseline RV-PA uncoupling remained an independent predictor of the primary endpoint at 2 years (HR: 1.92; 95% CI: 1.04-3.57; P = 0.038).
CONCLUSIONS
In patients with symptomatic severe AS at low surgical risk undergoing transcatheter aortic valve replacement or surgical aortic valve replacement, baseline RV-PA uncoupling defined by TAPSE/PASP ≤ 0.55 mm Hg was associated with adverse clinical outcomes at 2 years, including all-cause mortality, cardiovascular mortality, and rehospitalization.
Identifiants
pubmed: 36137685
pii: S1936-8798(22)01342-5
doi: 10.1016/j.jcin.2022.07.005
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1823-1833Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2022 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Funding Support and Author Disclosures Statistical analyses were performed by employees of Edwards Lifesciences. Dr Pibarot has received funding from Edwards Lifesciences, Medtronic, Pi-Cardia, and Cardiac Phoenix for echocardiography core laboratory analyses and research studies in the field of transcatheter valve therapies for which he received no personal compensation; has also received lecture fees from Edwards Lifesciences and Medtronic. Dr Yu is an employee of Edwards Lifesciences. Dr Babaliaros is a consultant for Edwards Lifesciences and Abbott; and has shares in Transmural Systems. Dr Blanke has served as a consultant for Tendyne, Neovasc, and Circle Cardiovascular Imaging; and has received funding from Edwards Lifesciences for computed tomography laboratory analyses in the context of transcatheter valve therapy trials with no direct compensation. Dr Clavel has received funding from Edwards Lifesciences and Medtronic for computed tomography core laboratory analyses and research studies in the field of surgical bioprostheses. Dr Khalique has received consulting fees from Edwards Lifesciences and Abbott Structural. Dr Leipsic has served as a consultant for and owns stock options in Circle Cardiovascular Imaging; and has received funding from Edwards Lifesciences for computed tomography laboratory analyses in the context of transcatheter valve therapy trials with no direct compensation. Dr Makkar has received research grants from Edwards Lifesciences, Abbott, Medtronic, and Boston Scientific; national PI for Portico (Abbott) and Acurate (Boston Scientific) US IDE trials; has received personal proctoring fees from Edwards Lifesciences; and has received travel support from Edwards, Abbott, and Boston Scientific. Ms Rogers is an employee of Edwards Lifesciences. Ms Alu’s institution receives research funding from Edwards Lifesciences and Abbott Structural Heart (no direct compensation). Dr Kodali has received institutional research grants from Edwards Lifesciences, Medtronic, and Abbott; has received consulting fees from Abbott, Admedus, and Meril Lifesciences; and has equity options from Biotrace Medical and Thubrikar Aortic Valve Inc. Dr Mack served as coprimary investigator for the PARTNER Trial for Edwards Lifesciences and COAPT trial for Abbott and served as study chair for the APOLLO trial for Medtronic; he received no direct compensation for any of these activities. Dr Leon has received institutional research support from Edwards Lifesciences, Medtronic, Boston Scientific, and Abbott; and has consulted/participated on the advisory board for Medtronic, Boston Scientific, Gore, Meril Lifescience, and Abbott. Dr Hahn has received speaker fees from Abbott Structural, Baylis Medical, and Edwards Lifesciences; has institutional educational and consulting contracts for which she receives no direct compensation with Abbott Structural, Boston Scientific, Edwards Lifesciences, and Medtronic; has equity with Navigate; and is chief scientific officer for the Echocardiography Core Laboratory at the Cardiovascular Research Foundation for multiple industry-sponsored trials for which she receives no direct industry compensation. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.