Evolution and Prognostic Impact of Cardiac Damage After Aortic Valve Replacement.


Journal

Journal of the American College of Cardiology
ISSN: 1558-3597
Titre abrégé: J Am Coll Cardiol
Pays: United States
ID NLM: 8301365

Informations de publication

Date de publication:
23 08 2022
Historique:
received: 06 05 2022
revised: 12 05 2022
accepted: 12 05 2022
pubmed: 21 5 2022
medline: 23 8 2022
entrez: 20 5 2022
Statut: ppublish

Résumé

The impact of aortic valve replacement (AVR) on progression/regression of extravalvular cardiac damage and its association with subsequent prognosis is unknown. The purpose of this study was to describe the evolution of cardiac damage post-AVR and its association with outcomes. Patients undergoing transcatheter or surgical AVR from the PARTNER (Placement of Aortic Transcatheter Valves) 2 and 3 trials were pooled and classified by cardiac damage stage at baseline and 1 year (stage 0, no damage; stage 1, left ventricular damage; stage 2, left atrial or mitral valve damage; stage 3, pulmonary vasculature or tricuspid valve damage; and stage 4, right ventricular damage). Proportional hazards models determined association between change in cardiac damage post-AVR and 2-year outcomes. Among 1,974 patients, 121 (6.1%) were stage 0, 287 (14.5%) stage 1, 1,014 (51.4%) stage 2, 412 (20.9%) stage 3, and 140 (7.1%) stage 4 pre-AVR. Two-year mortality was associated with extent of cardiac damage at baseline and 1 year. Compared with baseline, cardiac damage improved in ∼15%, remained unchanged in ∼60%, and worsened in ∼25% of patients at 1 year. The 1-year change in cardiac damage stage was independently associated with mortality (adjusted HR for improvement: 0.49; no change: 1.00; worsening: 1.95; P = 0.023) and composite of death or heart failure hospitalization (adjusted HR for improvement: 0.60; no change: 1.00; worsening: 2.25; P < 0.001) at 2 years. In patients undergoing AVR, extent of extravalvular cardiac damage at baseline and its change at 1 year have important prognostic implications. These findings suggest that earlier detection of aortic stenosis and intervention before development of irreversible cardiac damage may improve global cardiac function and prognosis. (PARTNER II Trial: Placement of AoRTic TraNscathetER Valves II - XT Intermediate and High Risk [PII A], NCT01314313; The PARTNER II Trial: Placement of AoRTic TraNscathetER Valves - PII B [PARTNERII B], NCT02184442; and PARTNER 3 Trial: Safety and Effectiveness of the SAPIEN 3 Transcatheter Heart Valve in Low Risk Patients With Aortic Stenosis [P3], NCT02675114).

Sections du résumé

BACKGROUND
The impact of aortic valve replacement (AVR) on progression/regression of extravalvular cardiac damage and its association with subsequent prognosis is unknown.
OBJECTIVES
The purpose of this study was to describe the evolution of cardiac damage post-AVR and its association with outcomes.
METHODS
Patients undergoing transcatheter or surgical AVR from the PARTNER (Placement of Aortic Transcatheter Valves) 2 and 3 trials were pooled and classified by cardiac damage stage at baseline and 1 year (stage 0, no damage; stage 1, left ventricular damage; stage 2, left atrial or mitral valve damage; stage 3, pulmonary vasculature or tricuspid valve damage; and stage 4, right ventricular damage). Proportional hazards models determined association between change in cardiac damage post-AVR and 2-year outcomes.
RESULTS
Among 1,974 patients, 121 (6.1%) were stage 0, 287 (14.5%) stage 1, 1,014 (51.4%) stage 2, 412 (20.9%) stage 3, and 140 (7.1%) stage 4 pre-AVR. Two-year mortality was associated with extent of cardiac damage at baseline and 1 year. Compared with baseline, cardiac damage improved in ∼15%, remained unchanged in ∼60%, and worsened in ∼25% of patients at 1 year. The 1-year change in cardiac damage stage was independently associated with mortality (adjusted HR for improvement: 0.49; no change: 1.00; worsening: 1.95; P = 0.023) and composite of death or heart failure hospitalization (adjusted HR for improvement: 0.60; no change: 1.00; worsening: 2.25; P < 0.001) at 2 years.
CONCLUSIONS
In patients undergoing AVR, extent of extravalvular cardiac damage at baseline and its change at 1 year have important prognostic implications. These findings suggest that earlier detection of aortic stenosis and intervention before development of irreversible cardiac damage may improve global cardiac function and prognosis. (PARTNER II Trial: Placement of AoRTic TraNscathetER Valves II - XT Intermediate and High Risk [PII A], NCT01314313; The PARTNER II Trial: Placement of AoRTic TraNscathetER Valves - PII B [PARTNERII B], NCT02184442; and PARTNER 3 Trial: Safety and Effectiveness of the SAPIEN 3 Transcatheter Heart Valve in Low Risk Patients With Aortic Stenosis [P3], NCT02675114).

Identifiants

pubmed: 35595203
pii: S0735-1097(22)04979-8
doi: 10.1016/j.jacc.2022.05.006
pii:
doi:

Banques de données

ClinicalTrials.gov
['NCT02675114', 'NCT01314313', 'NCT02184442']

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

783-800

Commentaires 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 The PARTNER II and PARTNER 3 Trials were Sponsored by Edwards Lifesciences. Dr Généreux has served as a consultant for, advisor for, and received speaker fees from Abbott Vascular, Abiomed, BioTrace Medical, and Medtronic; has served as a consultant for Boston Scientific, CARANX Medical, GE Healthcare, iRhythm Technologies, Opsens, Teleflex, and Siemens; has served as a consultant and PI for the Eclipse Trial for Cardiovascular System Inc; has served as a consultant, advisor, and proctor, and received speaker fees and institutional research grants for PI EARLY-TAVR and PI PROGRESS trials from Edwards Lifesciences; has received equity from and served as a consultant for Pi-Cardia, Puzzle Medical, Saranas, and Soundbite Medical Inc; has served as a consultant for and received speaker fees from Shockwave; and has served as consultant for and PI of the Feasibility study for 4C Medical. 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; and has received lecture fees from Edwards Lifesciences and Medtronic. The Cardiovascular Research Foundation (Drs Redfors, Vincent, Alu, Hahn, Leon, and Cohen) receives research funding from Edwards Lifesciences (no direct compensation). Dr Bax’s department (Department of Cardiology, LUMC, the Netherlands) has received research grants from Medtronic, Biotronik, Edwards Lifesciences, and Boston Scientific; and he has received speaker fees from Abbott Vascular. Dr Zhao is an employee of Edwards Lifesciences. Dr Makkar has received grant support/research contracts from Edwards Lifesciences and St. Jude Medical; and has received consultant fees/honoraria from/served on the speaker's bureau for Abbott Vascular, Cordis Corporation, and Medtronic. Dr Thourani has served on the Advisory Board of Edwards Lifesciences, Abbott Vascular, Atricure, Cryolife, Jenavalve, Shockwave, and Boston Scientific. Dr Mack has served as coprimary investigator for the PARTNER Trial for Edwards Lifesciences and COAPT trial for Abbott; and has served as study chair for the APOLLO trial for Medtronic (all activities unpaid). Dr Nazif is a consultant for Edwards Lifesciences, Medtronic, and Boston Scientific. Dr Lindman has served on the Scientific Advisory Board for Roche Diagnostics; and has received research grants from Edwards Lifesciences and Roche Diagnostics. Dr Babaliaros has received consulting fees from Edwards Lifesciences and Abbott. Dr Russo has received grants from Edwards Lifesciences; and has served as a consultant for Abbott, Boston Scientific, and Edwards Lifesciences. Dr McCabe has served as a consultant for Edwards, Medtronic, Boston Scientific, and Cardiovascular System Inc; and has equity in ConKay Medical. Dr Gillam has served as a consultant for Edwards Lifesciences; and has received core laboratory contracts from Edwards Lifesciences and Medtronic. Dr Hahn has received speaker fees from Abbott Vascular, Baylis Medical, and Edwards Lifesciences; has institutional consulting agreements for which she receives no direct compensation with Abbott Vascular, Boston Scientific, Edwards Lifesciences, Medtronic, and Novartis; has equity with Navigate; and is the Chief Scientific Officer for the Echocardiography Core Laboratory at the Cardiovascular Research Foundation. Dr Webb is a consultant for Edwards Lifesciences. Dr Leon serves on the PARTNER Trial Executive Committee for Edwards Lifesciences (nonpaid); has received institutional research grants from and is a nonpaid advisor for Abbott, Boston Scientific, and Medtronic; has served as a nonpaid advisor for Sinomed; and has equity in Medinol. Dr Cohen has received research grant support and consulting income from Edwards Lifesciences, Medtronic, Boston Scientific, and Abbott. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Auteurs

Philippe Généreux (P)

Gagnon Cardiovascular Institute, Morristown Medical Center, Morristown, New Jersey, USA. Electronic address: philippe.genereux@atlantichealth.org.

Philippe Pibarot (P)

Department of Medicine, Laval University, Quebec, Quebec, Canada.

Björn Redfors (B)

Clinical Trials Center, Cardiovascular Research Foundation, New York, New York, USA; Columbia University Irving Medical Center, New York, New York, USA; Department of Cardiology, Sahlgrenska University Hospital, Gothenburg, Sweden.

Jeroen J Bax (JJ)

Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands.

Yanglu Zhao (Y)

Edwards Lifesciences, Irvine, California, USA.

Raj R Makkar (RR)

Cedars Sinai Medical Center, Los Angeles, California, USA.

Samir Kapadia (S)

Cleveland Clinic, Cleveland, Ohio, USA.

Vinod H Thourani (VH)

Piedmont Heart Institute, Atlanta, Georgia, USA.

Michael J Mack (MJ)

Baylor Scott and White Research Institute, Plano, Texas, USA.

Tamim M Nazif (TM)

Columbia University Irving Medical Center, New York, New York, USA.

Brian R Lindman (BR)

Vanderbilt University Medical Center, Nashville, Tennessee, USA.

Vasilis Babaliaros (V)

Emory University School of Medicine, Atlanta, Georgia, USA.

Flavien Vincent (F)

Clinical Trials Center, Cardiovascular Research Foundation, New York, New York, USA; Lille University Hospital, Lille, France.

Mark Russo (M)

Rutgers-Robert Wood Johnson Medical School, New Brunswick, New Jersey, USA.

James M McCabe (JM)

University of Washington, Seattle, Washington, USA.

Linda D Gillam (LD)

Gagnon Cardiovascular Institute, Morristown Medical Center, Morristown, New Jersey, USA.

Maria C Alu (MC)

Clinical Trials Center, Cardiovascular Research Foundation, New York, New York, USA; Columbia University Irving Medical Center, New York, New York, USA.

Rebecca T Hahn (RT)

Clinical Trials Center, Cardiovascular Research Foundation, New York, New York, USA; Columbia University Irving Medical Center, New York, New York, USA.

John G Webb (JG)

St. Paul's Hospital, Vancouver, British Columbia, Canada.

Martin B Leon (MB)

Clinical Trials Center, Cardiovascular Research Foundation, New York, New York, USA; Columbia University Irving Medical Center, New York, New York, USA.

David J Cohen (DJ)

Clinical Trials Center, Cardiovascular Research Foundation, New York, New York, USA; St. Francis Hospital and Heart Center, Roslyn, New York, USA.

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