Extracellular Myocardial Volume in Patients With Aortic Stenosis.
Aged
Aged, 80 and over
Aortic Valve Stenosis
/ diagnostic imaging
Extracellular Fluid
/ physiology
Female
Follow-Up Studies
Humans
Longitudinal Studies
Magnetic Resonance Imaging, Cine
/ methods
Male
Middle Aged
Mortality
/ trends
Myocardium
/ pathology
Prospective Studies
Stroke Volume
/ physiology
Ventricular Dysfunction, Left
/ diagnostic imaging
T1 mapping
aortic stenosis
cardiovascular magnetic resonance
diffuse myocardial fibrosis
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:
28 01 2020
28 01 2020
Historique:
received:
03
10
2019
revised:
31
10
2019
accepted:
04
11
2019
entrez:
25
1
2020
pubmed:
25
1
2020
medline:
13
8
2020
Statut:
ppublish
Résumé
Myocardial fibrosis is a key mechanism of left ventricular decompensation in aortic stenosis and can be quantified using cardiovascular magnetic resonance (CMR) measures such as extracellular volume fraction (ECV%). Outcomes following aortic valve intervention may be linked to the presence and extent of myocardial fibrosis. This study sought to determine associations between ECV% and markers of left ventricular decompensation and post-intervention clinical outcomes. Patients with severe aortic stenosis underwent CMR, including ECV% quantification using modified Look-Locker inversion recovery-based T1 mapping and late gadolinium enhancement before aortic valve intervention. A central core laboratory quantified CMR parameters. Four-hundred forty patients (age 70 ± 10 years, 59% male) from 10 international centers underwent CMR a median of 15 days (IQR: 4 to 58 days) before aortic valve intervention. ECV% did not vary by scanner manufacturer, magnetic field strength, or T1 mapping sequence (all p > 0.20). ECV% correlated with markers of left ventricular decompensation including left ventricular mass, left atrial volume, New York Heart Association functional class III/IV, late gadolinium enhancement, and lower left ventricular ejection fraction (p < 0.05 for all), the latter 2 associations being independent of all other clinical variables (p = 0.035 and p < 0.001). After a median of 3.8 years (IQR: 2.8 to 4.6 years) of follow-up, 52 patients had died, 14 from adjudicated cardiovascular causes. A progressive increase in all-cause mortality was seen across tertiles of ECV% (17.3, 31.6, and 52.7 deaths per 1,000 patient-years; log-rank test; p = 0.009). Not only was ECV% associated with cardiovascular mortality (p = 0.003), but it was also independently associated with all-cause mortality following adjustment for age, sex, ejection fraction, and late gadolinium enhancement (hazard ratio per percent increase in ECV%: 1.10; 95% confidence interval [1.02 to 1.19]; p = 0.013). In patients with severe aortic stenosis scheduled for aortic valve intervention, an increased ECV% is a measure of left ventricular decompensation and a powerful independent predictor of mortality.
Sections du résumé
BACKGROUND
Myocardial fibrosis is a key mechanism of left ventricular decompensation in aortic stenosis and can be quantified using cardiovascular magnetic resonance (CMR) measures such as extracellular volume fraction (ECV%). Outcomes following aortic valve intervention may be linked to the presence and extent of myocardial fibrosis.
OBJECTIVES
This study sought to determine associations between ECV% and markers of left ventricular decompensation and post-intervention clinical outcomes.
METHODS
Patients with severe aortic stenosis underwent CMR, including ECV% quantification using modified Look-Locker inversion recovery-based T1 mapping and late gadolinium enhancement before aortic valve intervention. A central core laboratory quantified CMR parameters.
RESULTS
Four-hundred forty patients (age 70 ± 10 years, 59% male) from 10 international centers underwent CMR a median of 15 days (IQR: 4 to 58 days) before aortic valve intervention. ECV% did not vary by scanner manufacturer, magnetic field strength, or T1 mapping sequence (all p > 0.20). ECV% correlated with markers of left ventricular decompensation including left ventricular mass, left atrial volume, New York Heart Association functional class III/IV, late gadolinium enhancement, and lower left ventricular ejection fraction (p < 0.05 for all), the latter 2 associations being independent of all other clinical variables (p = 0.035 and p < 0.001). After a median of 3.8 years (IQR: 2.8 to 4.6 years) of follow-up, 52 patients had died, 14 from adjudicated cardiovascular causes. A progressive increase in all-cause mortality was seen across tertiles of ECV% (17.3, 31.6, and 52.7 deaths per 1,000 patient-years; log-rank test; p = 0.009). Not only was ECV% associated with cardiovascular mortality (p = 0.003), but it was also independently associated with all-cause mortality following adjustment for age, sex, ejection fraction, and late gadolinium enhancement (hazard ratio per percent increase in ECV%: 1.10; 95% confidence interval [1.02 to 1.19]; p = 0.013).
CONCLUSIONS
In patients with severe aortic stenosis scheduled for aortic valve intervention, an increased ECV% is a measure of left ventricular decompensation and a powerful independent predictor of mortality.
Identifiants
pubmed: 31976869
pii: S0735-1097(19)38514-6
doi: 10.1016/j.jacc.2019.11.032
pmc: PMC6985897
pii:
doi:
Types de publication
Journal Article
Multicenter Study
Observational Study
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
304-316Subventions
Organisme : British Heart Foundation
ID : FS/19/35/34374
Pays : United Kingdom
Organisme : British Heart Foundation
ID : FS/14/78/31020
Pays : United Kingdom
Organisme : Department of Health
ID : PDF-2011-04-051
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RE/18/5/34216
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RG/16/10/32375
Pays : United Kingdom
Organisme : British Heart Foundation
ID : FS/16/47/32190
Pays : United Kingdom
Organisme : Wellcome Trust
ID : WT103782AIA
Pays : United Kingdom
Organisme : Department of Health
ID : CDF 2014-07-045
Pays : United Kingdom
Organisme : Medical Research Council
ID : G0701127
Pays : United Kingdom
Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : CIHR
ID : FDN 143225
Pays : Canada
Organisme : CIHR
ID : MOP-114997
Pays : Canada
Organisme : British Heart Foundation
ID : CH/09/002
Pays : United Kingdom
Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.
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