Cardiac-MRI Predicts Clinical Worsening and Mortality in Pulmonary Arterial Hypertension: A Systematic Review and Meta-Analysis.


Journal

JACC. Cardiovascular imaging
ISSN: 1876-7591
Titre abrégé: JACC Cardiovasc Imaging
Pays: United States
ID NLM: 101467978

Informations de publication

Date de publication:
05 2021
Historique:
received: 20 07 2020
revised: 17 08 2020
accepted: 21 08 2020
pubmed: 4 10 2020
medline: 28 8 2021
entrez: 3 10 2020
Statut: ppublish

Résumé

This meta-analysis evaluates assessment of pulmonary arterial hypertension (PAH), with a focus on clinical worsening and mortality. Cardiac magnetic resonance (CMR) has prognostic value in the assessment of patients with PAH. However, there are limited data on the prediction of clinical worsening, an important composite endpoint used in PAH therapy trials. The Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, and Web of Science databases were searched in May 2020. All CMR studies assessing clinical worsening and the prognosis of patients with PAH were included. Pooled hazard ratios of univariate regression analyses for CMR measurements, for prediction of clinical worsening and mortality, were calculated. Twenty-two studies with 1,938 participants were included in the meta-analysis. There were 18 clinical worsening events and 8 deaths per 100 patient-years. The pooled hazard ratios show that every 1% decrease in right ventricular (RV) ejection fraction is associated with a 4.9% increase in the risk of clinical worsening over 22 months of follow-up and a 2.1% increase in the risk of death over 54 months. For every 1 ml/m This review confirms CMR as a powerful prognostic marker in PAH in a large cohort of patients. In addition to confirming previous observations that RV function and RV and left ventricular volumes predict mortality, RV function and volumes also predict clinical worsening. This study provides a strong rationale for considering CMR as a clinically relevant endpoint for trials of PAH therapies.

Sections du résumé

OBJECTIVES
This meta-analysis evaluates assessment of pulmonary arterial hypertension (PAH), with a focus on clinical worsening and mortality.
BACKGROUND
Cardiac magnetic resonance (CMR) has prognostic value in the assessment of patients with PAH. However, there are limited data on the prediction of clinical worsening, an important composite endpoint used in PAH therapy trials.
METHODS
The Cochrane Central Register of Controlled Trials, MEDLINE, EMBASE, and Web of Science databases were searched in May 2020. All CMR studies assessing clinical worsening and the prognosis of patients with PAH were included. Pooled hazard ratios of univariate regression analyses for CMR measurements, for prediction of clinical worsening and mortality, were calculated.
RESULTS
Twenty-two studies with 1,938 participants were included in the meta-analysis. There were 18 clinical worsening events and 8 deaths per 100 patient-years. The pooled hazard ratios show that every 1% decrease in right ventricular (RV) ejection fraction is associated with a 4.9% increase in the risk of clinical worsening over 22 months of follow-up and a 2.1% increase in the risk of death over 54 months. For every 1 ml/m
CONCLUSIONS
This review confirms CMR as a powerful prognostic marker in PAH in a large cohort of patients. In addition to confirming previous observations that RV function and RV and left ventricular volumes predict mortality, RV function and volumes also predict clinical worsening. This study provides a strong rationale for considering CMR as a clinically relevant endpoint for trials of PAH therapies.

Identifiants

pubmed: 33008758
pii: S1936-878X(20)30731-2
doi: 10.1016/j.jcmg.2020.08.013
pmc: PMC7525356
pii:
doi:

Types de publication

Journal Article Meta-Analysis Research Support, Non-U.S. Gov't Systematic Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

931-942

Subventions

Organisme : Medical Research Council
ID : MR/M008894/1
Pays : United Kingdom
Organisme : British Heart Foundation
ID : SP/14/6/31350
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 215799/Z/19/Z
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 205188/Z/16/Z
Pays : United Kingdom

Commentaires et corrections

Type : CommentIn
Type : ErratumIn

Informations de copyright

Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Funding Support and Author Disclosures The study was supported by the Wellcome Trust grants 215799/Z/19/Z and 205188/Z/16/Z. The funder did not have any role in the design and conduct of the study; in the collection, analysis, and interpretation of the data; or in the preparation, review, and approval of the paper. The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Auteurs

Samer Alabed (S)

Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom; Department of Clinical Radiology, Sheffield Teaching Hospitals, Sheffield, United Kingdom. Electronic address: s.alabed@nhs.net.

Yousef Shahin (Y)

Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom; Department of Clinical Radiology, Sheffield Teaching Hospitals, Sheffield, United Kingdom.

Pankaj Garg (P)

Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom.

Faisal Alandejani (F)

Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom.

Christopher S Johns (CS)

Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom; Department of Clinical Radiology, Sheffield Teaching Hospitals, Sheffield, United Kingdom.

Robert A Lewis (RA)

Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom; Sheffield Pulmonary Vascular Disease Unit, Royal Hallamshire Hospital, Sheffield, United Kingdom.

Robin Condliffe (R)

Sheffield Pulmonary Vascular Disease Unit, Royal Hallamshire Hospital, Sheffield, United Kingdom.

James M Wild (JM)

Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom; INSIGNEO, Institute for In Silico Medicine, University of Sheffield, United Kingdom.

David G Kiely (DG)

Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom; Sheffield Pulmonary Vascular Disease Unit, Royal Hallamshire Hospital, Sheffield, United Kingdom; INSIGNEO, Institute for In Silico Medicine, University of Sheffield, United Kingdom.

Andrew J Swift (AJ)

Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom; Department of Clinical Radiology, Sheffield Teaching Hospitals, Sheffield, United Kingdom; INSIGNEO, Institute for In Silico Medicine, University of Sheffield, United Kingdom.

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