Myocardial Contractile Mechanics in Ischemic Mitral Regurgitation: Multicenter Data Using Stress Perfusion Cardiovascular Magnetic Resonance.


Journal

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

Informations de publication

Date de publication:
07 2022
Historique:
received: 20 09 2021
revised: 24 02 2022
accepted: 04 03 2022
entrez: 7 7 2022
pubmed: 8 7 2022
medline: 12 7 2022
Statut: ppublish

Résumé

Left ventricular (LV) ischemia has been variably associated with functional mitral regurgitation (FMR). Determinants of FMR in patients with ischemia are poorly understood. This study sought to test whether contractile mechanics in ischemic myocardium underlying the mitral valve have an impact on likelihood of FMR. Vasodilator stress perfusion cardiac magnetic resonance was performed in patients with coronary artery disease (CAD) at multiple centers. FMR severity was confirmed quantitatively via core lab analysis. To test relationship of contractile mechanics with ischemic FMR, regional wall motion and strain were assessed in patients with inducible ischemia and minimal (≤5% LV myocardium, nontransmural) infarction. A total of 2,647 patients with CAD were studied; 34% had FMR (7% moderate or greater). FMR severity increased with presence (P < 0.001) and extent (P = 0.01) of subpapillary ischemia: patients with moderate or greater FMR had more subpapillary ischemia (odds ratio [OR]: 1.13 per 10% LV; 95% CI: 1.05-1.21; P = 0.001) independent of ischemia in remote regions (P = NS); moderate or greater FMR prevalence increased stepwise with extent of ischemia and infarction in subpapillary myocardium (P < 0.001); stronger associations between FMR and infarction paralleled greater wall motion scores in infarct-affected territories. Among patients with inducible ischemia and minimal infarction (n = 532), wall motion and radial strain analysis showed impaired subpapillary contractile mechanics to associate with moderate or greater FMR (P < 0.05) independent of remote regions (P = NS). Conversely, subpapillary ischemia without contractile dysfunction did not augment FMR likelihood. Mitral and interpapillary dimensions increased with subpapillary radial strain impairment; each remodeling parameter associated with impaired subpapillary strain (P < 0.05) independent of remote strain (P = NS). Subpapillary radial strain (OR: 1.13 per 5% [95% CI: 1.02-1.25]; P = 0.02) and mitral tenting area (OR: 1.05 per 10 mm Among patients with CAD and ischemia, FMR severity and adverse mitral apparatus remodeling increase in proportion to contractile dysfunction underlying the mitral valve.

Sections du résumé

BACKGROUND
Left ventricular (LV) ischemia has been variably associated with functional mitral regurgitation (FMR). Determinants of FMR in patients with ischemia are poorly understood.
OBJECTIVES
This study sought to test whether contractile mechanics in ischemic myocardium underlying the mitral valve have an impact on likelihood of FMR.
METHODS
Vasodilator stress perfusion cardiac magnetic resonance was performed in patients with coronary artery disease (CAD) at multiple centers. FMR severity was confirmed quantitatively via core lab analysis. To test relationship of contractile mechanics with ischemic FMR, regional wall motion and strain were assessed in patients with inducible ischemia and minimal (≤5% LV myocardium, nontransmural) infarction.
RESULTS
A total of 2,647 patients with CAD were studied; 34% had FMR (7% moderate or greater). FMR severity increased with presence (P < 0.001) and extent (P = 0.01) of subpapillary ischemia: patients with moderate or greater FMR had more subpapillary ischemia (odds ratio [OR]: 1.13 per 10% LV; 95% CI: 1.05-1.21; P = 0.001) independent of ischemia in remote regions (P = NS); moderate or greater FMR prevalence increased stepwise with extent of ischemia and infarction in subpapillary myocardium (P < 0.001); stronger associations between FMR and infarction paralleled greater wall motion scores in infarct-affected territories. Among patients with inducible ischemia and minimal infarction (n = 532), wall motion and radial strain analysis showed impaired subpapillary contractile mechanics to associate with moderate or greater FMR (P < 0.05) independent of remote regions (P = NS). Conversely, subpapillary ischemia without contractile dysfunction did not augment FMR likelihood. Mitral and interpapillary dimensions increased with subpapillary radial strain impairment; each remodeling parameter associated with impaired subpapillary strain (P < 0.05) independent of remote strain (P = NS). Subpapillary radial strain (OR: 1.13 per 5% [95% CI: 1.02-1.25]; P = 0.02) and mitral tenting area (OR: 1.05 per 10 mm
CONCLUSIONS
Among patients with CAD and ischemia, FMR severity and adverse mitral apparatus remodeling increase in proportion to contractile dysfunction underlying the mitral valve.

Identifiants

pubmed: 35798397
pii: S1936-878X(22)00179-6
doi: 10.1016/j.jcmg.2022.03.014
pmc: PMC9273017
mid: NIHMS1793960
pii:
doi:

Types de publication

Journal Article Multicenter Study Research Support, Non-U.S. Gov't Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

1212-1226

Subventions

Organisme : NHLBI NIH HHS
ID : R01 HL141917
Pays : United States
Organisme : NHLBI NIH HHS
ID : K23 HL140092
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL128099
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL128278
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL007854
Pays : United States
Organisme : NHLBI NIH HHS
ID : K23 HL132011
Pays : United States

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 Supported by National Institutes of Health grants R01 HL128278 (to Drs Weinsaft, Levine, and J. Kim), R01 HL128099 and R01 HL141917 (to Dr Levine), K23 HL140092 (to Dr J. Kim), K23 HL132011 (to Dr Shenoy), and T32 HL7854-23 (to Dr Kochav), as well as by the Glorney-Raisbeck Fellowship/New York Academy of Medicine (to Dr Kochav). Dr Judd has an equity interest in and has been a consultant for Heart Imaging Technologies. Dr Klem has been a consultant and speaker for Bayer; and has received funding from Medtronic. Dr Leon has received funding from Abbott Vascular, Boston Scientific, and Medtronic. Dr R. Kim has served on the Board of Directors of Heart Imaging Technologies. Dr Weinsaft has received a speaker honorarium from General Electric Healthcare; and has been a consultant for Lexeo Therapeutics. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

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Auteurs

Jonathan D Kochav (JD)

Division of Cardiology, Weill Cornell Medicine, New York, New York, USA; Division of Cardiology, Columbia University Irving Medical Center, New York, New York, USA. Electronic address: jww2001@med.cornell.edu.

Jiwon Kim (J)

Division of Cardiology, Weill Cornell Medicine, New York, New York, USA.

Robert Judd (R)

Duke Cardiovascular Magnetic Resonance Center, Duke University Medical Center, Durham, North Carolina, USA.

Katherine A Tak (KA)

Division of Cardiology, Weill Cornell Medicine, New York, New York, USA.

Emmad Janjua (E)

Division of Cardiology, Weill Cornell Medicine, New York, New York, USA; Weill Cornell Medicine-Qatar, Doha, Qatar.

Abigail J Maciejewski (AJ)

Division of Cardiology, Weill Cornell Medicine, New York, New York, USA.

Han W Kim (HW)

Duke Cardiovascular Magnetic Resonance Center, Duke University Medical Center, Durham, North Carolina, USA.

Igor Klem (I)

Duke Cardiovascular Magnetic Resonance Center, Duke University Medical Center, Durham, North Carolina, USA.

John Heitner (J)

Division of Cardiology, New York Presbyterian Brooklyn Methodist Hospital, New York, New York, USA.

Dipan Shah (D)

Division of Cardiology, Houston Methodist DeBakey Heart and Vascular Center, Houston, Texas, USA.

William A Zoghbi (WA)

Division of Cardiology, Houston Methodist DeBakey Heart and Vascular Center, Houston, Texas, USA.

Chetan Shenoy (C)

Division of Cardiology, University of Minnesota Medical Center, Minneapolis, Minnesota, USA.

Afshin Farzaneh-Far (A)

Division of Cardiology, University of Illinois at Chicago, Chicago, Illinois, USA.

Venkateshwar Polsani (V)

Piedmont Atlanta Hospital, Atlanta, Georgia, USA.

Pablo Villar-Calle (P)

Division of Cardiology, Weill Cornell Medicine, New York, New York, USA.

Michele Parker (M)

Duke Cardiovascular Magnetic Resonance Center, Duke University Medical Center, Durham, North Carolina, USA.

Kevin M Judd (KM)

Heart Imaging Technologies, Durham, North Carolina, USA.

Omar K Khalique (OK)

Division of Cardiology, Columbia University Irving Medical Center, New York, New York, USA.

Martin B Leon (MB)

Division of Cardiology, Columbia University Irving Medical Center, New York, New York, USA.

Richard B Devereux (RB)

Division of Cardiology, Weill Cornell Medicine, New York, New York, USA.

Robert A Levine (RA)

Division of Cardiology, Massachusetts General Hospital, Boston, Massachusetts, USA.

Raymond J Kim (RJ)

Duke Cardiovascular Magnetic Resonance Center, Duke University Medical Center, Durham, North Carolina, USA.

Jonathan W Weinsaft (JW)

Division of Cardiology, Weill Cornell Medicine, New York, New York, USA.

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Classifications MeSH