Ischemia-Mediated Dysfunction in Subpapillary Myocardium as a Marker of Functional Mitral Regurgitation.


Journal

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

Informations de publication

Date de publication:
04 2021
Historique:
received: 13 08 2020
revised: 28 12 2020
accepted: 06 01 2021
pubmed: 22 3 2021
medline: 28 8 2021
entrez: 21 3 2021
Statut: ppublish

Résumé

The goal of this study was to test whether ischemia-mediated contractile dysfunction underlying the mitral valve affects functional mitral regurgitation (FMR) and the prognostic impact of FMR. FMR results from left ventricular (LV) remodeling, which can stem from myocardial tissue alterations. Stress cardiac magnetic resonance can assess ischemia and infarction in the left ventricle and papillary muscles; relative impact on FMR is uncertain. Vasodilator stress cardiac magnetic resonance was performed in patients with known or suspected coronary artery disease at 7 sites. Images were centrally analyzed for MR etiology/severity, mitral apparatus remodeling, and papillary ischemia. A total of 8,631 patients (mean age 60.0 ± 14.1 years; 55% male) were studied. FMR was present in 27%, among whom 16% (n = 372) had advanced (moderate or severe) FMR. Patients with ischemia localized to subpapillary regions were more likely to have advanced FMR (p = 0.003); those with ischemia localized to other areas were not (p = 0.17). Ischemic/dysfunctional subpapillary myocardium (odds ratio: 1.24/10% subpapillary myocardium; confidence interval: 1.17 to 1.31; p < 0.001) was associated with advanced FMR controlling for infarction. Among a subgroup with (n = 372) and without (n = 744) advanced FMR matched (1:2) on infarct size/distribution, patients with advanced FMR had increased adverse mitral apparatus remodeling, paralleled by greater ischemic/dysfunctional subpapillary myocardium (p < 0.001). Although posteromedial papillary ischemia was more common with advanced FMR (p = 0.006), subpapillary ischemia with dysfunction remained associated (p < 0.001), adjusting for posteromedial papillary ischemia (p = 0.074). During follow-up (median 5.1 years), 1,473 deaths occurred in the overall cohort; advanced FMR conferred increased mortality risk (hazard ratio: 1.52; 95% confidence interval: 1.25 to 1.86; p < 0.001) controlling for left ventricular ejection fraction, infarction, and ischemia. Ischemic and dysfunctional subpapillary myocardium provides a substrate for FMR, which predicts mortality independent of key mechanistic substrates.

Sections du résumé

OBJECTIVES
The goal of this study was to test whether ischemia-mediated contractile dysfunction underlying the mitral valve affects functional mitral regurgitation (FMR) and the prognostic impact of FMR.
BACKGROUND
FMR results from left ventricular (LV) remodeling, which can stem from myocardial tissue alterations. Stress cardiac magnetic resonance can assess ischemia and infarction in the left ventricle and papillary muscles; relative impact on FMR is uncertain.
METHODS
Vasodilator stress cardiac magnetic resonance was performed in patients with known or suspected coronary artery disease at 7 sites. Images were centrally analyzed for MR etiology/severity, mitral apparatus remodeling, and papillary ischemia.
RESULTS
A total of 8,631 patients (mean age 60.0 ± 14.1 years; 55% male) were studied. FMR was present in 27%, among whom 16% (n = 372) had advanced (moderate or severe) FMR. Patients with ischemia localized to subpapillary regions were more likely to have advanced FMR (p = 0.003); those with ischemia localized to other areas were not (p = 0.17). Ischemic/dysfunctional subpapillary myocardium (odds ratio: 1.24/10% subpapillary myocardium; confidence interval: 1.17 to 1.31; p < 0.001) was associated with advanced FMR controlling for infarction. Among a subgroup with (n = 372) and without (n = 744) advanced FMR matched (1:2) on infarct size/distribution, patients with advanced FMR had increased adverse mitral apparatus remodeling, paralleled by greater ischemic/dysfunctional subpapillary myocardium (p < 0.001). Although posteromedial papillary ischemia was more common with advanced FMR (p = 0.006), subpapillary ischemia with dysfunction remained associated (p < 0.001), adjusting for posteromedial papillary ischemia (p = 0.074). During follow-up (median 5.1 years), 1,473 deaths occurred in the overall cohort; advanced FMR conferred increased mortality risk (hazard ratio: 1.52; 95% confidence interval: 1.25 to 1.86; p < 0.001) controlling for left ventricular ejection fraction, infarction, and ischemia.
CONCLUSIONS
Ischemic and dysfunctional subpapillary myocardium provides a substrate for FMR, which predicts mortality independent of key mechanistic substrates.

Identifiants

pubmed: 33744130
pii: S1936-878X(21)00067-X
doi: 10.1016/j.jcmg.2021.01.007
pmc: PMC8086776
mid: NIHMS1665395
pii:
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

826-839

Subventions

Organisme : NHLBI NIH HHS
ID : R01 HL141917
Pays : United States
Organisme : NHLBI NIH HHS
ID : K23 HL140092
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL128278
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL063348
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL007854
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL151686
Pays : United States
Organisme : NHLBI NIH HHS
ID : K23 HL132011
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL128099
Pays : United States
Organisme : NHLBI NIH HHS
ID : R61 HL151355
Pays : United States
Organisme : NHLBI NIH HHS
ID : K23 HL102249
Pays : United States
Organisme : NHLBI NIH HHS
ID : R33 HL151355
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2021 American College of Cardiology Foundation. All rights reserved.

Déclaration de conflit d'intérêts

Funding Support and Author Disclosures This study was supported by the National Institutes of Health grants R01 HL128278 (Drs. Weinsaft, Ratcliffe, Levine, and J. Kim), R01 HL128099 and R01 HL141917 (Dr. Levine), R01-HL63348 (Dr. Ratcliffe), K23 HL140092 (Dr. J. Kim), K23 HL132011 (Dr. Shenoy), and T32 HL7854-23 (Dr. Kochav). It was also funded by the Glorney-Raisbeck Fellowship/NY Academy of Medicine (Dr. Kochav). Dr. Judd has an equity interest. Dr. R. Kim serves on the Board of Directors. Mr. Cargile is an employee of Heart Imaging Technologies. Dr. Klem is a consultant for and receives speaker honorarium from Bayer; and receives funding from Medtronic. Dr. Karmpaliotis receives funding from Abbott Vascular, Boston Scientific, and Abiomed; and has equity in Saranas, Soundbite, and Traverse Vascular. Dr. Leon receives funding from Abbott Vascular, Boston Scientific, and Medtronic. Dr. Weinsaft has received speaker honoraria from GE Healthcare. 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.

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.

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, NewYork-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.

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)

Peidmont Heart Institute, Peidmont Atlanta Hospital, Atlanta Georgia, USA.

Ramsey Kalil (R)

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

Pablo Villar-Calle (P)

Department of Cardiology, Sant Pau Hospital, Barcelona, Spain.

Lakshmi Nambiar (L)

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

Razia Sultana (R)

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.

Preston Cargile (P)

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.

Dimitrios Karmpaliotis (D)

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

Mark Ratcliffe (M)

Division of Cardiac Surgery, University of California, San Francisco, California, USA.

Robert Levine (R)

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

William A Zoghbi (WA)

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

Richard B Devereux (RB)

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

Chaya S Moskowitz (CS)

Department of Epidemiology and Biostatics, Memorial Sloan Kettering Cancer Center, New York, New York, USA.

Raymond Kim (R)

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. Electronic address: jww2001@med.cornell.edu.

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Classifications MeSH