Diastolic dysfunction in women with ischemia and no obstructive coronary artery disease: Mechanistic insight from magnetic resonance imaging.


Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
15 05 2021
Historique:
received: 25 07 2020
revised: 11 12 2020
accepted: 25 01 2021
pubmed: 6 2 2021
medline: 29 5 2021
entrez: 5 2 2021
Statut: ppublish

Résumé

Ischemia with no obstructive coronary artery disease (INOCA) is prevalent in women and is associated with increased risk of developing heart failure with preserved ejection fraction (HFpEF); however, the mechanism(s) contributing to this progression remains unclear. Given that diastolic dysfunction is common in women with INOCA, defining mechanisms related to diastolic dysfunction in INOCA could identify therapeutic targets to prevent HFpEF. Cardiac MRI was performed in 65 women with INOCA and 12 reference controls. Diastolic function was defined by left ventricular early diastolic circumferential strain rate (eCSRd). Contributors to diastolic dysfunction were chosen a priori as coronary vascular dysfunction (myocardial perfusion reserve index [MPRI]), diffuse myocardial fibrosis (extracellular volume [ECV]), and aortic stiffness (aortic pulse wave velocity [aPWV]). Compared to controls, eCSRd was lower in INOCA (1.61 ± 0.33/s vs. 1.36 ± 0.31/s, P = 0.016); however, this difference was not exaggerated when the INOCA group was sub-divided by low and high MPRI (P > 0.05) nor was ECV elevated in INOCA (29.0 ± 1.9% vs. 28.0 ± 3.2%, control vs. INOCA; P = 0.38). However, aPWV was higher in INOCA vs. controls (8.1 ± 3.2 m/s vs. 6.1 ± 1.5 m/s; P = 0.045), and was associated with eCSRd (r = -0.50, P < 0.001). By multivariable linear regression analysis, aPWV was an independent predictor of decreased eCSRd (standardized β = -0.39, P = 0.003), as was having an elevated left ventricular mass index (standardized β = -0.25, P = 0.024) and lower ECV (standardized β = 0.30, P = 0.003). These data provide mechanistic insight into diastolic dysfunction in women with INOCA, identifying aortic stiffness and ventricular remodeling as putative therapeutic targets.

Sections du résumé

BACKGROUND
Ischemia with no obstructive coronary artery disease (INOCA) is prevalent in women and is associated with increased risk of developing heart failure with preserved ejection fraction (HFpEF); however, the mechanism(s) contributing to this progression remains unclear. Given that diastolic dysfunction is common in women with INOCA, defining mechanisms related to diastolic dysfunction in INOCA could identify therapeutic targets to prevent HFpEF.
METHODS
Cardiac MRI was performed in 65 women with INOCA and 12 reference controls. Diastolic function was defined by left ventricular early diastolic circumferential strain rate (eCSRd). Contributors to diastolic dysfunction were chosen a priori as coronary vascular dysfunction (myocardial perfusion reserve index [MPRI]), diffuse myocardial fibrosis (extracellular volume [ECV]), and aortic stiffness (aortic pulse wave velocity [aPWV]).
RESULTS
Compared to controls, eCSRd was lower in INOCA (1.61 ± 0.33/s vs. 1.36 ± 0.31/s, P = 0.016); however, this difference was not exaggerated when the INOCA group was sub-divided by low and high MPRI (P > 0.05) nor was ECV elevated in INOCA (29.0 ± 1.9% vs. 28.0 ± 3.2%, control vs. INOCA; P = 0.38). However, aPWV was higher in INOCA vs. controls (8.1 ± 3.2 m/s vs. 6.1 ± 1.5 m/s; P = 0.045), and was associated with eCSRd (r = -0.50, P < 0.001). By multivariable linear regression analysis, aPWV was an independent predictor of decreased eCSRd (standardized β = -0.39, P = 0.003), as was having an elevated left ventricular mass index (standardized β = -0.25, P = 0.024) and lower ECV (standardized β = 0.30, P = 0.003).
CONCLUSIONS
These data provide mechanistic insight into diastolic dysfunction in women with INOCA, identifying aortic stiffness and ventricular remodeling as putative therapeutic targets.

Identifiants

pubmed: 33545261
pii: S0167-5273(21)00146-7
doi: 10.1016/j.ijcard.2021.01.064
pmc: PMC8026746
mid: NIHMS1669611
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1-7

Subventions

Organisme : NHLBI NIH HHS
ID : U01 HL064829
Pays : United States
Organisme : NHLBI NIH HHS
ID : N01HV68162
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR000064
Pays : United States
Organisme : NIA NIH HHS
ID : R03 AG032631
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL069751
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR000124
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL153430
Pays : United States
Organisme : NHLBI NIH HHS
ID : U01 HL064924
Pays : United States
Organisme : NCRR NIH HHS
ID : M01 RR000425
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL151266
Pays : United States
Organisme : American Heart Association-American Stroke Association
ID : 18PRE33960358
Pays : United States
Organisme : NHLBI NIH HHS
ID : K23 HL105787
Pays : United States
Organisme : NHLBI NIH HHS
ID : R00 HL124323
Pays : United States
Organisme : NHLBI NIH HHS
ID : K23 HL125941
Pays : United States
Organisme : NHLBI NIH HHS
ID : N01HV68163
Pays : United States
Organisme : NHLBI NIH HHS
ID : K23 HL127262
Pays : United States
Organisme : NHLBI NIH HHS
ID : N01 HV068164
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2021 Elsevier B.V. All rights reserved.

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Auteurs

T Jake Samuel (TJ)

The University of Texas at Arlington, Arlington, TX, USA.

Janet Wei (J)

Barbra Streisand Women's Heart Center, Cedars-Sinai Smidt Heart Institute, Los Angeles, CA, USA.

Behzad Sharif (B)

Biomedical Imaging Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Balaji K Tamarappoo (BK)

Mark S. Taper Imaging Center, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Varun Pattisapu (V)

Barbra Streisand Women's Heart Center, Cedars-Sinai Smidt Heart Institute, Los Angeles, CA, USA.

Jenna Maughan (J)

Barbra Streisand Women's Heart Center, Cedars-Sinai Smidt Heart Institute, Los Angeles, CA, USA.

Daisha J Cipher (DJ)

The University of Texas at Arlington, Arlington, TX, USA.

Nissi Suppogu (N)

Barbra Streisand Women's Heart Center, Cedars-Sinai Smidt Heart Institute, Los Angeles, CA, USA.

Haider Aldiwani (H)

Barbra Streisand Women's Heart Center, Cedars-Sinai Smidt Heart Institute, Los Angeles, CA, USA.

Louise E J Thomson (LEJ)

Mark S. Taper Imaging Center, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Chrisandra Shufelt (C)

Barbra Streisand Women's Heart Center, Cedars-Sinai Smidt Heart Institute, Los Angeles, CA, USA.

Daniel S Berman (DS)

Mark S. Taper Imaging Center, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

Debiao Li (D)

Biomedical Imaging Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.

C Noel Bairey Merz (CN)

Barbra Streisand Women's Heart Center, Cedars-Sinai Smidt Heart Institute, Los Angeles, CA, USA.

Michael D Nelson (MD)

The University of Texas at Arlington, Arlington, TX, USA; Barbra Streisand Women's Heart Center, Cedars-Sinai Smidt Heart Institute, Los Angeles, CA, USA. Electronic address: Michael.nelson3@uta.edu.

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Classifications MeSH