Effect of early versus late onset mitral regurgitation on left ventricular remodeling in ischemic cardiomyopathy in an animal model.

Autor:	Kono T; Structural Heart Research and Innovation Laboratory, Carlyle Fraser Heart Center, Emory University Hospital Midtown, Atlanta, Ga., Onohara D; Structural Heart Research and Innovation Laboratory, Carlyle Fraser Heart Center, Emory University Hospital Midtown, Atlanta, Ga; Division of Cardiothoracic Surgery, Emory University, Atlanta, Ga., Amedi A; Structural Heart Research and Innovation Laboratory, Carlyle Fraser Heart Center, Emory University Hospital Midtown, Atlanta, Ga., Corporan D; Structural Heart Research and Innovation Laboratory, Carlyle Fraser Heart Center, Emory University Hospital Midtown, Atlanta, Ga; Division of Cardiothoracic Surgery, Emory University, Atlanta, Ga., Padala M; Structural Heart Research and Innovation Laboratory, Carlyle Fraser Heart Center, Emory University Hospital Midtown, Atlanta, Ga; Division of Cardiothoracic Surgery, Emory University, Atlanta, Ga. Electronic address: spadala@emory.edu.
Jazyk:	angličtina
Zdroj:	The Journal of thoracic and cardiovascular surgery [J Thorac Cardiovasc Surg] 2022 Dec; Vol. 164 (6), pp. e333-e347. Date of Electronic Publication: 2021 Nov 16.
DOI:	10.1016/j.jtcvs.2021.11.024
Abstrakt:	Background: Patients who survive a myocardial infarction have progressive cardiac dysfunction and ventricular remodeling. Mitral regurgitation is often diagnosed in these patients, and is a risk factor that portends poor prognosis. Whether such postinfarction mitral regurgitation magnifies adverse left ventricular remodeling is unclear, which was studied in an animal model. Methods: Forty-one adult rats were induced with myocardial infarction using left coronary artery ligation and assigned to 3 groups: group 1, myocardial infarction only; group 2, myocardial infarction with severe mitral regurgitation introduced after 4 weeks; and group 3, myocardial infarction with severe mitral regurgitation introduced after 10 weeks. Valve regurgitation was introduced by advancing a transapical ultrasound-guided needle into the mitral valve anterior leaflet. Animals were survived to 20 weeks from the index procedure, with biweekly cardiac ultrasound, and invasive hemodynamics and histology at termination. Results: At 20 weeks, end diastolic volume was largest in the groups with mitral regurgitation, compared with the group without the valve lesion (group 1, 760.9 ± 124.6 μL; group 2, 958.0 ± 115.1 μL; group 3, 968.3 ± 214.9 μL). Similarly, end systolic volume was larger in groups with regurgitation (group 1, 431.2 ± 152.6 μL; group 2, 533.2 ± 130.8 μL; group 3, 533.1 ± 177.5 μL). In the infarction-only group, left ventricular remodeling was maximal until 6 weeks and plateaued thereafter. In groups with mitral regurgitation, left ventricular remodeling was significantly elevated at the onset of regurgitation and persisted. Conclusions: Mitral regurgitation is a potent driver of adverse cardiac remodeling after a myocardial infarction, irrespective of the timing of its onset. (Copyright © 2021 The American Association for Thoracic Surgery. Published by Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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