Takanori Kono1, Daisuke Onohara2, Alan Amedi1, Daniella Corporan2, Muralidhar Padala3. 1. Structural Heart Research and Innovation Laboratory, Carlyle Fraser Heart Center, Emory University Hospital Midtown, Atlanta, Ga. 2. Structural Heart Research and Innovation Laboratory, Carlyle Fraser Heart Center, Emory University Hospital Midtown, Atlanta, Ga; Division of Cardiothoracic Surgery, Emory University, Atlanta, Ga. 3. 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.
Abstract
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.
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.
Authors: Lawrence S Lee; Michael H Kwon; Marisa Cevasco; Jan D Schmitto; Suyog A Mokashi; Siobhan McGurk; Lawrence H Cohn; R Morton Bolman; Frederick Y Chen Journal: Ann Thorac Surg Date: 2012-06-21 Impact factor: 4.330
Authors: Sohaib A Virk; David H Tian; Arunan Sriravindrarajah; Douglas Dunn; Hugh D Wolfenden; Rakesh M Suri; Stine Munkholm-Larsen; Christopher Cao Journal: J Thorac Cardiovasc Surg Date: 2017-03-22 Impact factor: 5.209
Authors: Jerry Braun; Jeroen J Bax; Michel I M Versteegh; Pieter G Voigt; Eduard R Holman; Robert J M Klautz; Eric Boersma; Robert A E Dion Journal: Eur J Cardiothorac Surg Date: 2005-05 Impact factor: 4.191
Authors: Christos G Mihos; Steve Xydas; Evin Yucel; Romain Capoulade; Roy F Williams; Maurice Mawad; Guillermo Garcia; Orlando Santana Journal: J Thorac Dis Date: 2017-06 Impact factor: 2.895