Daisuke Onohara1, Daniella Corporan1, Roberto Hernandez-Merlo1, Robert A Guyton2, 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, Joseph P. Whitehead Department of Surgery, Emory University School of Medicine, Atlanta, Ga. 3. Structural Heart Research and Innovation Laboratory, Carlyle Fraser Heart Center, Emory University Hospital Midtown, Atlanta, Ga; Division of Cardiothoracic Surgery, Joseph P. Whitehead Department of Surgery, Emory University School of Medicine, Atlanta, Ga. Electronic address: spadala@emory.edu.
Abstract
OBJECTIVE: Mitral regurgitation (MR) developing concomitant with ischemic cardiomyopathy is a frequently diagnosed valvular lesion, for which an optimal therapeutic strategy is unknown. The contribution of MR to the ongoing cardiac remodeling from myocardial infarction (MI) remains controversial. We have developed a novel experimental model in which MI and severe MR can be independently introduced, to study the role of MR in chronic remodeling of the ischemic heart. METHODS: A total of 98 rats were induced with MI+MR (group 1), MI (group 2), MR (group 3), or sham surgery (group 4). MR was induced by inserting a needle into the anterior mitral leaflet via the ventricular apex in a beating heart. MI was induced by ligating the left coronary artery. Biweekly ultrasound examinations were performed after surgery, and invasive hemodynamic assessments were performed in some rats at 2, 10, and 20 weeks. RESULTS: At 2 weeks postsurgery, the mean end-diastolic volume was 432 ± 103 μL in ischemic hearts with MR, compared with 390 ± 76.3 μL in ischemic hearts without MR (a 10.76% difference). By 20 weeks, the mean volume was significantly greater in the former group (767 ± 246 μL vs 580 ± 85 μL; a 32.24% difference). At 2 weeks, mean end-systolic volume was 147 ± 46.8 μL in the ischemic hearts with MR and 147 ± 45.7 μL in those without MR. By 20 weeks, the mean volumes had increased to 357 ± 136.4 μL and 271 ± 82.3 μL, respectively (a 31.73% difference). CONCLUSIONS: MR in ischemic hearts significantly increased end-diastolic and end-systolic volumes of the left ventricle, indicating adverse cardiac remodeling and worse systolic function.
OBJECTIVE: Mitral regurgitation (MR) developing concomitant with ischemic cardiomyopathy is a frequently diagnosed valvular lesion, for which an optimal therapeutic strategy is unknown. The contribution of MR to the ongoing cardiac remodeling from myocardial infarction (MI) remains controversial. We have developed a novel experimental model in which MI and severe MR can be independently introduced, to study the role of MR in chronic remodeling of the ischemic heart. METHODS: A total of 98 rats were induced with MI+MR (group 1), MI (group 2), MR (group 3), or sham surgery (group 4). MR was induced by inserting a needle into the anterior mitral leaflet via the ventricular apex in a beating heart. MI was induced by ligating the left coronary artery. Biweekly ultrasound examinations were performed after surgery, and invasive hemodynamic assessments were performed in some rats at 2, 10, and 20 weeks. RESULTS: At 2 weeks postsurgery, the mean end-diastolic volume was 432 ± 103 μL in ischemic hearts with MR, compared with 390 ± 76.3 μL in ischemic hearts without MR (a 10.76% difference). By 20 weeks, the mean volume was significantly greater in the former group (767 ± 246 μL vs 580 ± 85 μL; a 32.24% difference). At 2 weeks, mean end-systolic volume was 147 ± 46.8 μL in the ischemic hearts with MR and 147 ± 45.7 μL in those without MR. By 20 weeks, the mean volumes had increased to 357 ± 136.4 μL and 271 ± 82.3 μL, respectively (a 31.73% difference). CONCLUSIONS: MR in ischemic hearts significantly increased end-diastolic and end-systolic volumes of the left ventricle, indicating adverse cardiac remodeling and worse systolic function.
Authors: Peter K Smith; John D Puskas; Deborah D Ascheim; Pierre Voisine; Annetine C Gelijns; Alan J Moskowitz; Judy W Hung; Michael K Parides; Gorav Ailawadi; Louis P Perrault; Michael A Acker; Michael Argenziano; Vinod Thourani; James S Gammie; Marissa A Miller; Pierre Pagé; Jessica R Overbey; Emilia Bagiella; François Dagenais; Eugene H Blackstone; Irving L Kron; Daniel J Goldstein; Eric A Rose; Ellen G Moquete; Neal Jeffries; Timothy J Gardner; Patrick T O'Gara; John H Alexander; Robert E Michler Journal: N Engl J Med Date: 2014-11-18 Impact factor: 91.245
Authors: M R Llaneras; M L Nance; J T Streicher; J A Lima; J S Savino; D K Bogen; R F Deac; M B Ratcliffe; L H Edmunds Journal: Ann Thorac Surg Date: 1994-02 Impact factor: 4.330
Authors: Jonathan Beaudoin; Robert A Levine; J Luis Guerrero; Chaim Yosefy; Suzanne Sullivan; Susan Abedat; Mark D Handschumacher; Catherine Szymanski; Dan Gilon; Nicholas O Palmeri; Gus J Vlahakes; Roger J Hajjar; Ronen Beeri Journal: Circulation Date: 2013-09-10 Impact factor: 29.690
Authors: Weiwei Shi; Bryant V McIver; Kanika Kalra; Eric L Sarin; Susan Schmarkey; Michael Duggan; Vinod H Thourani; Robert A Guyton; Muralidhar Padala Journal: J Cardiovasc Transl Res Date: 2017-06-02 Impact factor: 4.132
Authors: Ronen Beeri; Chaim Yosefy; J Luis Guerrero; Suzan Abedat; Mark D Handschumacher; Robert E Stroud; Suzanne Sullivan; Miguel Chaput; Dan Gilon; Gus J Vlahakes; Francis G Spinale; Roger J Hajjar; Robert A Levine Journal: Circulation Date: 2007-09-11 Impact factor: 29.690
Authors: Matthew H Park; Yuanjia Zhu; Annabel M Imbrie-Moore; Hanjay Wang; Mateo Marin-Cuartas; Michael J Paulsen; Y Joseph Woo Journal: Front Cardiovasc Med Date: 2021-07-08