Jaume Aguero1, Carlos Galan-Arriola2, Rodrigo Fernandez-Jimenez3, Javier Sanchez-Gonzalez4, Nina Ajmone5, Victoria Delgado5, Jorge Solis6, Gonzalo J Lopez7, Antonio de Molina-Iracheta7, Roger J Hajjar8, Jeroen J Bax5, Valentin Fuster9, Borja Ibáñez10. 1. Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain; CIBER de enfermedades CardioVasculares, Madrid, Spain; Hospital Universitari i Politecnic La Fe, Valencia, Spain. 2. Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain; CIBER de enfermedades CardioVasculares, Madrid, Spain. 3. Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain; CIBER de enfermedades CardioVasculares, Madrid, Spain; The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York. 4. Philips Healthcare, Madrid, Spain. 5. Department of Cardiology, Heart Lung Center, Leiden University Medical Center, Leiden, the Netherlands. 6. Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain; Hospital 12 de Octubre, Madrid, Spain. 7. Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain. 8. The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York. 9. Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain; The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York. 10. Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain; CIBER de enfermedades CardioVasculares, Madrid, Spain; Cardiology Department, IIS-Fundación Jiménez Díaz Hospital, Madrid, Spain. Electronic address: bibanez@cnic.es.
Abstract
BACKGROUND: Left atrial (LA) remodeling after an acute myocardial infarction (MI) is poorly characterized regarding its determinants or its effect on ischemic mitral regurgitation (MR) development. OBJECTIVES: The purpose of this study was: 1) to compare LA structural remodeling in experimental MI swine models recapitulating the effects of left ventricular (LV) dysfunction, ischemic MR, and left atrial infarction (LAI); and 2) to analyze how LA remodeling influences ischemic MR development. METHODS: Three models of MI were generated: 1) proximal left circumflex (LCx) coronary artery occlusion involving the LA branch (LAI group); 2) proximal LCx occlusion not involving the LA branch (LCx group); and 3) left anterior descending (LAD) occlusion (LAD group). Serial cardiac magnetic resonance scans were performed to define LA and LV remodeling and ischemic MR, and were correlated with histology. RESULTS: Occlusion of the LA branch (LAI group) induced a greater degree of LA dilation at 1 and 8 weeks post-MI than the LCx and LAD groups, along with early and severe impairment of LA function. In the LCx and LAD groups, LA dysfunction was less pronounced and not consistent. Development of ischemic MR was more pronounced in the LAI group than in the LCx group. Histology confirmed atrial infarction with extensive fibrosis in the LAI group and interstitial fibrosis in the LCx group. In the LAD group, LA remodeling was not observed by cardiac magnetic resonance or histology. CONCLUSIONS: We provide the first experimental evidence of the deleterious effect of acute LAI on atrial structural remodeling, characterized by early LA dilation, dysfunction, and fibrosis, and early occurrence of ischemic MR.
BACKGROUND: Left atrial (LA) remodeling after an acute myocardial infarction (MI) is poorly characterized regarding its determinants or its effect on ischemic mitral regurgitation (MR) development. OBJECTIVES: The purpose of this study was: 1) to compare LA structural remodeling in experimental MI swine models recapitulating the effects of left ventricular (LV) dysfunction, ischemic MR, and left atrial infarction (LAI); and 2) to analyze how LA remodeling influences ischemic MR development. METHODS: Three models of MI were generated: 1) proximal left circumflex (LCx) coronary artery occlusion involving the LA branch (LAI group); 2) proximal LCx occlusion not involving the LA branch (LCx group); and 3) left anterior descending (LAD) occlusion (LAD group). Serial cardiac magnetic resonance scans were performed to define LA and LV remodeling and ischemic MR, and were correlated with histology. RESULTS: Occlusion of the LA branch (LAI group) induced a greater degree of LA dilation at 1 and 8 weeks post-MI than the LCx and LAD groups, along with early and severe impairment of LA function. In the LCx and LAD groups, LA dysfunction was less pronounced and not consistent. Development of ischemic MR was more pronounced in the LAI group than in the LCx group. Histology confirmed atrial infarction with extensive fibrosis in the LAI group and interstitial fibrosis in the LCx group. In the LAD group, LA remodeling was not observed by cardiac magnetic resonance or histology. CONCLUSIONS: We provide the first experimental evidence of the deleterious effect of acute LAI on atrial structural remodeling, characterized by early LA dilation, dysfunction, and fibrosis, and early occurrence of ischemicMR.
Authors: Hans Erik Bøtker; Derek Hausenloy; Ioanna Andreadou; Salvatore Antonucci; Kerstin Boengler; Sean M Davidson; Soni Deshwal; Yvan Devaux; Fabio Di Lisa; Moises Di Sante; Panagiotis Efentakis; Saveria Femminò; David García-Dorado; Zoltán Giricz; Borja Ibanez; Efstathios Iliodromitis; Nina Kaludercic; Petra Kleinbongard; Markus Neuhäuser; Michel Ovize; Pasquale Pagliaro; Michael Rahbek-Schmidt; Marisol Ruiz-Meana; Klaus-Dieter Schlüter; Rainer Schulz; Andreas Skyschally; Catherine Wilder; Derek M Yellon; Peter Ferdinandy; Gerd Heusch Journal: Basic Res Cardiol Date: 2018-08-17 Impact factor: 17.165
Authors: Rodrigue Garcia; Mathilde Clouard; Fabian Plank; Bruno Degand; Séverine Philibert; Gabriel Laurent; Pierre Poupin; Saliman Sakhy; Matthieu Gras; Markus Stühlinger; Nándor Szegedi; Szilvia Herczeg; Judit Simon; Harry J G M Crijns; Eloi Marijon; Luc Christiaens; Charles Guenancia Journal: Front Cardiovasc Med Date: 2022-09-26