Hui-Chen Han1, Sarah A Parsons2, Claire L Curl3, Andrew W Teh4, Antonia J A Raaijmakers3, Anoop N Koshy1, Trishe Leong5, Louise M Burrell6, David O'Donnell1, Jitendra K Vohra7, Jonathan M Kalman7, Prashanthan Sanders8, David L Hare1, Omar Farouque1, Lea M D Delbridge3, Han S Lim9. 1. Department of Cardiology, Austin Health and University of Melbourne, Victoria, Australia. 2. Victorian Institute of Forensic Medicine and Monash University Department of Forensic Medicine, Victoria, Australia. 3. Department of Physiology, University of Melbourne, Victoria, Australia. 4. Department of Cardiology, Austin Health and University of Melbourne, Victoria, Australia; Department of Cardiology, Eastern Health and Monash University, Victoria, Australia. 5. Department of Anatomical Pathology, Austin Health and University of Melbourne, Victoria, Australia. 6. Department of Medicine, Austin Health and University of Melbourne, Victoria, Australia. 7. Department of Cardiology, Royal Melbourne Hospital and University of Melbourne, Victoria, Australia. 8. Centre for Heart Rhythm Disorders, University of Adelaide and Royal Adelaide Hospital, South Australia, Australia. 9. Department of Cardiology, Austin Health and University of Melbourne, Victoria, Australia; Department of Cardiology, Northern Health and University of Melbourne, Victoria, Australia. Electronic address: lim.h@unimelb.edu.au.
Abstract
BACKGROUND: Cardiac fibrosis in mitral valve prolapse (MVP) is implicated in the development of sudden cardiac death (SCD); however, the pattern remains poorly characterized. OBJECTIVE: The purpose of this study was to systematically quantify left and right ventricular fibrosis in individuals with isolated MVP and SCD (iMVP-SCD), whereby other potential causes of death are excluded, compared to a control cohort. METHODS: Individuals with iMVP-SCD were identified from the Victorian Institute of Forensic Medicine, Australia, and matched for age, sex, and body mass index to control cases with noncardiac death. Cardiac tissue sections were analyzed to determine collagen deposition in the left ventricular free wall (anterior, lateral, and posterior portions), interventricular septum, and right ventricle. Within the iMVP-SCD cases, the endocardial-to-epicardial distribution of fibrosis within the left ventricle was specifically characterized. RESULTS: Seventeen cases with iMVP-SCD were matched 1:1 with 17 controls, yielding 149 samples and 1788 histologic regions. The iMVP-SCD group had increased left ventricular (anterior, lateral, and posterior; all P <.001) and interventricular septum fibrosis (P <.001), but similar amounts of right ventricular fibrosis (P = .62) compared to controls. In iMVP-SCD, left ventricular fibrosis was significantly higher in the lateral and posterior walls compared to the anterior wall and interventricular septum (all P <.001). Within the lateral and posterior walls, iMVP-SCD cases had a significant endocardial-to-epicardial gradient of cardiac fibrosis (P <.01) similar to other known conditions that cause cardiac remodeling. CONCLUSION: Our study indicates that nonuniform left ventricular remodeling with both localized and generalized left ventricular fibrosis is important in the pathogenesis of SCD in individuals with MVP.
BACKGROUND: Cardiac fibrosis in mitral valve prolapse (MVP) is implicated in the development of sudden cardiac death (SCD); however, the pattern remains poorly characterized. OBJECTIVE: The purpose of this study was to systematically quantify left and right ventricular fibrosis in individuals with isolated MVP and SCD (iMVP-SCD), whereby other potential causes of death are excluded, compared to a control cohort. METHODS: Individuals with iMVP-SCD were identified from the Victorian Institute of Forensic Medicine, Australia, and matched for age, sex, and body mass index to control cases with noncardiac death. Cardiac tissue sections were analyzed to determine collagen deposition in the left ventricular free wall (anterior, lateral, and posterior portions), interventricular septum, and right ventricle. Within the iMVP-SCD cases, the endocardial-to-epicardial distribution of fibrosis within the left ventricle was specifically characterized. RESULTS: Seventeen cases with iMVP-SCD were matched 1:1 with 17 controls, yielding 149 samples and 1788 histologic regions. The iMVP-SCD group had increased left ventricular (anterior, lateral, and posterior; all P <.001) and interventricular septum fibrosis (P <.001), but similar amounts of right ventricular fibrosis (P = .62) compared to controls. In iMVP-SCD, left ventricular fibrosis was significantly higher in the lateral and posterior walls compared to the anterior wall and interventricular septum (all P <.001). Within the lateral and posterior walls, iMVP-SCD cases had a significant endocardial-to-epicardial gradient of cardiac fibrosis (P <.01) similar to other known conditions that cause cardiac remodeling. CONCLUSION: Our study indicates that nonuniform left ventricular remodeling with both localized and generalized left ventricular fibrosis is important in the pathogenesis of SCD in individuals with MVP.
Authors: Monica Chivulescu; Eivind W Aabel; Erik Gjertsen; Einar Hopp; Esther Scheirlynck; Bernard Cosyns; Erik Lyseggen; Thor Edvardsen; Øyvind H Lie; Lars A Dejgaard; Kristina H Haugaa Journal: Europace Date: 2022-07-21 Impact factor: 5.486
Authors: Jordan E Morningstar; Cortney Gensemer; Reece Moore; Diana Fulmer; Tyler C Beck; Christina Wang; Kelsey Moore; Lilong Guo; Franz Sieg; Yasufumi Nagata; Philippe Bertrand; Ricardo A Spampinato; Janiece Glover; Stephen Poelzing; Robert G Gourdie; Kelsey Watts; William J Richardson; Robert A Levine; Michael A Borger; Russell A Norris Journal: J Am Heart Assoc Date: 2021-12-07 Impact factor: 6.106