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dc.contributor.authorHan, Hui-Chen-
dc.contributor.authorParsons, Sarah A-
dc.contributor.authorCurl, Claire L-
dc.contributor.authorTeh, Andrew W-
dc.contributor.authorRaaijmakers, Antonia J A-
dc.contributor.authorKoshy, Anoop N-
dc.contributor.authorLeong, Trishe-
dc.contributor.authorBurrell, Louise Men
dc.contributor.authorO'Donnell, David-
dc.contributor.authorVohra, Jitendra K-
dc.contributor.authorKalman, Jonathan M-
dc.contributor.authorSanders, Prashanthan-
dc.contributor.authorHare, David L-
dc.contributor.authorFarouque, Omar-
dc.contributor.authorDelbridge, Lea M D-
dc.contributor.authorLim, Han S-
dc.identifier.citationHeart Rhythm 2020; online first: 24 Decemberen
dc.description.abstractCardiac fibrosis in mitral valve prolapse (MVP) is implicated in the development of sudden cardiac death (SCD), however, the pattern remains poorly characterized. This study aimed 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. 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 non-cardiac 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-epicardial distribution of fibrosis within the LV was specifically characterized. There were 17 cases with iMVP-SCD matched 1:1 with 17 controls yielding 149 samples and 1,788 histological regions. The iMVP-SCD group had increased left ventricular (anterior, lateral and posterior; all p<0.001) and interventricular septum fibrosis (p<0.001), but similar amounts of right ventricular fibrosis (p=0.62) compared to controls. In iMVP-SCD, left ventricular fibrosis was significantly higher in the lateral and posterior wall compared to the anterior wall and interventricular septum (all p<0.001). Within the lateral and posterior wall, iMVP-SCD cases had a significant endocardial-to-epicardial gradient of cardiac fibrosis (p<0.01) similar to other known conditions which cause cardiac remodeling. Our study indicates that non-uniform left ventricular remodeling with both localized and generalized left ventricular fibrosis is important in the pathogenesis of SCD in individuals with MVP.en
dc.subjectcardiac fibrosisen
dc.subjectmitral valve diseaseen
dc.subjectmitral valve prolapseen
dc.subjectsudden deathen
dc.subjectvalvular heart diseaseen
dc.titleSystematic Quantification of Histological Ventricular Fibrosis in Isolated Mitral Valve Prolapse and Sudden Cardiac Death.en
dc.typeJournal Articleen
dc.identifier.journaltitleHeart Rhythmen
dc.identifier.affiliationDepartment of Cardiology, Eastern Health and Monash University, Victoria, Australiaen
dc.identifier.affiliationDepartment of Cardiology, Northern Health and University of Melbourne, Victoria, Australiaen
dc.identifier.affiliationVictorian Institute of Forensic Medicine and Monash University Department of Forensic Medicine, Victoria, Australiaen
dc.identifier.affiliationDepartment of Cardiology, Royal Melbourne Hospital and University of Melbourne, Victoria, Australiaen
dc.identifier.affiliationDepartment of Physiology, University of Melbourne, Victoria, Australiaen
dc.identifier.affiliationCentre for Heart Rhythm Disorders, University of Adelaide and Royal Adelaide Hospital, South Australia, Australiaen
dc.identifier.affiliationMedicine (University of Melbourne)en
dc.identifier.affiliationAnatomical Pathologyen
dc.identifier.affiliationUniversity of Melbourne, Victoria, Australiaen
dc.identifier.pubmedid33359875, Louise M
item.fulltextNo Fulltext-
item.openairetypeJournal Article-
item.grantfulltextnone- Medicine- (University of Melbourne)-
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