Department of Cardiology, Austin Health and University of Melbourne, Victoria, Australia.
Victorian Institute of Forensic Medicine and Monash University Department of Forensic Medicine, Victoria, Australia.
Heart Rhythm. 2021 Apr;18(4):570-576. doi: 10.1016/j.hrthm.2020.12.021. Epub 2020 Dec 24.
Cardiac fibrosis in mitral valve prolapse (MVP) is implicated in the development of sudden cardiac death (SCD); however, the pattern remains poorly characterized.
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.
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.
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.
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.
二尖瓣脱垂(MVP)中的心脏纤维化与心脏性猝死(SCD)的发生有关;然而,其模式仍未得到充分描述。
本研究旨在系统性地定量评估孤立性 MVP 和 SCD(iMVP-SCD)个体以及排除其他潜在死因的对照队列的左、右心室纤维化程度。
从澳大利亚维多利亚法医研究所确定 iMVP-SCD 个体,并根据年龄、性别和体重指数与非心脏性死亡的对照病例相匹配。分析心脏组织切片以确定左心室游离壁(前壁、侧壁和后壁)、室间隔和右心室的胶原沉积。在 iMVP-SCD 病例中,特别描述了左心室内心膜到心外膜的纤维化分布。
17 例 iMVP-SCD 病例与 17 例对照病例 1:1 匹配,共获得 149 个样本和 1788 个组织学区域。iMVP-SCD 组的左心室(前壁、侧壁和后壁;均 P <.001)和室间隔纤维化程度增加(P <.001),但右心室纤维化程度与对照组相似(P =.62)。在 iMVP-SCD 中,左心室侧壁和后壁的纤维化程度明显高于前壁和室间隔(均 P <.001)。在侧壁和后壁,iMVP-SCD 病例存在显著的内心膜到心外膜的心脏纤维化梯度(P <.01),与其他导致心脏重构的已知疾病相似。
本研究表明,非均匀性左心室重构伴有局灶性和弥漫性左心室纤维化是 MVP 个体 SCD 发病机制中的重要因素。