Abstract 16731: Novel CMR Anatomical Predictors of Mitral Regurgitation Presence and Severity in Mitral Valve Prolapse

Aalap Chokshi, Angelica Romero Daza, Patricia Pardo Marinez, Nicolas Maneiro Melon,Adam Jacobi,Michael Chung,Matthew Cham,Gina LaRocca, Jorge Solis Martin,Leticia Fernández Friera,Javier Sanz

Circulation(2018)

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摘要
Introduction: Mitral valve (MV) prolapse (MVP) is often associated with mitral regurgitation (MR). The determinants of MR in MVP are incompletely understood. Methods: We retrospectively identified 86 consecutive patients with MVP and preserved ejection fraction undergoing CMR with velocity encoding for MR quantification between 2005 and 2017. On 3-chamber cine images we measured, in end-diastole (Figure), end-systole, and their percentage change during the cardiac cycle, the following parameters: basal and mid inferolateral wall thickness, posterior papillary muscle length, annulus diameter, LV diameter and distance from the posterior papillary muscle to anterior and posterior annulus. In addition, we measured anterior and posterior leaflet thickness in diastole and maximal prolapse distance in end-systole. We explored the associations between these parameters and mitral regurgitant fraction (RF) using multivariate linear regression. Results: Median age was 52.6 years and 48% were males. There was posterior MVP in 49 (57%), bileaflet MVP in 35 (41%) patients, and isolated anterior MVP in 2 (2%) patients. MR was present in 73 (85%) and, in these, median RF was 23% (IQR 13-33%). In multivariate analyses, diastolic papillary muscle to posterior annulus distance, maximal prolapse distance, maximal posterior leaflet thickness, and LV basal inferolateral diastolic thickness were independent predictors of mitral RF (p<0.05 for all). Conclusions: Beyond known determinants of MR in MVP such as maximal prolapse and leaflet thickness, we identified novel anatomical predictors of MR severity, namely increased diastolic papillary muscle to posterior annulus distance and LV basal inferolateral thickness. Whether these abnormalities represent secondary changes to MVP (i.e. basal inferolateral “stretch” and compensatory regional LV hypertrophy, respectively) or primary phenotypic features of the MVP syndrome is uncertain.
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