Introduction
Mitral valve (MV) prolapse (MVP), as the most common finding in degenerative mitral regurgitation, is defined by superior displacement during systole of the free edge of leaflet beyond the annular level, resulting in coaptation failure and mitral regurgitation (MR).[1, 2] Conventional two-dimensional (2D) echocardiographic studies showed it frequently accompanied with varied degrees of annular dilation, leaflet redundancy, and chordal dysfunction.[3, 4]
MVP tends to progress over time with increase in volume overload. Moreover, left ventricular remodelling can begin with even mild MR as a continuous adaptive process to volume overload and progresses that paralleled to MR severity. [5-7]
Three-dimensional (3D) transesophageal echocardiography (TEE) could provide excellent images of MV apparatus and accurate measurements of the mitral complex and has increase our understanding of DMR disease. Recent study using 3D TEE has revealed that left ventricular remodelling in MVP patients can exacerbate mal-coaptation through apical tethering of non-prolapsed leaflet segments, constituting a vicious MR-tethering cycle.[8] Subsequently, leaflet tethering in MVP patients has been reported to be associated with residual MR after surgical repair and transcatheter edge-to-edge repair.[9-11] However, it remains unclear about how severe the MR is when the MR-tethering cycle is triggered. One of the possible reasons may be lack of specific criteria for differentiating normal from pathological leaflet tethering in MVP patients. Indeed, limitations existed with the small population and narrow spectrum of MR severity in the previous study.[8]
The goals of this study were using 3D TEE determine the association between vena contracta area (VCA) and secondary leaflet tethering among MVP patients, and thus to further identify and characterize an MVP with pathological leaflet tethering (MVPt+) phenotype.