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.