Determinants of degenerative mitral regurgitation severity
MR severity for MVP patients varies from trivial to severe according to the failure of coaptation driven by leaflet prolapse or chordal elongation and annular enlargement. [3, 15] It tends to progress over time with increase in volume overload (regurgitant volume) due to increase in regurgitant orifice. Progression of MVP is determined by progression of lesions, particular a new flail leaflet, or mitral annulus size. [4, 16] In addition, left ventricular enlargement is a continuous adaptive process that begins with even mild MR and progresses paralleled to MR severity.[5, 17, 18]
Otani et al. first reported AML tenting volume was proportional to papillary muscle displacement attributed to both annular and LV dilatation, suggesting that degenerative MV prolapse causes secondary LV dilatation and mitral leaflet tethering, especially in non-prolapsed leaflets. [8] More recently, Morningstar[19] et al demonstrated that mechanical changes induced by a prolapsing valve can engender fibrosis within the inferobasal wall and attached PM that are physically and mechanically linked to the prolapsing leaflets. These changes may also contribute to leaflet tethering in MVP.[20]
Previous studies have revealed that prolapse and tenting volume, annular dimension and AHCWR correlated with MR severity in MVP patients.[4, 7] We tested these factors in the multivariate model and found that only PVi and TVi was associated with 3D VCA, independent of annular dimension. Indeed, in functional MR (FMR), isolated annular dilation does not usually cause important MR without leaflet tethering caused by LV dilation and dysfunction.[8, 21] Although annular dilation is not the most significant determinant of 3D VCA, it contributed to the severity of leaflet tethering. [8]
Despite further annular dilatation, our MVPt+ group showed similar AHCWR with normal controls and MVPt- patients. Flattening of annular saddle shape is commonly seen in MAD patients as an intrinsic annular abnormality, which is our exclusion criteria for the current study. Flattening of annular saddle shape also recently has been demonstrated to be correlated with reduction of LV longitudinal contraction (GLS) in atrial FMR. [22, 23] Indeed, annular saddle shape is more preserved in FED phenotype[6], which represents the majority of our patients.
It had been widely accepted that leaflet tethering plays a fundamental role in the pathogenesis of FMR[12, 21], whereas leaflet tethering in MVP patients was not commonly recognized until Otani et al. Although Otani et al[12] firstly elaborated the mechanism, limitations existed with the small population and narrow spectrum of MR severity in the previous study. Furthermore, data on clinical and echocardiographic characteristics MVPt+ patients are sparse. One of the reasons may be attributed to lack of specific criteria for differentiating normal from pathological leaflet tethering in MVP patients.
Under normal physiological circumstances, longitudinal LV fiber contraction translates the posterior annulus apically during the systole as to fold the annulus into a saddle shape. Accordingly, the anterior annulus has to tilt posteriorly, thus made the anterior leaflet tethered at the aortic root.[24, 25]The value of TVi in healthy controls and MVPt- group represents the above conformational changes of the anterior leaflet.
Our study also suggested that within MVP patients both AML and PML could occur secondary leaflet tethering, as quantitated by TVi and leaflet angle. Reduction of PML TVi and leaflet angle in MVPt- patients was probably a morphological consequence of PML prolapse.