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.