LAVIs by both 2DE and 3DE are powerful predictors of future cardiac events. 3D LAVImin tended to have a stronger and additive prognostic value than 3D LAVImax.

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ObjectiveMitral annular/leaflet calcification (MALC) is frequently observed in patients with degenerative aortic stenosis (AS). However, the impact of MALC on mitral valve function has not been established. We aimed to investigate whether MALC reduces mitral annular area and restricts leaflet opening, resulting in non-rheumatic mitral stenosis.MethodsReal-time three-dimensional transoesophageal images of the mitral valve were acquired in 101 patients with degenerative AS and 26 control participants. The outer and inner borders of the mitral annular area (MAA) and the maximal leaflet opening angle were measured at early diastole. The mitral valve area (MVA) was calculated as the left ventricular stroke volume divided by the velocity time integral of the transmitral flow velocity.ResultsAlthough the outer MAA was significantly larger in patients with AS compared to control participants (8.2±1.3 vs 7.3±0.9 cm2, p<0.001), the inner MAA was significantly smaller (4.5±1.1 vs 5.9±0.9 cm2, p<0.001), resulting in an average decrease of 45% in the effective MAA. The maximal anterior and posterior leaflet opening angle was also significantly smaller in patients with AS (64±10 vs 72±8°, p<0.001, 71±12 vs 87±7°, p<0.001). Thus, MVA was significantly smaller in patients with AS (2.5±1.0 vs 3.8±0.8 cm2, p<0.001). Twenty-four (24%) patients with AS showed MVA <1.5 cm2. Multivariate regression analysis including parameters for mitral valve geometry revealed that a decrease in effective MAA and a reduced posterior leaflet opening angle were independent predictors for MVA.ConclusionsCalcific extension to the mitral valve in patients with AS reduced effective MAA and the leaflet opening, resulting in a significant non-rheumatic mitral stenosis in one-fourth of the patients.

Progressive superior shift of the mitral valve (MV) during systole is associated with abnormal papillary muscle (PM) superior shift in late systolic MV prolapse (MVP). The causal relation of these superior shifts remains unclarified. We hypothesized that the MV superior shift is related to augmented MV superiorly pushing force by systolic left ventricular pressure due to MV annular dilatation, which can be corrected by surgical MV plasty, leading to postoperative disappearance of these superior shifts. In 35 controls, 28 patients with holosystolic MVP, and 28 patients with late systolic MVP, the MV coaptation depth from the MV annulus was measured at early and late systole by two-dimensional echocardiography. The PM tip superior shift was monitored by echocardiographic speckle tracking. MV superiorly pushing force was obtained as MV annular area × (systolic blood pressure − 10). Measurements were repeated after MV plasty in 14 patients with late systolic MVP. Compared with controls and patients with holosystolic MVP, MV and PM superior shifts and MV superiorly pushing force were greater in patients with late systolic MVP [1.3 (0.5) vs. 0.9 (0.6) vs. 3.9 (1.0) mm/m2, 1.3 (0.5) vs. 1.2 (1.0) vs. 3.3 (1.3) mm/m2, and 487 (90) vs. 606 (167) vs. 742 (177) mmHg·cm2·m−2, respectively, means (SD), P < 0.001]. MV superior shift was correlated with PM superior shift ( P < 0.001), which was further related to augmented MV superiorly pushing force ( P < 0.001). MV and PM superior shift disappeared after surgical MV plasty for late systolic MVP. These data suggest that MV annulus dilatation augmenting MV superiorly pushing force may promote secondary superior shift of the MV (equal to late systolic MVP) that causes subvalvular PM traction in patients with late systolic MVP. NEW & NOTEWORTHY Late systolic mitral valve prolapse (MVP) is associated with mitral valve (MV) and papillary muscle (PM) abnormal superior shifts during systole, but the causal relation remains unclarified. MV and PM superior shifts were correlated with augmented MV superiorly pushing force by annular dilatation and disappeared after surgical MV plasty with annulus size and MV superiorly pushing force reduction. This suggests that MV annulus dilatation may promote secondary superior shifts of the MV (late systolic MVP) that cause subvalvular PM traction.

The new DD grade is frequently observed and has a prognosis similar to that of the pseudonormal group but significantly worse than that of the impaired relaxation group. However, LA booster function was maintained at the expense of LA volume enlargement. Thus, the new grade should be a distinct entity for routine DD grading.