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Competing Interests: Competing interests: None declared.

The mechanism of systolic annular expansion in mitral valve prolapse (MVP) is not clarified. Since annular expansion is systolic outward shift of MV leaflet/chorda tissue complex at superior and outer ends, annular expansion could be related to inward (superior) shift of the complex at another inferior and inner end of the papillary muscle (PM) tip and/or systolic lengthening of the tissue complex, especially MV leaflets.MV annulus systolic expansion, PMs' systolic superior shift, and MV leaflets' systolic lengthening were evaluated by echocardiography with a speckle tracking analysis in 25 normal subjects, 25 subjects with holo-systolic MVP and 20 subjects with late-systolic MVP.PMs' superior shift, MV leaflets' lengthening, MV annular area at the onset of systole and subsequent MV annulus expansion were significantly greater in late-systolic MVP than in holo-systolic MVP (4.6 ± 1.6 versus 1.5 ± 0.7 mm/m 2 , 2.5 ± 1.4 versus 0.6 ± 2.0 mm/m 2 , 6.8 ± 2.5 versus 5.7 ± 1.0 cm 2 /m 2 and 1.6 ± 0.8 versus 0.1 ± 0.5 cm 2 /m 2 , P < 0.001, respectively). Multivariate analysis identified MV leaflets' lengthening and PMs' superior shift as independent factors associated with MV annular expansion.Conclusions: These results suggest that systolic MV annular expansion in MVP is related to abnormal MV leaflets' lengthening and PMs' superior shift.

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/m 2 , 1.3 (0.5) vs. 1.2 (1.0) vs. 3.3 (1.3) mm/m 2 , and 487 (90) vs. 606 (167) vs. 742 (177) mmHg·cm 2 ·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.

Background: Prominent mitral valve (MV) annular dilatation with only modest left ventricular (LV) dilatation in patients with MV prolapse (MVP) suggests predominant dilatation in adjacent basal LV, which may augment regional wall tension and attenuate contraction by Laplace's law. We hypothesized that MV annular dilatation in patients with MVP is associated with the basal predominance of LV dilatation and attenuated contraction, which can be altered by surgical MV plasty with annulus reduction., Methods and Results: Echocardiography with speckle-tracking analysis to assess regional cross-sectional short-axis area and longitudinal contraction (strain) of basal, middle, and apical LV was performed in 30 controls and 130 patients with MVP. The basal value/averaged middle and apical values (B/M·A ratio) of LV cross-sectional area and strain were obtained. Patients with MVP showed significantly greater MV annular area (6.4±1.6 versus 3.7±0.6 cm 2 /m 2 ), increased B/M·A LV area ratio (2.4±0.5 versus 1.8±0.2), and reduced B/M·A LV strain ratio (0.83±0.14 versus 0.96±0.09) than controls (P<0.001). Multivariable analyses identified that MV annular dilatation was independently associated with increased B/M·A LV area ratio (β=0.60, P<0.001), which was associated with reduced B/M·A LV strain ratio (β=-0.32, P<0.001). In 35 patients with MVP, B/M·A LV area and strain ratio significantly altered after surgical MV plasty with annulus reduction (2.5±0.5-1.8±0.3 and 0.73±0.10-0.89±0.17, P<0.001, respectively)., Conclusions: In patients with MVP, MV annular dilatation was associated with the basal predominance of LV dilatation and reduced contraction, which can be altered by surgical MV plasty with annulus reduction, suggesting unfavorable influence from MV annular dilatation on basal LV., (© 2016 American Heart Association, Inc.)