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Background: Recent studies have shown that mitral valve leaflets enlarge as a response to increased systolic stress produced by subvalvular tenting. This adaptative mechanism is mediated by systolic leaflet stress and reduces the degree of functional mitral regurgitation. However, flow-mediated shear-stress is the most important hemodynamic force responsible for physiological development of most vascular structures. Eccentric aortic regurgitation in pts. with a bicuspid aortic valve BAV rises diastolic shear-stress on the anterior mitral leaflet during diastole and could be responsible for triggering leaflet remodeling.Objective: We aimed to characterize mitral valve geometry in patients with (BAV) with and without aortic regurgitation (AR).Methods: 50 patients (43 ± 14 years old, 82% male) with BAV were studied. Mitral valve annular diameter (MAD), leaflet length and thickness, leaflet coaptation pattern (% of anterior leaflet projection onto the MAD), tenting area (area between leaftet and mitral annulus) and LV volumes were measured using 2D echocardiography. AR was graded as absent or nonsignificant (Group I), or moderate or severe (Group II), based on American Society Echocardiography guidelines.Results: 19 patients had significant AR; these GII patients showed significantly higher values of anterior leaflet length compared with GI (4.6 ± 0.3 vs. 3.5 ± 0.5 cm p <0.001). This caused posterior displacement of the coaptation point (72 ± 6 vs. 59 ± 12 %. p <0.001). Valve thickness was not different between both groups. Despite larger LV volumes in GII (143 ± 60 vs 105 ± 35 ml, p= 0.01), tethering forces were not higher (tenting area GI:1.9 ± 0.2 vs GII:1.01 ± 0.2 cm2. p = 0.5). In a multivariate linear regression analysis we observed an independent association between the grade of AR and the length of the anterior leaflet and not to the LV diastolic volumes.Conclusion: Diastolic shear-stress on the mitral valve is associated with remodeling changes in mitral valve geometry. Diastolic jet impact seems responsible of anterior mitral length enlargement and posterior displacement of coaptation point. These changes in mitral valve geometry are independent of tethering forces. This hemodynamic mechanism and not intrinsic congenital abnormalities are most probably responsible for abnormal mitral structural findings frequently observed in patients with BAV.