Impact of Dynamic Mitral Annular Deformation on Systolic Anterior Motion in Patients With Hypertrophic Cardiomyopathy

The role of annular deformation on mitral valve systolic anterior motion (SAM) is unclear. We aimed to examine the contribution of mitral annular deformation to the pathophysiology of SAM using 3-D echocardiography, as well as assess the relationship between mitral annular deformation and SAM and explore its impact on left ventricular outflow tract (LVOT) obstruction in hypertrophic cardiomyopathy (HCM).

A 3-D echocardiography database was examined for patients with HCM. Patients were divided into two groups based on the presence of SAM, and mitral annular geometry was quantified and compared in SAM versus non-SAM patients. In total, 55 HCM patients (SAM group N = 27, non-SAM group N = 28) and 29 healthy controls were included. Mitral annular diameter, coaptation-to-septum distance and coaptation-to-anterior annulus (C-Ant MA) distance were measured at end diastole (ED) and late systole (LS). The dynamic residual anterior leaflet (DRAL), reflecting SAM involvement, was calculated as DRAL = (C-Ant MA ED) - (C-Ant MA LS). Mitral annular area deformation was quantified using 3-D echocardiography. Segmental wall motion was assessed using 3-D strain analysis, measuring longitudinal/radial strain and displacement in the basal anterior, basal anterior-lateral, basal inferior-lateral and basal inferior walls.

Compared with the non-SAM and control groups, the SAM group showed reduced mitral annular deformation (all p < 0.001), smaller coaptation-to-septum distance at ED and LS (p < 0.001) and increased DRAL (p < 0.001), which correlated with annular area deformation (R = 0.65) and LVOT gradient (R = 0.79). Radial strain and displacement in basal anterior-lateral and inferior-lateral segments were higher in the SAM group (p < 0.05).

Deformation of the mitral annulus is associated with SAM and LVOT gradient. Mitral annular deformation in SAM relates to greater left ventricular basal lateral wall radial displacement compared with non-SAM. These findings suggest a novel mechanism for SAM and LVOT obstruction in hypertrophic cardiomyopathy.