Abstract 20501: Left Ventricular Flow Dynamics in the Presence of Severe Mitral Annular Calcification - An In Vitro Study
Introduction: Normal flow patterns within the left ventricle (LV) optimize energy efficiency. Cardiac disease leads to disturbed flow and suboptimal LV performance. Mitral annular calcification (MAC) is common in the elderly and those with renal insufficiency and occasionally causes mitral stenosis or regurgitation. However, its effects on LV flow patterns have not been explored.
Objective: To investigate the effects of MAC on LV flow dynamics and viscous energy losses using a patient-specific 3D print of a MAC valve placed in a cardiac simulator.
Methods: Full-volume 3D TEE images of the mitral valve were acquired in a patient with severe MAC. Images were exported in Cartesian format and loaded into ITK-SNAP (Version 3.4.0-rc1) open source software. The valve was segmented, from annulus to leaflet tip, in early diastole. Surface meshes of the segmented structures were converted to stereolithography files and 3D printed to produce an exact replica of the patient’s valve in silicone. This was then tested in a double-pulse duplicator under physiological conditions. The velocity field in the LV was investigated using time-resolved particle image velocimetry (PIV) and compared with normal LV flow (measured with a bioprosthetic valve placed in the duplicator). Velocity measurements were used to evaluate the time evolution of viscous energy loss in the LV.
Results: LV flow patterns were significantly altered in the presence of MAC compared to the normal case. Severe MAC produced a turbulent jet which entered the LV with a peak velocity as high as 1.3 m/s vs. 0.6 m/s in the normal situation. The viscous energy loss in the LV was ~10 times greater with severe MAC when compared to normal (0.0237 vs. 0.0023 W/m, p < 0.001).
Conclusions: The presence of mitral annular calcification disturbs flow in the LV leading to markedly increased viscous energy losses. This contributes to suboptimal LV pumping function and might explain symptoms of dyspnea and fatigue in affected patients.
Author Disclosures: B. El Sayegh: None. G. DiLabbio: None. G.S. Pressman: None. E. Obasare: None. L. Kadem: None.
- © 2016 by American Heart Association, Inc.