Patient-Specific Analysis of Ventricular Vortex Formation and Flow Energetics in Rheumatic and Calcific Mitral Stenosis

Abstract Purpose Mitral stenosis (MS) accounts for 12% of cardiac patients with single valve disease. There are two main causes: rheumatic disease of the mitral valve (MV) and mitral annular calcification (MAC). While both result in increased transmitral pressure gradients, each has unique effects on valve morphology and pathophysiology. We aimed to study differences in transmitral vortex formation and stroke energetics between the two valve types. We created an in silico experimental system using an immersed finite element-finite difference fluid-structure interaction (FSI) scheme and performed three-dimensional flow field analysis. Materials and Methods Patient-specific, echocardiographic-derived geometries from a healthy MV, a MAC-associated MS valve, and a rheumatic disease-associated MS (RMS) valve were translated into finite element meshes and situated within a left ventricle model driven by a pump-approximating pressure boundary condition at 70 bpm and cardiac outputs of 1.5, 3, 3.5, and 5 L/min over eight cycles. Results RMS had smaller geometric and effective orifice areas than MAC, but the RMS–MAC differences in mean transmitral pressure gradient and peak transmitral velocity depended on cardiac output. Across equivalent cardiac output conditions, the MAC case required greater pump stroke work and exhibited higher three-dimensional ventricular kinetic energy and viscous energy dissipation than the RMS case. Both diseased cases showed disrupted mitral vortex formation. Conclusion Three-dimensional FSI simulations suggest that MAC-associated MS may impose a greater energetic burden on ventricular flow than RMS, revealing etiology-specific hemodynamic signatures and providing potential mechanistic insight for improved characterization of MS, warranting further investigation with an expanded valve cohort.