Evaluation of mitral valve dynamics.

Mitral valve (mv) repair is the preferred treatment for patients with mv insufficiency. The unsolved problem in MV repair surgery is predicting the optimal repair for each patient. This is in part due to lack of physiological imaging modalities to provide this information prior to or at the time of valve repair. Moreover, the majority of cases have complex pathophysiological involvement including annular enlargement, chordal lengthening, chordal rupture, calcification, and ultimately lack of proper leaflet coaptation. Current clinical 3-dimensional (3D) transesophageal echocardiography (TEE) can demonstrate volumetric morphology of the MV apparatus. However, biomechanical information is not available from 3D echocardiography. If imaging techniques can be combined with appropriate computational MV evaluation methods, then improved diagnosis and therapeutic approaches to MV repair can be developed. In the present study, we describe a novel comprehensive evaluation protocol to improve diagnosis and treatment of MV pathology by combining 3D TEE and computational simulation techniques (Fig. 1). Virtual MV models were created by utilizing 3D TEE data of patients with normal and pathological MVs followed by computational simulations of MV function. Computational simulations clearly demonstrated deformation and stress distribution of the MV structure across the cardiac cycle at a microsecond scale and corresponded well to 3D TEE data (Figs. 2 and ​and3,3, Online Videos 1, 2, 3, and 4). Here we present 4 case studies (1 normal and 3 different types of pathological MVs). Figure 1 Flow Chart for Virtual MV Modeling and Computational Simulation of MV Function Figure 2 Images of a Normal MV Figure 3 Images of a Pathological MV With Posterior Chordal Rupture Case 1 (Fig. 4): a normal MV demonstrated complete coaptation with no regurgitation when closed. Figure 4 Case 1: A Normal MV With Complete Coaptation; A to D (Peak Systole), E to H (End Diastole) Case 2 (Fig. 5): this MV showed mild regurgitation with relatively small annular dilation. Computational simulation indicated increased leaflet stress values and reduced contact pressure between the leaflets. Figure 5 Case 2: A Degenerative MV With Mild Regurgitation and Small Annular Dilation; A to D (Peak Systole), E to H (End Diastole) Case 3 (Fig. 6): a degenerative MV with large annular dilation demonstrated severe regurgitation by 3D Doppler TEE and the lesion corresponded to regions with no leaflet contact in the computational simulation. Figure 6 Case 3: A Degenerative MV With Severe Regurgitation and Large Annular Dilation; A to D (Peak Systole), E to H (End Diastole) Case 4 (Fig. 7): chordal rupture of this MV caused posterior leaflet prolapse inducing the regurgitant jet. Computational simulation demonstrated an extremely asymmetric and large stress distribution over the leaflets and lack of leaflet coaptation in the regurgitant region. Figure 7 Case 4: A Degenerative MV With Severe Regurgitation due to Ruptured Chordae; A to D (Peak Systole), E to H (End Diastole) Comparative studies of the normal MV (Case 1) and the pathological MV with ruptured chordae (Case 4) clearly demonstrated differences in annular reaction forces and chordal stresses (Fig. 8), and in the degree of leaflet coaptation (Fig. 9, Online Videos 5 and 6). Figure 8 Assessment of Annular Reaction Force and Chordal Stress Distribution; Normal MV (Case 1) Versus MV With Ruptured Chordae (Case 4) Figure 9 Contact Pressure Distribution Between the Leaflets; Normal MV (Case 1) Versus MV With Ruptured Chordae (Case 4) Although MV morphology obtained with 3D TEE image data may demonstrate relatively normal function with no regurgitation, the leaflets may be under extremely high stresses which can result in annular dilation and MV deterioration. Biomechanical information from computational simulation further provides information to help better understand MV pathophysiology. This novel computational strategy has the potential to predict pathophysiological alterations in MV structure, help cardiologists to quantitatively evaluate the extent and severity of MV pathology, and help surgeons to better understand MV dynamics before and following repair to determine more suitable patient-specific repair techniques.