Mixed Valvular Disease Following Transcatheter Aortic Valve Replacement: Quantification and Systematic Differentiation Using Clinical Measurements and Image‐Based Patient‐Specific In Silico Modeling

Abstract

Background Mixed valvular disease (MVD), mitral regurgitation (MR) from pre‐existing disease in conjunction with paravalvular leak (PVL) following transcatheter aortic valve replacement (TAVR), is one of the most important stimuli for left ventricle (LV) dysfunction, associated with cardiac mortality. Despite the prevalence of MVD, the quantitative understanding of the interplay between pre‐existing MVD, PVL, LV, and post‐TAVR recovery is meager. Methods and Results We quantified the effects of MVD on valvular‐ventricular hemodynamics using an image‐based patient‐specific computational framework in 72 MVD patients. Doppler pressure was reduced by TAVR (mean, 77%; N=72; P <0.05), but it was not always accompanied by improvements in LV workload. TAVR had no effect on LV workload in 22 patients, and LV workload post‐TAVR significantly rose in 32 other patients. TAVR reduced LV workload in only 18 patients (25%). PVL significantly alters LV flow and increases shear stress on transcatheter aortic valve leaflets. It interacts with mitral inflow and elevates shear stresses on mitral valve and is one of the main contributors in worsening of MR post‐TAVR. MR worsened in 32 patients post‐TAVR and did not improve in 18 other patients. Conclusions PVL limits the benefit of TAVR by increasing LV load and worsening of MR and heart failure. Post‐TAVR, most MVD patients (75% of N=72; P <0.05) showed no improvements or even worsening of LV workload, whereas the majority of patients with PVL, but without that pre‐existing MR condition (60% of N=48; P <0.05), showed improvements in LV workload. MR and its exacerbation by PVL may hinder the success of TAVR.

A diagnostic, monitoring, and predictive tool for patients with complex valvular, vascular and ventricular diseases

“…In the second step, R SA , C SVC , and C ao were optimized so that maximum and minimum of the aorta pressure were respectively equal to the systolic and diastolic pressures measured using a sphygmomanometer in each patient. Table 2 for patients characteristics) between 2011 and 2018 at St. Joseph's Healthcare and Hamilton Health Sciences (Hamilton, ON, Canada) and Hospital Universitario Marques de Valdecilla (IDIVAL, Santander, Spain) were retrospectively considered 6 . The protocols were reviewed and approved by the Institutional Review Boards of each institution as follows: the Hamilton Integrated Research Ethics Board (HiREB) of Hamilton Health Sciences and St. Joseph's Healthcare, both affiliated to McMaster University and Comité de ética de la investigación con medicamentos de Cantabria of the Hospital Universitario Marques de Valdecilla.…”

“…The development and validation of the proposed method require the retrospective clinical data routinely measured in clinics (Doppler ultrasound and catheter data). These data were transferred as the de-identified & anonymized data from St. Joseph's Healthcare and Hamilton Health Sciences (Hamilton, ON, Canada) and Hospital Universitario Marques de Valdecilla (IDIVAL, Santander, Spain) 6 . The code and the optimization algorithm used for C3VI-CMF are available from the author upon request.…”

“…Validation of C3VI-CMF, against cardiac catheterization in forty-nine patients with complex cardiovascular diseases, showed very good agreement with the measurements.prediction of effects of interventions, allowing timely and personalized interventions, and helping critical clinical decision making about life-threatening risks based on quantitative data.The heart resides in a sophisticated vascular network whose loads impose boundary conditions on the heart function 6,7,14-16 . Effective diagnosis and prediction hinge on quantifications of the global hemodynamics (heart workload) and of the local hemodynamics (detailed information of the dynamics of the circulatory system, e.g., flow and pressure) of the cardiovascular system as all are very important for long-term health of the heart 6,14,16 . However, there is no method to invasively or noninvasively quantify the heart workload (global hemodynamics) and to provide contribution breakdown of each component of the cardiovascular diseases.…”

“…It is expected to remain the first cause of death by 2030 in the world 1 . Complex valvular-vascular-ventricular interactions (C3VI) is the most general and fundamentally challenging condition in which multiple valvular, vascular and ventricular pathologies have mechanical interactions with one another wherein physical phenomena associated with each pathology amplify effects of others on the cardiovascular system [2][3][4][5][6] . Examples of components of C3VI include: valvular disease (e.g., aortic valve stenosis, mitral valve stenosis, aortic valve regurgitation and mitral valve insufficiency), ventricular disease (e.g., left ventricle dysfunction and heart failure), vascular disease (e.g., hypertension), paravalvular leaks, and LV outflow tract obstruction in patients with implanted cardiovascular devices such as transcatheter valve replacement (TVR), changes due to surgical procedures for C3VI (e.g., valve replacement and left ventricular reconstructive surgery) and etc 2,[4][5][6][7] .…”

Towards non-invasive computational-mechanics and imaging-based diagnostic framework for personalized cardiology for coarctation

“…The heart resides in a sophisticated vascular network whose loads impose boundary conditions on the heart function 6,7,[10][11][12] . Effective diagnosis of COA hinges on: (1) quantifications of the global hemodynamics (heart function metrics, e.g., left ventricle workload and instantaneous pressure), and (2) quantifications of the local hemodynamics (detailed information of the 3-D flow dynamics in COA).…”