A virtual sizing tool for mitral valve annuloplasty.

Functional mitral regurgitation, a backward leakage of the mitral valve, is a result of left ventricular growth and mitral annular dilatation. Its gold standard treatment is mitral annuloplasty, the surgical reduction in mitral annular area through the implantation of annuloplasty rings. Recurrent regurgitation rates may, however, be as high as 30% and more. While the degree of annular downsizing has been linked to improved long-term outcomes, too aggressive downsizing increases the risk of ring dehiscences and significantly impairs repair durability. Here, we prototype a virtual sizing tool to quantify changes in annular dimensions, surgically induced tissue strains, mitral annular stretches, and suture forces in response to mitral annuloplasty. We create a computational model of dilated cardiomyopathy onto which we virtually implant annuloplasty rings of different sizes. Our simulations confirm the common intuition that smaller rings are more invasive to the surrounding tissue, induce higher strains, and require larger suture forces than larger rings: The total suture force was 2.2 N for a 24-mm ring, 1.9 N for a 28-mm ring, and 0.8 N for a 32-mm ring. Our model predicts the highest risk of dehiscence in the septal and postero-lateral annulus where suture forces are maximal. These regions co-localize with regional peaks in myocardial strain and annular stretch. Our study illustrates the potential of realistic predictive simulations in cardiac surgery to identify areas at risk for dehiscence, guide the selection of ring size and shape, rationalize the design of smart annuloplasty rings and, ultimately, improve long-term outcomes after surgical mitral annuloplasty. Copyright © 2016 John Wiley & Sons, Ltd.

Partial LVAD restores ventricular outputs and normalizes LV but not RV stress distributions in the acutely failing heart in silico.

PURPOSE: Heart failure is a worldwide epidemic that is unlikely to change as the population ages and life expectancy increases. We sought to detail significant recent improvements to the Dassault Systèmes Living Heart Model (LHM) and use the LHM to compute left ventricular (LV) and right ventricular (RV) myofiber stress distributions under the following 4 conditions: (1) normal cardiac function; (2) acute left heart failure (ALHF); (3) ALHF treated using an LV assist device (LVAD) flow rate of 2 L/min; and (4) ALHF treated using an LVAD flow rate of 4.5 L/min. METHODS AND RESULTS: Incorporating improved systolic myocardial material properties in the LHM resulted in its ability to simulate the Frank-Starling law of the heart. We decreased myocardial contractility in the LV myocardium so that LV ejection fraction decreased from 56% to 28%. This caused mean LV end diastolic (ED) stress to increase to 508% of normal, mean LV end systolic (ES) stress to increase to 113% of normal, mean RV ED stress to decrease to 94% of normal and RV ES to increase to 570% of normal. When ALHF in the model was treated with an LVAD flow rate of 4.5 L/min, most stress results normalized. Mean LV ED stress became 85% of normal, mean LV ES stress became 109% of normal and mean RV ED stress became 95% of normal. However, mean RV ES stress improved less dramatically (to 342% of normal values). CONCLUSIONS: These simulations strongly suggest that an LVAD is effective in normalizing LV stresses but not RV stresses that become elevated as a result of ALHF.

Human Cardiac Function Simulator for the Optimal Design of a Novel Annuloplasty Ring with a Sub-valvular Element for Correction of Ischemic Mitral Regurgitation.

Ischemic mitral regurgitation is associated with substantial risk of death. We sought to: (1) detail significant recent improvements to the Dassault Systèmes human cardiac function simulator (HCFS); (2) use the HCFS to simulate normal cardiac function as well as pathologic function in the setting of posterior left ventricular (LV) papillary muscle infarction; and (3) debut our novel device for correction of ischemic mitral regurgitation. We synthesized two recent studies of human myocardial mechanics. The first study presented the robust and integrative finite element HCFS. Its primary limitation was its poor diastolic performance with an LV ejection fraction below 20% caused by overly stiff ex vivo porcine tissue parameters. The second study derived improved diastolic myocardial material parameters using in vivo MRI data from five normal human subjects. We combined these models to simulate ischemic mitral regurgitation by computationally infarcting an LV region including the posterior papillary muscle. Contact between our novel device and the mitral valve apparatus was simulated using Dassault Systèmes SIMULIA software. Incorporating improved cardiac geometry and diastolic myocardial material properties in the HCFS resulted in a realistic LV ejection fraction of 55%. Simulating infarction of posterior papillary muscle caused regurgitant mitral valve mechanics. Implementation of our novel device corrected valve dysfunction. Improvements in the current study to the HCFS permit increasingly accurate study of myocardial mechanics. The first application of this simulator to abnormal human cardiac function suggests that our novel annuloplasty ring with a sub-valvular element will correct ischemic mitral regurgitation.

The Living Heart Project: A robust and integrative simulator for human heart function.

The heart is not only our most vital, but also our most complex organ: Precisely controlled by the interplay of electrical and mechanical fields, it consists of four chambers and four valves, which act in concert to regulate its filling, ejection, and overall pump function. While numerous computational models exist to study either the electrical or the mechanical response of its individual chambers, the integrative electro-mechanical response of the whole heart remains poorly understood. Here we present a proof-of-concept simulator for a four-chamber human heart model created from computer topography and magnetic resonance images. We illustrate the governing equations of excitation-contraction coupling and discretize them using a single, unified finite element environment. To illustrate the basic features of our model, we visualize the electrical potential and the mechanical deformation across the human heart throughout its cardiac cycle. To compare our simulation against common metrics of cardiac function, we extract the pressure-volume relationship and show that it agrees well with clinical observations. Our prototype model allows us to explore and understand the key features, physics, and technologies to create an integrative, predictive model of the living human heart. Ultimately, our simulator will open opportunities to probe landscapes of clinical parameters, and guide device design and treatment planning in cardiac diseases such as stenosis, regurgitation, or prolapse of the aortic, pulmonary, tricuspid, or mitral valve.