| description abstract | The mitral valve (MV) is the left atrioventricular heart valve that regulates blood flow between the left atrium and left ventricle (LV) during the cardiac cycle. Contrary to the aortic valve (AV), the MV is an intimately coupled, fully functional part of the LV. In situations where the MV fails to fully close during systole, the resulting blood regurgitation into the left atrium typically causes pulmonary congestion, leading to heart failure and/or stroke. The causes of MV regurgitation can be either primary (e.g., myxomatous degeneration) where the valvular tissue is organically diseased, or secondary (typically induced by ischemic cardiomyopathy) termed ischemic mitral regurgitation (IMR), is brought on by adverse LV remodeling. IMR is present in up to 40% of patients and more than doubles the probability of cardiovascular morbidity after 3.5 years. There is now agreement that adjunctive procedures are required to treat IMR caused by leaflet tethering. However, there is no consensus regarding the best procedure. Multicenter registries and randomized trials would be necessary to prove which procedure is superior. Given the number of proposed procedures and the complexity and duration of such studies, it is highly unlikely that IMR procedure optimization will be achieved by prospective clinical trials. There is thus an urgent need for cell and tissue physiologically based quantitative assessments of MV function to better design surgical solutions and associated therapies. Novel computational approaches directed toward optimized surgical repair procedures can substantially reduce the need for such trial-and-error approaches. We present the details of our MV modeling techniques, with an emphasis on what is known and investigated at various length scales. Moreover, we show the state-of-the-art means to produce patient-specific MV computational models to develop quantitatively optimized devices and procedures for MV repair. | |
