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In the field of cardiology, the current ability to accurately detect diastolic dysfunction is unsatisfactory due to the lack of an effective diagnostic index. Currently, assessments of diastolic dysfunction are based on echocardiographic measurements that are assumed to be correlated with progression from mild dysfunction to more severe disease. However, relying on existing ultrasonic indices for diagnosis of diastolic failure leads us to underestimate the progress of dysfunction. The presence of vortical flow that develops along with a strong propulsive trans-mitral jet during diastole in a normal left ventricle has been demonstrated by different imaging modalities. Thus, physical characteristics of these vortical structures may provide more effective indices of diastolic function than existing ones. In the first few chapters of this thesis, I fully describe the relationship between physical characteristics of these vortices and the dynamics of mitral valve during diastole. We found that regardless of the valve size and the pressure drop time-constant, the mitral annuls recoil computed would be maximized when the trans-mitral vortex ring pinches off in a range of formation time between three and five.
In chapter five, I introduce a novel technique that can estimate the viscoelastic properties of the left ventricle based on harmonic behavior of the ventricular chamber. Elastic deformations resulting from the changes in the ventricular mechanical properties of myocardium are represented as a time-varying spring, while the viscous components of the model include a time-varying viscous damper, representing relaxation and the frictional energy loss.
In the final chapter, I discussed about effect of isovolumic relaxation phase on diastolic rapid filling in the process of post-infarction cardiac remodeling in sheep. The results of this study confirmed that the post-infarction changes in isovolumic relaxation phase have direct influence on diastolic rapid filling phase, which leads to complex variations in end-diastolic lengthening and end-systolic shortening of the LV contractile elements.