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The goal of this study is to understand the role of structural-and-functional inhomogeneity (SFI) in the left ventricular (LV) wall. According to the peculiarities of heart diseases development, we supposed the existence of causal relationship between SFI and the heart functional reserve, i.e. an ability to maintain pump function in case of additional load. Here, we looked into the functional aspect of SFI phenomenon. Sixteen IHD patients with a different extent of coronary artery stenotic lesion were chosen for this investigation. The patients were underwent the transesophageal ultrasound examinations, and LV 3D reconstruction was performed. To estimate the extent of the functional non-uniformity, the myocardium elastic properties in LV wall regions and LV regional motion were defined. We found out a strong inverse correlation between the extent of LV functional non-uniformity and the heart functional reserve, estimated as a patients' tolerance to physical load. We concluded that the transition of functional myocardium non-uniformity due to IHD development reflects the exhaust of heart functional reserve.
The main objective of this work is to study the effect of blood pressure and viscosity on flow in a pathological and healthy anatomy. The method chosen for this project is the numerical simulation of fluid dynamics. First, a radiological database from Tlemcen hospital was studied in order to select a patient whose aortic anatomy is representative of the pathology studied in this research project. The left ventricle was segmented using SolidWork software. The exported data made it possible to model this geometry on Comsol software. The geometry has been idealized to make it comparable to a given healthy left ventricle geometry and present the main parameters which influence the ventricular hemodynamics. A first series of numerical simulations made it possible to highlight the hemodynamic disturbances associated with the pathology of interest and described extensively in the literature. A second series of numerical simulations made it possible to model the effect of blood viscosity on flow. All the results obtained, the modeling of the left ventricle, must be valid experimentally. This study therefore does not completely justify the treatment of ventricular dilation with a flow modulator but constitutes an important first step towards a proof of concept.