Computational Analysis of Flow Structures in Turbulent Ventricular Blood Flow Associated With Mitral Valve Intervention

Abstract

Cardiac disease and clinical intervention may both lead to an increased risk for thrombosis events due to a modified blood flow in the heart, and thereby a change in the mechanical stimuli of blood cells passing through the chambers of the heart. Specifically, the degree of platelet activation is influenced by the level and type of mechanical stresses in the blood flow. In this article we analyze the blood flow in the left ventricle of the heart through a computational model constructed from patient-specific data. The blood flow in the ventricle is modelled by the Navier-Stokes equations, and the flow through the mitral valve by a parameterized model which represents the projected opening of the valve. A finite element method is used to solve the equations, from which a simulation of the velocity and pressure of the blood flow is constructed. The intraventricular blood flow is complex, in particular in diastole when the inflow jet from the atrium breaks down into turbulent flow on a range of scales. A triple decomposition of the velocity gradient tensor is then used to distinguish between rigid body rotational flow, irrotational straining flow, and shear flow. The triple decomposition enables the separation of three fundamentally different flow structures, that each generates a distinct type of mechanical stimulus on the blood cells in the flow. We compare the results in a simulation where a mitral valve clip intervention is modelled, which leads to a significant modification of the intraventricular flow. Further, we perform a sensitivity study of the results with respect to the positioning of the clip. It was found that the shear in the simulation cases treated with clips increased more compared to the untreated case than the rotation and strain did. A decrease in valve opening area of 64% in one of the cases led to a 90% increase in rotation and strain, but a 150% increase in shear. The computational analysis opens up for improvements in models of shear-induced platelet activation, by offering an algorithm to distinguish shear from other modalities in intraventricular blood flow.

Management of Intracranial Hemorrhage in the Setting of Mechanical Heart Valve Replacement Therapy

“…Slow blood flow Turbulence Incomplete apposition [80,81], Hypercoagulability [82,83], Turbulence [84,85], and Incomplete apposition [86,87] can be found through the cited sources. See [2] for a more detailed list of factors involved in prosthetic valve thrombosis.…”

“…Hemostatic and hemodynamic factors involved in the development of prosthetic valve thromboses. Additional information regarding Slow blood flow[80,81], Hypercoagulability[82,83], Turbulence[84,85], and Incomplete apposition[86,87] can be found through the cited sources. See[2] for a more detailed list of factors involved in prosthetic valve thrombosis.…”

A mathematical model that integrates cardiac electrophysiology, mechanics, and fluid dynamics: Application to the human left heart

“…Several mathematical and numerical heart models have been proposed in recent years. Most of them focus on some specific feature of the heart function, by surrogating the remaining ones with models of reduced dimensionality: electrophysiology, 13–20 cardiac mechanics and electromechanics 2,21–33 or computational fluid dynamics (CFD) of the blood 4,34–43 . Only few works also consider the interplay between hemodynamics and cardiac mechanics in a fluid–structure interaction (FSI) framework, 44–48 while neglecting or simplifying the electrical processes generating the contraction 49–52 …”

“…Most of them focus on some specific feature of the heart function, by surrogating the remaining ones with models of reduced dimensionality: electrophysiology, [13][14][15][16][17][18][19][20] cardiac mechanics and electromechanics 2,[21][22][23][24][25][26][27][28][29][30][31][32][33] or computational fluid dynamics (CFD) of the blood. 4,[34][35][36][37][38][39][40][41][42][43] Only few works also consider the interplay between hemodynamics and cardiac mechanics in a fluid-structure interaction (FSI) framework, [44][45][46][47][48] while neglecting or simplifying the electrical processes generating the contraction. [49][50][51][52] Albeit each of the above-mentioned models can provide meaningful insight into the cardiac function in both healthy and pathological conditions, they often neglect the feedback mechanisms that relate the different components.…”