Cardiovascular Biomechanics
Hadi Taghizadeh; Faezeh Amini
Volume 16, Issue 1 , May 2022, , Pages 11-21
Abstract
Atherosclerosis, a common cardiovascular disease, is among the leading causes of death. Many of the heart attacks results from ruptured atherosclerotic lesion and emboli formation. Then, the susceptibility of the lesion is a key factor in preventing negative outcomes of the rupture. Mechanisms of plaque ...
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Atherosclerosis, a common cardiovascular disease, is among the leading causes of death. Many of the heart attacks results from ruptured atherosclerotic lesion and emboli formation. Then, the susceptibility of the lesion is a key factor in preventing negative outcomes of the rupture. Mechanisms of plaque rupture are under debate. However, a general agreement on the bold contribution of hemodynamic factors including the blood pressure is established. In the current study, biomechanical impacts of plaque calcification procedure and the changed thickness of fibrous cap were investigated. To do so, a cross-section of the constricted coronary artery is reconstructed from the histological images and extruded in the axial direction of the artery to produce the three dimensional configuration of the coronary model. Holzapfel strain energy density function is utilized for mechanical description of the arterial tissue and the fibrous cap which enables us to adopt collagen fiber orientation into the mechanical model. Furthermore, since the constricted vessel configuration is asymmetrical, instead of simplified cylindrical coordinates for collagen orientation, a discrete coordinate system is assigned to every element and respective circumferential, axial and radial directions were assigned. With calcification, plaque is more stable and produces monotonic stress patterns in its vicinity. Also, the fibrous cap thickness plays an important role as a barrier to inhibit stress concentration from soft lipid core and disturb the mechanical loads to the neighboring regions. These two parameters, provide useful insight on mechanical load distribution around an atherosclerotic lesion and the pathway of arterial tissue toward a new homeostasis.