Probing the possibility of lesion formation/progression in vicinity of a primary atherosclerotic plaque: A fluid-solid interaction study and angiographic evidences.

It is shown that certain locations in the arterial tree, such as coronary and cerebral arteries, are more prevalent to plaque formation. Endothelial activation and consequent plaque development are attributed to local hemodynamic parameters such as wall shear stress (WSS), oscillatory shear index (OSI), relative residence time (RRT), and stress phase angle. After a certain level of plaque progression, these hemodynamic parameters are disturbed before and after the plaque. In the current study, it is hypothesized that the vicinity of a primary lesion is susceptible for further degeneration and second plaque formation. A fluid-solid interaction (FSI) model of the coronary artery with different levels of asymmetric constriction, is simulated and the trend of hemodynamic parameters were studied in both of the plaque side (PS) and the opposite wall (facing the plaque [PF]). Also, a novel factor is introduced that can identify the high-risk regions associated with WSS oscillations to negative values. Our results indicate that when more than half of the artery is constricted, the downstream of the plaque is highly exposed to endothelial pathogenesis the PS, such that negative WSS, and as well, critical values of OSI and RRT, that is, -1.2 Pa, 0.42 and 6.5 s, respectively arise in this region. PS endothelial cells in this region exposed to the highest risk of atherosclerosis based on the proposed index (3 out of 3). As well, three cases of angiographic images are provided that confirms existence of secondary lesion close to the primary one as predicted by our computational simulations.

Contribution of atherosclerotic plaque location and severity to the near-wall hemodynamics of the carotid bifurcation: an experimental study and FSI modeling.

Atherosclerosis is initiated by endothelial injury that is related to abnormal values of hemodynamic parameters such as wall shear stress (WSS), oscillatory shear index (OSI) and stress phase angle (SPA), which are more common in arterial bifurcations due to the complex structure. An experimental model of human carotid bifurcation with accurate geometrical and mechanical features was set up, and using realistic pulsatile flow rates, the inlet and outlet pressure pulses were measured for normal and stenosed models with 40% and 80% severities at common carotid (CCA), internal carotid (ICA) and external carotid (ECA) arteries. Based on the obtained experimental data, fluid-structure models were developed to obtain WSS, OSI, and SPA and evaluate pathological consequences at different locations. Mild severity had minor impact, however, inducing severe 80% stenosis in each branch led to considerable localized changes of hemodynamic parameters both in the stenosis site and other locations. This included sharp increases in WSS values accompanied by very low values close to zero before and after the peaks. Severe stenosis not only caused significant changes in the local artery, but also in other branches. OSI and SPA were less sensitive to stenosis, although high peaks were observed on bifurcation site for the stenosis at ECA. The interconnection of arteries at carotid bifurcation results in altered pressure/flow patterns in all branches when a stenosis is applied in any site. Such effect confirms pathological findings that atherosclerotic plaques are observed simultaneously in different carotid branches, although with different degrees of plaque growth and severity.