Evolution and rupture of vulnerable plaques: a review of mechanical effects

Atherosclerosis occurs as a result of the buildup and infiltration of lipid streaks in artery walls, leading to plaques. Understanding the development of atherosclerosis and plaque vulnerability is of critical importance, since plaque rupture can result in heart attack or stroke. Plaques can be divided into two distinct types: those that rupture (vulnerable) and those that are less likely to rupture (stable). In the last few decades, researchers have been interested in studying the influence of the mechanical effects (blood shear stress, pressure forces, and structural stress) on the plaque formation and rupture processes. In the literature, physiological experimental studies are limited by the complexity of in vivo experiments to study such effects, whereas the numerical approach often uses simplified models compared with realistic conditions, so that no general agreement of the mechanisms responsible for plaque formation has yet been reached. In addition, in a large number of cases, the presence of plaques in arteries is asymptomatic. The prediction of plaque rupture remains a complex question to elucidate, not only because of the interaction of numerous phenomena involved in this process (biological, chemical, and mechanical) but also because of the large time scale on which plaques develop. The purpose of the present article is to review the current mechanical models used to describe the blood flow in arteries in the presence of plaques, as well as reviewing the literature treating the influence of mechanical effects on plaque formation, development, and rupture. Finally, some directions of research, including those being undertaken by the authors, are described

Imaging-Based Patient-Specific Biomechanical Evaluation of Atherosclerosis and Aneurysm: A Comparison Between Structural-Only, Fluid-Only and Fluid–Structure Interaction Analysis

Cardiovascular diseases (CVD) are the leading cause of morbidity and mortality worldwide. Atherosclerosis is the dominating underlying cause of CVD, that occurs at susceptible locations such as coronary and carotid arteries. The progression of atherosclerosis is a gradual process and most of the time asymptomatic until a catastrophic event occurs. Similarly, an intracranial aneurysm is the bulging of the cerebral artery due to a weakened area of the vessel wall. The progression of the aneurysm could result in the rupture of the vessel wall leading to a subarachnoid haemorrhage. The formation and progression of atherosclerosis and aneurysm are closely linked to abnormal blood flow behaviour and mechanical forces acting on the vessel wall. Recent technologies in medical imaging, modeling, and computation are used to estimate critical parameters from patient-specific data. However, there is still a need to develop protocols that are reproducible and efficient. This article focuses on the methods for biomechanical analysis of the cerebral aneurysms and atherosclerotic arteries including carotid & coronary. In this study, patient-specific 3D models were reconstructed from optical coherence imaging (OCT) for coronary and magnetic resonance imaging (MRI) for the carotid and cerebral arteries. The reconstructed models were used for computational fluid dynamics (CFD), structural-only, and fluid–structure interaction (FSI) simulations. The results of the FSI were compared against structural and CFD-only simulations to identify the most suitable method for each artery. The comparison between FSI and structural only simulations for the coronary artery showed similar mechanical stress values across the cardiac cycle with a maximum difference of 1.8%. However, the results for the carotid and cerebral arteries showed a maximum difference of 5% and 20% respectively. Additionally, with relation to the hemodynamic WSS calculated from FSI and CFD-only, the coronary artery presented a significant difference of 87%. Conversely, the results for the carotid and cerebral arteries showed a maximum difference of 9 and 6.4% at systole. Based on the results it can be concluded that the shape & location of the artery will influence the selection of the model that can be used for solving the numerical problem

High shear stress relates to intraplaque haemorrhage in asymptomatic carotid plaques

Background and aims Carotid artery plaques with vulnerable plaque components are related to a higher risk of cerebrovascular accidents. It is unknown which factors drive vulnerable plaque development. Shear stress, the frictional force of blood at the vessel wall, is known to influence plaque formation. We evaluated the association between shear stress and plaque components (intraplaque haemorrhage (IPH), lipid rich necrotic core (LRNC) and/or calcifications) in relatively small carotid artery plaques in asymptomatic persons. Methods Participants (n = 74) from the population-based

Ultrasound Assessment of the Relation Between Local Hemodynamic Parameters and Plaque Morphology

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High shear stress relates to intraplaque haemorrhage in asymptomatic carotid plaques

AbstractBackground and aimsCarotid artery plaques with vulnerable plaque components are related to a higher risk of cerebrovascular accidents. It is unknown which factors drive vulnerable plaque development. Shear stress, the frictional force of blood at the vessel wall, is known to influence plaque formation. We evaluated the association between shear stress and plaque components (intraplaque haemorrhage (IPH), lipid rich necrotic core (LRNC) and/or calcifications) in relatively small carotid artery plaques in asymptomatic persons.MethodsParticipants (n = 74) from the population-based Rotterdam Study, all with carotid atherosclerosis assessed on ultrasound, underwent carotid MRI. Multiple MRI sequences were used to evaluate the presence of IPH, LRNC and/or calcifications in plaques in the carotid arteries. Images were automatically segmented for lumen and outer wall to obtain a 3D reconstruction of the carotid bifurcation. These reconstructions were used to calculate minimum, mean and maximum shear stresses by applying computational fluid dynamics with subject-specific inflow conditions. Associations between shear stress measures and plaque composition were studied using generalized estimating equations analysis, adjusting for age, sex and carotid wall thickness.ResultsThe study group consisted of 93 atherosclerotic carotid arteries of 74 participants. In plaques with higher maximum shear stresses, IPH was more often present (OR per unit increase in maximum shear stress (log transformed) = 12.14; p = 0.001). Higher maximum shear stress was also significantly associated with the presence of calcifications (OR = 4.28; p = 0.015).ConclusionsHigher maximum shear stress is associated with intraplaque haemorrhage and calcifications

Physiological predictors of acute coronary syndromes: emerging insights from the plaque to the vulnerable patient

In this review, the authors explore the evolving evidence linking physiological assessment of coronary artery disease with plaque progression and vulnerability. Reducing adverse clinical events remains the ultimate goal for diagnostic tests, and this review highlights evidence supporting the prognostic value of physiological metrics in predicting outcomes. Historical and contemporary studies support synergy among lesion severity, ischemia, plaque vulnerability, and patient prognosis. Ischemia contributes to clinical events through association with plaque burden, but this review addresses the emerging concept that it associates with atherothrombosis via disturbed lesion hemodynamics. Biomechanical pathophysiological forces including endothelial shear stress-the frictional force generated by blood flow on the vessel wall-are increasingly linked with atherogenesis, vulnerable plaque morphology, and platelet and leukocyte activation. The authors conclude by transitioning from the model of the vulnerable plaque to the concept of the "vulnerable patient," looking more broadly at physiological contributors to Virchow's triad underpinning acute coronary syndrome

The Need to Shift from Morphological to Structural Assessment for Carotid Plaque Vulnerability

Degree of luminal stenosis is generally considered to be an important indicator for judging the risk of atherosclerosis burden. However, patients with the same or similar degree of stenosis may have significant differences in plaque morphology and biomechanical factors. This study investigated three patients with carotid atherosclerosis within a similar range of stenosis. Using our developed fluid–structure interaction (FSI) modelling method, this study analyzed and compared the morphological and biomechanical parameters of the three patients. Although their degrees of carotid stenosis were similar, the plaque components showed a significant difference. The distribution range of time-averaged wall shear stress (TAWSS) of patient 2 was wider than that of patient 1 and patient 3. Patient 2 also had a much smaller plaque stress compared to the other two patients. There were significant differences in TAWSS and plaque stresses among three patients. This study suggests that plaque vulnerability is not determined by a single morphological factor, but rather by the combined structure. It is necessary to transform the morphological assessment into a structural assessment of the risk of plaque rupture

Sequential Structural and Fluid Dynamics Analysis of Balloon-Expandable Coronary Stents.

As in-stent restenosis following coronary stent deployment has been strongly linked with stent-induced arterial injury and altered vessel hemodynamics, the sequential numerical analysis of the mechanical and hemodynamic impact of stent deployment within a coronary artery is likely to provide an excellent indication of coronary stent performance. Despite this observation, very few numerical studies have considered both the mechanical and hemodynamic impact of stent deployment. In light of this observation, the aim of this research is to develop a robust numerical methodology for investigating the performance of balloon-expandable coronary stents in terms of their mechanical and hemodynamic impact within a coronary artery. The proposed methodology is divided into two stages. In the first stage, a numerical model of the stent is generated and a computational structural analysis is carried out to simulate its deployment within a coronary artery. In the second stage, the results of the structural analysis are used to generate a realistic model of the stented coronary lumen and a computational fluid dynamics analysis is carried out to simulate pulsatile blood flow within a coronary artery. Following the completion of the analyses, the mechanical impact of the stent is evaluated in terms of the stress distribution predicted within the artery whilst the hemodynamic impact of the stent is evaluated in terms of the wall shear stress distribution predicted upon the luminal surface of the artery. In order to demonstrate its application, the proposed numerical methodology was applied to six generic stents. Comparing the predicted performance of the generic stents revealed that strut thickness is likely to have a significant influence upon both the mechanical and hemodynamic impact of coronary stent deployment. Additionally, comparing the predicted performance of three of the investigated stents to the clinical performance of three comparable commercial stents, as reported in two large-scale clinical trials, revealed that that the proposed numerical methodology successfully identified the stents that resulted in higher rates of angiographic in-stent restenosis, late lumen loss and target-vessel revascularisation at short-term follow-up. In light of the conflicting requirements of coronary stent design, the proposed numerical methodology should prove useful in the design and optimisation of future coronary stents