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Hemodynamics and atherosclerosis. Insights and perspectives gained from studies of human arteries
S Glagov1, C Zarins, D P Giddens
1Department of Pathology, University of Chicago, IL 60637.
Insights
Atherosclerosis plaque formation is linked to reduced blood flow and shear stress in arteries. Hemodynamic forces influence plaque growth and vessel diameter, but their role in plaque destabilization needs further study.
Area of Science:
- Cardiovascular Biology
- Biomedical Engineering
- Pathology
Background:
- Atherosclerosis affects major arteries, with specific sites like the carotid bifurcation and coronary arteries being high-risk areas.
- The distribution of atherosclerotic lesions suggests a role for local mechanical factors in disease initiation and progression.
Purpose of the Study:
- To investigate the relationship between hemodynamic forces, such as wall shear stress and mural tensile stress, and the localization of atherosclerotic plaques.
- To explore how flow patterns and mechanical stresses influence plaque development, arterial remodeling, and potential destabilization.
Main Methods:
- Analysis of human vessels at high risk for atherosclerosis.
- Utilizing computational models to study flow characteristics and mechanical stresses in arterial segments.
- Quantitative assessment of plaque distribution in relation to hemodynamic parameters.
Main Results:
- Plaques predominantly form in regions with reduced flow velocity and shear stress, and where flow deviates from laminar patterns.
- Altered flow patterns, particularly during systole, increase particle residence time in susceptible areas.
- Arterial remodeling, driven by hemodynamic forces, aims to maintain lumen patency, while tensile stress relates to wall architecture.
Conclusions:
- Hemodynamic forces, specifically wall shear stress, are critical in determining atherosclerotic plaque localization.
- Tensile stress influences arterial wall structure and composition.
- Further research is needed to clarify the interplay between hemodynamic forces, tensile stress, and arterial wall metabolism in atherosclerosis progression and complication.
Abstract:
Atherosclerosis affects the major elastic and muscular arteries, but some vessels are largely spared while others may be markedly diseased. The carotid bifurcation, the coronary arteries, the infrarenal abdominal aorta, and the vessels supplying the lower extremities are at highest risk. The propensity for plaque formation at bifurcations, branchings, and curvatures has led to conjectures that local mechanical factors such as wall shear stress and mural tensile stress potentiate atherogenesis. Recent studies of the human vessels at high risk, and of corresponding models, have provided quantitative evidence that plaques tend to occur where flow velocity and shear stress are reduced and flow departs from a laminar, unidirectional pattern. Such flow characteristics tend to increase the residence time of circulating particles in susceptible regions while particles are cleared rapidly from regions of relatively high wall shear stress and laminar unidirectional flow. The flow patterns associated with plaque localization are most prominent during systole. Long-term consequences are therefore likely to be greatly enhanced by elevated heart rate and may exert a selective effect on the coronary arteries. The point-by-point redistribution of wall tension at regions of geometric transition has not been quantitatively related to plaque localization. Enlargement of arteries as plaques increase in size and the associated modeling of plaque and wall configuration tend to preserve an adequate and regular lumen cross section. Hemodynamic forces appear to determine changes in vessel diameter so as to restore normal levels of wall shear stress, while wall thickness architecture, and composition are closely related to tensile stress. Hemodynamic forces may also be implicated in the symptom-producing destabilization of plaques, especially in relation to wall instabilities near stenoses. The relative roles of wall shear stress, tensile stress, and the metabolism of the artery wall in the progression and complication of atherosclerosis remain to be clarified. Development of clinical techniques for relating hemodynamic and tensile properties to plaque location, stenosis, and composition should permit pathologists to provide new insights into the bases for the topographic and individual differences in plaque progression and outcome.