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Updated: Jul 12, 2025

Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
The site-specific distribution of atheromatous plaques in the coronary arteries
Jarosław Wasilewski1, Monika Zofia Czaja-Ziółkowska1, Mariusz Gąsior1
13 Department of Cardiology, School of Medical Sciences in Zabrze, Medical University of Silesia, Katowice, Poland.
Insights
Atherosclerosis plaque distribution is influenced by disturbed blood flow, not just cholesterol. Hemodynamics and low-density lipoprotein concentration at the arterial wall are key factors in plaque formation, explaining lesion patterns.
Area of Science:
- Cardiovascular Research
- Pathophysiology
- Biomedical Engineering
Background:
- Atherosclerosis etiology remains unclear, with current hypotheses focusing on cholesterol.
- Hypercholesterolemia is a risk factor, not a direct cause, and doesn't explain plaque distribution.
- Plaque distribution is uneven, concentrating in specific arterial regions like the left anterior descending artery.
Purpose of the Study:
- To review the interplay between hemodynamics and low-density lipoprotein concentration in atherosclerosis.
- To explain the non-uniform distribution of atheromatous plaques in coronary arteries.
- To discuss the hemodynamic theory of atherosclerosis as a response to wall shear stress.
Main Methods:
- Review of existing literature on atherosclerosis etiology and plaque distribution.
- Analysis of hemodynamic forces and their interaction with endothelial cells.
- Examination of coronary artery plaque distribution data from autopsy and imaging studies.
Main Results:
- Hemodynamic factors, specifically disturbed flow and reduced wall shear stress, are critical in plaque development.
- Low-density lipoprotein concentration at the luminal surface exacerbates plaque formation under disturbed flow conditions.
- Coronary artery plaque distribution patterns, such as proximal LAD lesions, are linked to specific hemodynamic profiles.
Conclusions:
- Atherosclerosis is a complex disease where hemodynamic forces significantly influence lesion localization.
- The hemodynamic theory provides a framework for understanding plaque distribution patterns in the coronary vasculature.
- Further research integrating hemodynamic analysis with lipid profiles is crucial for understanding atherosclerosis progression.
Abstract:
The etiology of atherosclerosis is still unknown, but there are several hypotheses trying to explain this complex disease. Most consider atherosclerosis as a cholesterol storage disease. However, hypercholesterolemia is not a cause but a risk factor. Besides, like other well-known systemic risk factors, it does not explain the uneven distribution of atheromatous plaques in the vasculature. Atherosclerotic lesions develop mainly at vulnerable "risk points" of the arterial wall such as curvatures and near side branches, and predominantly in the left anterior descending (LAD), while the left circumflex (LCx) artery is relatively spared. Furthermore, atheromatous plaques are present mainly in the proximal segments in the LAD and LCx, in contrast to the right coronary artery (RCA), where plaques are more evenly distributed. The hemodynamic theory explains to some extent the distribution of atherosclerotic lesions and considers atherosclerosis as a reactive biological response of endothelial cells to wall shear stress. In this review, we discuss the interplay of concentration of low-density lipoproteins at the luminal surface and local hemodynamic forces (disturbed flow) that reduce wall shear stress in the process of plaque formation. Moreover, we present the distribution of atheromatous plaques in the coronary arteries in autopsy studies and imaging methods such as cardiac computed tomography angiography and invasive coronary angiography.
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