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Wall Shear Stress (WSS) Analysis in Atherosclerosis in Partial Ligated Apolipoprotein E Knockout Mouse Model through
Minju Cho1, Joon Seup Hwang1, Kyeong Ryeol Kim1
1Department of Convergence Medicine, Brain Korea 21 Project, College of Medicine, University of Ulsan, Seoul 05505, Republic of Korea.
Insights
This study reveals that differences in wall shear stress (WSS) are linked to atherosclerosis development. Analyzing WSS variations in a mouse model demonstrated a correlation with plaque thickness and inflammatory factors, offering insights into vulnerable plaque formation.
Area of Science:
- Cardiovascular Science
- Biomedical Engineering
- Pathology
Background:
- Atherosclerosis, a leading cause of death, involves arterial plaque formation and inflammation.
- Contributing factors include hyperlipidemia, hypertension, obesity, diabetes, smoking, and altered wall shear stress (WSS).
- Understanding atherosclerosis mechanisms is vital for prevention and treatment.
Purpose of the Study:
- To investigate the correlation between wall shear stress (WSS) and atherosclerotic plaque development.
- To analyze the relationship between WSS variations, inflammatory factors, and plaque characteristics.
- To explore the role of WSS in the formation of vulnerable plaques.
Main Methods:
- Utilized an apolipoprotein E knockout (ApoE-KO) mouse model fed a high-fat diet.
- Employed computational fluid dynamics (CFD) to simulate blood flow and WSS.
- Reconstructed carotid artery blood flow using magnetic resonance imaging (MRI).
- Compared CFD analysis with inflammatory markers and pathological staining at 1, 2, and 4 weeks.
Main Results:
- The standard deviation of time-averaged wall shear stress (TAWSS) was analyzed to compare high and low WSS regions.
- A widening gap between low and high WSS areas was observed as the atherosclerosis model progressed over time.
- A correlation was found between atherosclerotic plaque thickness, inflammatory factors, and WSS variations.
Conclusions:
- Differences in WSS are significantly linked to the occurrence and progression of atherosclerosis.
- The study provides a novel approach to analyzing WSS standard deviation for understanding plaque development.
- Findings suggest WSS variations contribute to the formation of vulnerable atherosclerotic plaques.
Abstract:
Atherosclerosis involves an inflammatory response due to plaque formation within the arteries, which can lead to ischemic stroke and heart disease. It is one of the leading causes of death worldwide, with various contributing factors such as hyperlipidemia, hypertension, obesity, diabetes, and smoking. Wall shear stress (WSS) is also known as a contributing factor of the formation of atherosclerotic plaques. Since the causes of atherosclerosis cannot be attributed to a single factor, clearly understanding the mechanisms and causes of its occurrence is crucial for preventing the disease and developing effective treatment strategies. To better understand atherosclerosis and define the correlation between various contributing factors, computational fluid dynamics (CFD) analysis is primarily used. CFD simulates WSS, the frictional force caused by blood flow on the vessel wall with various hemodynamic changes. Using apolipoprotein E knockout (ApoE-KO) mice subjected to partial ligation and a high-fat diet at 1-week, 2-week, and 4-week intervals as an atherosclerosis model, CFD analysis was conducted along with the reconstruction of carotid artery blood flow via magnetic resonance imaging (MRI) and compared to the inflammatory factors and pathological staining. In this experiment, a comparative analysis of the effects of high WSS and low WSS was conducted by comparing the standard deviation of time-averaged wall shear stress (TAWSS) at each point within the vessel wall. As a novel approach, the standard deviation of TAWSS within the vessel was analyzed with the staining results and pathological features. Since the onset of atherosclerosis cannot be explained by a single factor, the aim was to find the correlation between the thickness of atherosclerotic plaques and inflammatory factors through standard deviation analysis. As a result, the gap between low WSS and high WSS widened as the interval between weeks in the atherosclerosis mouse model increased. This finding not only linked the occurrence of atherosclerosis to WSS differences but also provided a connection to the causes of vulnerable plaques.
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