Wall Shear Stress and Atherosclerotic Plaque Progression

Atherosclerotic plaque is the build-up of lipids, inflammatory cells and fibrotic tissue in the arterial wall. As disease progresses, atherosclerotic plaque progresses into various forms. Depending on their composition, plaques can be generally divided into two categories: stable and vulnerable. Rupture of a vulnerable plaque can lead to the sudden and unpredictable onset of stroke or heart attack.
Although risk factors for atherosclerosis, including smoking, diabetes, high blood pressure, hyperlipidemia, genetic susceptibility are systemic in nature, atherosclerosis develops at specific sites of the vasculature, i.e. near curvatures and bifurcations. This is due to the difference in the wall shear stress (WSS) environment.
WSS is the frictional force that blood flow applies on the endothelial lining of the arterial wall. Low WSS is known to induce inflammation and plaque initiation, while high WSS is anti-inflammatory and protect against plaque formation. However, the relationship between WSS and plaque vulnerability is not clear.
The aim of this thesis was to study the evolution of WSS during plaque progression and determine its correlation to plaque composition using a mouse model in which we surgically manipulate blood flow and induce the growth a vulnerable plaque.