Abstract
The fibrous cap is a protective layer of connective tissue that covers the core of an atherosclerotic plaque. The rupture of this layer has been commonly associated with acute myocardial infarctions. The thickness of the fibrous cap, the percentage of stenosed area, and the stiffness of the core were studied (commonly associated with vulnerable plaque characteristics) to quantify their effects on the cap’s mechanical stress state by performing analyses using computational fluid-structure interaction (FSI) methods. The mechanical stress levels are significantly increased within the fibrous cap structure at the upstream side of the plaque. As expected, the highest stresses occurred for a severe stenosis and a thin fibrous cap. Interestingly, a weak structural support such as a soft lipid pool beneath the fibrous cap allowed for the hemodynamic pressure gradient forces to displace the fibrous cap in the direction of the flow, resulting in higher strains and thus higher mechanical stresses in the upstream portion of the plaque cap, potentially increasing the risk of cap rupture. The peak stress behavior of the most critical cases (thin fibrous cap and soft lipid core) at various degrees of stenosis was analyzed. For mid-range stenosis from 43% to 75%, there was a plateau region revealing that mild and moderate plaques were quickly exposed to the high stress condition of severe plaques. In conclusion, the particular combination of a mild to severe stenosis, a thin fibrous cap and a soft lipid core resulted in the highest mechanical stresses calculated at the proximal side of the plaque. Mild and moderate plaques can be subjected to stresses similar to severe plaques, possibly contributing to their rupture.
Highlights
Atherosclerosis is a chronic inflammatory response in the arterial walls that narrows the lumen of vessels by the gradual deposition of fatty substances, cholesterol crystals, cellular waste products and calcium minerals, and the growth of connective tissue [1,2]
The particular combination of a mild to severe stenosis, a thin fibrous cap and a soft lipid core resulted in the highest mechanical stresses calculated at the proximal side of the plaque
Tang and colleagues have developed 3D fluid-structure interaction (FSI) models based on MRI scans and have displayed that regions of localized maximum stresses, solid stresses, correspond well with the location of plaque ulceration identified from histopathological evaluations
Summary
Atherosclerosis is a chronic inflammatory response in the arterial walls that narrows the lumen of vessels by the gradual deposition of fatty substances, cholesterol crystals, cellular waste products and calcium minerals, and the growth of connective tissue [1,2]. These localized pathological lesions are known as atheromatous plaques. It is estimated that two thirds to three quarters of all arterial thrombi are caused by plaque rupture [3] This event could potentially occlude the vessel and prevent blood perfusion downstream, resulting in an acute myocardial infarction. It is recognized that plaque vulnerability leading to rupture is an important cause of myocardial infarction, and sudden cardiac death
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