Abstract
In clinical practice, the risk of cerebrovascular events originating from carotid atherosclerotic plaques is correlated to the degree of luminal narrowing, commonly designated the degree of stenosis. Though the degree of stenosis is a proven marker of plaque vulnerability, it is widely recognized that better risk markers for cerebrovascular events are needed. Known morphological features of plaque vulnerability are large lipid-rich necrotic cores (LR-NC) with thin fibrous caps that generate localized elevated mechanical stresses within the fibrous cap separating arterial lumen from LR-NC. Thus, determination of local biomechanics using computational simulations may have clinical implications.
Highlights
In clinical practice, the risk of cerebrovascular events originating from carotid atherosclerotic plaques is correlated to the degree of luminal narrowing, commonly designated the degree of stenosis
Though the degree of stenosis is a proven marker of plaque vulnerability, it is widely recognized that better risk markers for cerebrovascular events are needed
Significant differences were apparent comparing the two different patient morphologies using surface plots of degree of stenosis, peak principal mechanical stresses, Objective Biomechanical stress levels could be indicative of plaque rupture risk
Summary
The risk of cerebrovascular events originating from carotid atherosclerotic plaques is correlated to the degree of luminal narrowing, commonly designated the degree of stenosis. Though the degree of stenosis is a proven marker of plaque vulnerability, it is widely recognized that better risk markers for cerebrovascular events are needed. Known morphological features of plaque vulnerability are large lipid-rich necrotic cores (LR-NC) with thin fibrous caps that generate localized elevated mechanical stresses within the fibrous cap separating arterial lumen from LR-NC. Determination of local biomechanics using computational simulations may have clinical implications. Mechanical stresses were evaluated using a widely adopted critical threshold of 300 kPa below which the plaque is not considered at risk of rupture
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