A mechanistic model of acute platelet accumulation in thrombogenic stenoses

Thrombosis on an atherosclerotic lesion can cause heart attack or stroke. Thrombosis may be triggered by plaque rupture or erosion, creating a thrombogenic stenosis. To measure and model this situation, collagen-coated stenoses have been exposed to nonanticoagulated blood in a baboon ex vivo shunt....

Full description

Saved in:
Bibliographic Details
Published in:Annals of biomedical engineering 2001-04, Vol.29 (4), p.321-329
Main Authors: Wootton, D M, Markou, C P, Hanson, S R, Ku, D N
Format: Article
Language:English
Subjects:
Accumulation
Animals
Arteriosclerosis - blood
Biomedical Engineering
Blood clots
Cardiovascular system
Collagen
Constriction, Pathologic
Hemodynamics
Humans
In Vitro Techniques
Mathematical models
Models, Cardiovascular
Papio
Platelet Activation - physiology
Platelet Adhesiveness - physiology
Risks
Thromboembolism
Thrombosis - blood
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Thrombosis on an atherosclerotic lesion can cause heart attack or stroke. Thrombosis may be triggered by plaque rupture or erosion, creating a thrombogenic stenosis. To measure and model this situation, collagen-coated stenoses have been exposed to nonanticoagulated blood in a baboon ex vivo shunt. The maximum rate of platelet accumulation, measured using a gamma camera, was highest in the throat region of moderate and severe stenoses, and increased with increasing stenosis severity. A species transport model of platelet accumulation was developed, which included mechanisms of convection, shear-enhanced diffusion, near-wall platelet concentration, and a kinetic model of platelet activation and aggregation. The model accurately reproduced the average spatial pattern and time rate of platelet accumulation in the upstream and throat regions of the stenosis, where shear-enhanced diffusivity increased platelet transport in the stenosis throat. Downstream of the throat where flow is complicated by recirculation, the model computed a transport-limited region with lower than measured platelet accumulation, suggesting that fluid-phase platelet activation may significantly affect both transport and adhesion rates in the poststenotic region. This model may provide an initial quantitative estimate of the likelihood of occlusive thrombus in individual patients due to plaque erosion, artery spasm, incomplete angioplasty, or plaque rupture.
ISSN:0090-6964
1573-9686
DOI:10.1114/1.1359449