EFFECT OF SHEAR-STRESS ON ACUTE PLATELET THROMBUS FORMATION IN CANINESTENOSED CAROTID ARTERIES - AN IN-VIVO QUANTITATIVE STUDY

Citation
N. Maalej et al., EFFECT OF SHEAR-STRESS ON ACUTE PLATELET THROMBUS FORMATION IN CANINESTENOSED CAROTID ARTERIES - AN IN-VIVO QUANTITATIVE STUDY, Journal of thrombosis and thrombolysis, 5(3), 1998, pp. 231-238
Citations number
31
Categorie Soggetti
Hematology,"Peripheal Vascular Diseas
ISSN journal
09295305
Volume
5
Issue
3
Year of publication
1998
Pages
231 - 238
Database
ISI
SICI code
0929-5305(1998)5:3<231:EOSOAP>2.0.ZU;2-9
Abstract
We investigated the in vivo effect of percent stenosis, trans-stenotic pressure, and shear stress (SS) on platelet accumulation (PA) in cani ne mechanically injured and stenosed carotid arteries. In 10 dogs, int imal damage and controlled variations in stenosis were produced on the carotid artery. Blood flow through the stenosis, trans-stenotic press ure, and stenosis geometry were measured. A NaI gamma detector was col limated and placed over the stenosis to detect gamma rays emitted by a utologous radiolabeled platelets as they accumulated inside the stenos is. The SS was obtained hom the finite difference solution of the Navi er-Stokes equations. As the flow declined during thrombus formation, t he radioactive count accumulated in an inverse fashion. The rate of fl ow decline directly correlated with the rate of PA during thrombus for mation (r(2) > 0.9). Compared with the undamaged and unstenosed artery , the PA increased by 52 +/- 34% due to mild stenosis (40-60%). PA inc reased by 94 +/- 66% due to severe stenosis (60-70%) and by 145 +/- 56 % due to critical stenosis (70-80%; P > 0.01). The platelet accumulati on produced totally occlusive thrombus formation at levels of stenosis higher than 70 +/- 5% (diameter narrowing), and for transstenotic pre ssure gradients higher than 50 +/- 5 mmHg producing SS greater than 10 0 +/- 10 Pa. The PA was maximum at the stenotic portion of the vessel where the level of SS is the highest (P < 0.001). In vivo platelet-med iated thrombosis increases with SS and occurs at the stenotic portion of the stenosis where the SS is the highest. Severe stenoses produce c ritical levels of SS that potentiate thrombosis and lead to life-threa tening arterial occlusion.