Mechanisms of arterial thrombosis in nonparallel streamlines: platelet thrombi grow on the apex of stenotic severely injured vessel wall. Experimental study in the pig model.

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Abstract
The role of thrombosis in various acute coronary syndromes has been established. However, the basic mechanism by which plaque rupture leads to a growing thrombus in the vicinity of stenotic lesions is not well understood. Using a characterized flow chamber in a rheologically controlled system, we have mimicked stenotic vessels and studied for the first time cell-vessel wall interaction in nonparallel streamlines. Stenoses ranging from 0 to 80% were produced with stripped tunica media to mimic severe vessel wall damage, and perfused with heparinized flowing blood. This perfusion device was placed within an extracorporeal system in swine, and blood was perfused for selected times from 1 to 30 min. Platelet deposition on the surface was evaluated by 111Indium-labeled platelets. As percent stenosis increased, platelet deposition significantly increased (P less than 0.001), indicating a shear-induced cell activation. Analysis of the axial distribution of platelet deposition indicated that the apex, and not the flow recirculation zone distal to the apex, was the segment of greater platelet accumulation within 30 min of blood perfusion (P less than 0.001). These results also indicate that the severity of the acute platelet response to plaque rupture probably depends on the location of the rupture with relation to the apex of the plaque.

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