Platelets play a primary role in
thrombus formation after plaque
rupture. Platelets recognize the exposed
collagen via
Von Willebrand factor (VWF) and become activated.
Saratin, an inhibitor of the VWF-dependent binding of platelets to
collagen, may reduce the thrombotic risk associated to
atherosclerosis. Our objective was to evaluate the antithrombotic effects of local treatment with
saratin on human atherosclerotic lesions.
Thrombus formation was assessed by the deposition of (111)In-platelets on different human atherosclerotic lesions under three local shear conditions (800,1700 and 3400/s) with blood derived from catheterized pigs. Human atherosclerotic lesions were locally treated with
saratin (30 microg/ml) at 37 degrees C for 5 min and placed in the chamber. Under stenotic shear conditions of 800/s,
saratin significantly (p<0.05) reduced platelet deposition triggered by human denuded vessel wall (44%), fatty streaks (47%), severely damaged vessel (50%) and
atherosclerotic plaque (57%).
Thrombus characterization by immunohistochemistry showed also a reduction in
fibrin deposition in treat-ed vessels. These results suggest that the local site-specific treatment with
saratin inhibits
atherosclerotic plaque thrombogenicity at haemodynamic conditions typical of moderately stenotic coronary arteries.