Why the study?
Thrombo-occlusive events causing heart attacks and strokes are mediated by platelets and thrombin and are not completely responsive to conventional aspirin and heparin therapy.
This text reviews the role of platelets and thrombin in vascular thrombosis, highlighting their resistance to conventional therapies like aspirin and heparin.
Heart attacks and strokes are usually caused by thrombo-occlusive events at sites of atherosclerotic stenosis and plaque rupture1. These thrombotic processes are generally mediated by thrombin, dependent on the action of platelets, and not completely responsive to conventional therapy with aspirin and heparin2,3. Resistant thrombi may also form after vascular procedures commonly performed for the treatment of symptomatic atherosclerotic disease, including coronary angioplasty, various types of atherectomy, placement of endovascular stents, endarterectomy, and implantation of small-caliber vascular grafts4,5. In fact, abrupt vessel closure and coronary restenosis are the two most difficult problems limiting the success . . .
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Laurence A. Harker (1994) conducted a review in Vascular Thrombosis.
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