Sticky platelet syndrome and thrombocythemia

Platelets play an important role in hemostasis, thrombosis, and atherosclerosis. Most of our understanding of platelets is based on their function in hemostasis, as it relates to quantitative and qualitative bleeding disorders. In hemostasis, platelets perform two major functions. First, because of their ability to adhere and aggregate at sites of endothelial injury, they facilitate the initial arrest of bleeding, also called primary hemostasis. Second, on ‘‘activation’’ at the site of vessel injury, they provide the surfaces onto which the factors of the coagulation system can be bound, thus keeping clot formation localized. The physiology and biochemistry of platelets has been the subject of extensive reviews [1–4] and will not be discussed in this context. Although the pathophysiology of the role of platelets in bleeding disorders is reasonably well understood, less is known about the involvement of platelets in thrombosis and atherosclerosis, though more patients have the latter than have bleeding problems. ‘‘Discovery of such abnormalities is the challenge of the future in platelet research’’ [2]. The role of platelets in the pathogenesis of arterial thrombosis in particular is relatively well known. Most arterial thrombotic events reside in clot formation at sites of atherosclerotic lesions, though other vascular diseases can also be involved. Ruptures at the base of the atherosclerotic plaques appear to precipitate thrombus formation [5,6]. As in normal hemostasis, platelets will adhere to exposed collagen fibers, aggregate, and initiate, together with tissue factor (TF), the activation of the coagulation system [7]. This leads to thrombus formation with temporary or permanent vascular occlusion. Atherosclerosis is the most prevalent reason for the development of acute myocardial infarction (AMI)