TIA and atherothrombotic stroke are platelet-dependent disease states since they are attributable to platelet-rich thrombi formed on an atheromatous plaque in major arteries. Cadioembolic stroke is attributable to fibrin-rich thrombi, although platelets might be strongly activated by thrombin generated as well. Recent studies have clarified that microatheroma, branch atheroma, and microemboli originated from major arteries, which might be platelet-dependent disease processes, contribute to the pathogenesis of lacunar stroke. In addition, it has been well known that platelet aggregation, release reaction, and procoagulant activity play important roles in the pathophysiology of acute ischemic stroke.
Findings of platelet activation were frequent in patients with atherothrombotic stroke or TIA. Platelet consumption and destruction were most prominent in patients with cardioembolic stroke. Mild platelet activation or consumption was also observed in some patients with lacunar stroke. Polymorphisms of platelet membrane glycoproteins have recently been reported to be a risk factor of stroke.
It might be finally proven by the efficacy of antiplatelet therapy whether platelet activation can be a risk factor of stroke. Meta-analyses by Antiplatelet and Antithrombotic Trialists' Collaborations have established the risk reduction by antiplatelet therapy in patients with atherothrombotic diseases. Clinical applications of more potent antiplatelet agents including platelet glycoprotein IIb/IIIa inhibitors may more clarify what disease states are platelet-dependent.
