Stroke is the third leading cause of death and the number one cause of disability in the US, with an estimated incidence of 780,000 strokes/ year.¹ Approximately 10% of all strokes are hemorrhagic, with the remainder being ischemic. Within the ischemic category, two major sub-classes are recognized. Ischemic strokes occurring within large blood vessels of the brain account for approximately 80% of the total and are thought to be the result of thromboembolic events originating in the heart or diseased large arteries. Lacunar strokes are the second major classification of ischemic stroke, occurring in small (200–300μm) penetrating arteries of the brain. The etiology of lacunar strokes is not considered to be embolic but rather represents endogenously generated clots, perhaps as a result of endothelial abnormalities. Largevessel strokes, subsequently referred to as cortical (or non-lacunar) strokes, have a worse prognosis for 30-day mortality, residual disability, and recurrence than do lacunar strokes.^2,3 Modifiable risk factors for ischemic stroke include hypertension, diabetes, smoking, and hyperlipidemia,¹ all factors that similarly contribute to atherosclerotic disease. While platelet participation is recognized as integral to the thrombotic process associated with ischemic strokes, there has been limited evidence to suggest that variations in platelet reactivity may also be a risk factor. This paucity of data is at least partially due to technical limitations in quantitating platelet reactivity, and also possibly due to the numerous platelet parameters that could affect thrombotic potential.

Coated-platelets
Our interest in the platelet’s role in ischemic stroke resulted from studies with coated-platelets, a subset of activated platelets with pro-thrombotic characteristics first described in 2000 by Alberio et al.⁴ The initial observation was that dual agonist activation with both thrombin and collagen resulted in enhanced prothrombinase activity and retention of coagulation factor V (FV) on the surface of a subgroup of activated platelets. Subsequently, Dale et al.5 demonstrated that several additional procoagulant proteins, including fibrinogen, von Willebrand factor, and thrombospondin, were also retained on the surface of these dual activated cells.

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