Clinical Application of Detecting Platelet Activation Markers in Cerebrovascular Disease

Background: Platelet activation and platelet-leukocyte crosstalk play important roles in the evolution and progress of coronary disease and diabetic angiopathy. Similar mechanisms are likely to occur in cerebrovascular disorders, too. Using the detection of specific epitopes on platelets, activation can be detected on a cellular level and used to gain further understanding of stroke pathophysiology and alternative treatment. Material and Methods: In patients with acute cerebral ischemia, platelet expression of activation-dependent epitopes CD62-P, CD63, and thrombospondin was investigated. Comparisons were made between patients and control subjects without cerebral ischemia and within the patient group with regard to the underlying etiology (pure vascular disease of brain-supplying arteries vs. pure cardiogenic disease). Another investigation addressed the quantification of platelet-leukocyte aggregates and a possible relation to infections preceding the ischemic stroke. Results: The patient group with macroangiopathic etiology of cerebral ischemia showed significantly increased expression of CD62-P and CD63 in comparison to patients with pure cardiogenic stroke. Cerebral ischemia that is preceded by infection seems to be accompanied by increased platelet-leukocyte aggregation. Conclusions: 1) Stroke of vascular origin may be due to a different pathogenetic mechanism than cardiogenic stroke. 2) The previously observed increase of ischemic stroke after infection may not only be explained by changes of soluble mediators of inflammation but also by proaggregatory platelet-leukocyte interaction. Both aspects need further investigation and may lead the way to different therapeutic strategies.