Clinical application of detecting platelet activation markers in cerebrovascular disease

Background: Platelet activation and platelet-leukocyte cross-talk play impo rtant roles in the evolution and progress of coronary disease and diabetic angiopathy. Similar mechanisms are likely to occur in cerebrovascular disor ders, too. Using the detection of specific epitopes on platelets, activatio n can be detected on a cellular level and used to gain further understandin g of stroke pathophysiology and alternative treatment. Material and Methods : in patients with acute cerebral ischemia, platelet expression of activati on-dependent epitopes CD62-P, CD63, and thrombospondin was investigated. Co mparisons were made between patients and control subjects without cerebral ischemia and within the patient group with regard to the underlying etiolog y (pure vascular disease of brain-supplying arteries vs. pure cardiogenic d isease). Another investigation addressed the quantification of platelet-leu kocyte aggregates and a possible relation to infections preceding the ische mic stroke. Results: The patient group with macroangiopathic etiology of ce rebral ischemia showed significantly increased expression of CD62-P and CD6 3 in comparison to patients with pure cardiogenic stroke. Cerebral ischemia that is preceded by infection seems to be accompanied by increased platele t-leukocyte aggregation. Conclusions: 1) Stroke of vascular origin may be d ue to a different pathogenetic mechanism than cardiogenic stroke. 2) The pr eviously observed increase of ischemic stroke after infection may not only be explained by changes of soluble mediators of inflammation but also by pr oaggregatory platelet-leukocyte interaction. Both aspects need further inve stigation and may lead the way to different therapeutic strategies.