Platelet-Leukocyte Interaction and Thrombosis

Cerebrocardiac thrombotic disease such as acute my-ocardial infarction and acute ischemic stroke cause significant morbidity and mortality. Present therapies for these diseases besides anttcoagulation and fibrinolysis mainly aim toward limiting platelet adhesion and aggregation processes. However, their incomplete effectiveness suggests that other mechanisms may be important. Although the underlying cellular and molecular mechanisms

Cerebrocardiac thrombotic disease such as acute myocardial infarction and acute ischemic stroke cause significant morbidity and mortality. Present therapies for these diseases besides anttcoagulation and fibrinolysis mainly aim toward limiting platelet adhesion and aggregation processes. However, their incomplete effectiveness suggests that other mechanisms may be important. Although the underlying cellular and molecular mechanisms of pathogenesis are complex, an early event in vessel injury is the adhesion of platelets and leukocytes to the damaged arterial wall. Recent studies havedemonstrated that the patients with acute coronary syndrome and ischemic stroke have not only increased interaction between platelets（ homotypic aggregates） but also increased interaction between platelets and leukocytes（heterotypic aggregates） detectable in circulating blood, and that the heterotypic aggregation contribute significantly to these disease progression.