Patients with acute coronary syndromes exhibit increased platelet-monocyte binding mediated by novel cation-independent adhesion mechanisms, suggesting a potential new therapeutic target.
There is evidence for a significant P-selectin-independent molecular component to the platelet-monocyte conjugation observed in peripheral blood. Patients with myocardial infarction and unstable angina demonstrate increased total binding of platelets to monocytes. Additionally, calcium-independent adhesion was significantly elevated in patients with evidence of myocardial infarction. These findings demonstrate that novel cation-independent adhesion mechanisms may mediate platelet-monocyte binding, representing a new therapeutic target after vascular injury associated with myocardial infarction.
Sarma et al. (2002) studied this question.