Background: Platelet activation that results from coronary plaque rupture is important in the pathogenesis of acute myocardial infarction (AMI). Soluble p-selectin (sP-selectin) is crucial in modulating leukocyte adhesion to both platelets and endothelial cells during inflammatory response and thrombus formation. We hypothesized that sP-selectin, an index of both platelet activation and acute inflammation, rapidly increases and modulates the recruitment of circulating white blood cells (WBC) in patients following AMI.
Methods: We conducted a prospective cohort study of 142 consecutive patients with ST-segment elevated AMI of onset < 12 h who were undergoing primary percutaneous coronary intervention. Blood samples for plasma levels of sP-selectin were obtained in the catheterization laboratory before coronary angiography was performed. The plasma levels of sP-selectin were also measured in 30 risk control subjects and 20 healthy control subjects.
Results: The plasma level of sP-selectin and the circulating WBC count were significantly higher in patients with AMI than in either the risk control or healthy subjects (all of p values < 0.0001). Additionally, repeated measures of ANOVA demonstrated that there were no significant differences in plasma levels of sP-selectin (p > 0.10) in three intervals from the start of chest pain to blood sample collection (< 180 min, > or = 180 < 360, and > or = 360 < 720) following AMI. Correlation analysis demonstrated that the increase in the plasma level of sP-selectin was significantly related to the circulating WBC count (r = 0.248, p = 0.003).
Conclusions: sP-selectin was markedly elevated in an early phase of AMI. sP-selectin may be involved in modulating the recruitment of circulating WBC during AMI. These findings raise the need for a prospective investigation of sP-selectin as a potential reliable clinical tool for rapidly diagnosing AMI.