Original Contributions |
From the Center for Thrombosis Research, Sinai Hospital of Baltimore, Baltimore, Md.
Correspondence to Victor L. Serebruany, MD, PhD, Center for Thrombosis Research, Sinai Hospital of Baltimore, 2401 W Belvedere Ave, Schapiro Research Building R202, Baltimore, MD 21215. E-mail Heartdrug{at}aol.com
AbstractAnimal studies have shown that the administration of antibodies against platelet/endothelial cell adhesion molecule-1 (PECAM-1) before reperfusion can reduce infarct size. The purpose of the present study was to define the effects of thrombolytic therapy in acute myocardial infarction (AMI) patients on the platelet expression and plasma concentrations of PECAM-1 at prespecified time points after attempted reperfusion. The plasma concentration and platelet expression of PECAM-1 were determined in 23 AMI patients enrolled in the Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO-III) trial before thrombolysis and at 3, 6, 12, and 24 hours thereafter and compared with 22 healthy controls. At baseline, PECAM-1 was expressed significantly more on the platelet surface in the AMI patients than in controls (P=0.027) while soluble PECAM-1 plasma levels were almost identical between groups. There were no significant diurnal variations in both plasma and platelet PECAM-1 levels in controls. A significant decrease in platelet PECAM-1 expression was observed 3 hours after thrombolysis (P=0.03) compared with baseline, followed by a significant increase (P=0.004) in fluorescence intensity later at 24 hours after thrombolysis. Conversely, a significant increase in soluble PECAM-1 was observed 3 hours after thrombolysis (P=0.02), followed by a significant decrease later at 24 hours after attempted reperfusion (P=0.03). The expression of platelet-bound PECAM-1 is increased in AMI patients. Discordantly directed changes in soluble and platelet PECAM-1 after the first 24 hours after thrombolytic therapy may represent redistribution of the whole PECAM-1 pool. Further investigation of the possible role of PECAM-1 and the relationship between its soluble and platelet fractions in AMI are warranted.
Key Words: PECAM-1 acute myocardial infarction thrombolysis humans
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