Background: P-Selectin mediates adhesive interactions between platelets, leukocytes and endothelium to form thrombi. Our purpose was to investigate plasma soluble(s) P-selectin levels in patients with acute myocardial infarction (aMI) and the effect of thrombolysis on P-selectin levels.
Methods: Patients with aMI within the first 6 h of chest pain were enrolled prospectively. sP-selectin levels were determined by ELISA in the plasma of patients with aMI (n=32), stable angina (n=18), and healthy controls (n=15). Samples were obtained before, 3 and 24 h after reperfusion therapy with tissue plasminogen activator. Seven patients showed recurrent angina or failure to reperfuse.
Results: sP-selectin levels were significantly higher in aMI group than other groups (86.7+/-8.7 ng/ml, P<0.05). sP-selectin levels were similar in stable angina and control groups (28.8+/-4.4 vs. 25.4+/-7.3 ng/ml, P=NS). A significant increase in sP-selectin levels was observed 3 h after successful thrombolysis and this was followed by a decrease to near the baseline level late after reperfusion. But patients with failed reperfusion showed sustained high sP-selectin levels after 24 h of thrombolysis (P<0.05).
Conclusion: The plasma sP-selectin level is elevated in aMI and it increases further following thrombolytic therapy. This increase is probably induced by activation of endothelial cells or platelets after myocardial ischemia and reperfusion during aMI. As the elevated levels are sustained in patients with failed reperfusion, serial P-selectin levels may be used as a non-invasive indicator of successful thrombolysis in aMI.