SOLUBLE E-SELECTIN LEVELS IN ACUTE HUMAN MYOCARDIAL-INFARCTION

It has been suggested that leukocyte adhesion mechanisms play a key ro le in experimental myocardial infarction. We have recently shown that E-selectin, an adhesion molecule belonging to the selectin family, is involved in the pathogenesis of experimental myocardial ischemia. We i nvestigated the circulating levels of E-selectin, studied as a marker of endothelial dysfunction, in acute myocardial infarction. Our study was carried out in 60 patients, 20 hospitalized for acute myocardial i nfarction, 20 suffered from angina pectoris and 20 healthy control sub jects. Patients with acute myocardial infarction had increased serum l evels of soluble E-selectin (sE-selectin = 255 +/- 12 ng/ml) compared to both patients with angina pectoris (sE-selectin = 46 +/- 10 ng/ml) and healthy control subjects (sE-selectin = 51 +/- 14 ng/ml). Thrombol ytic therapy with urokinase (1,000,000 IU as an intravenous bolus in 5 min, followed by an infusion of additional 1,000,000 IU for the follo wing 2 h) succeeded in producing reperfusion and reduced the serum lev els of sE-selectin (71 +/- 19 ng/ml). Our results confirm previous exp erimental data and indicate that adhesion mechanisms supporting leukoc yte-endothelium interaction may also be operative in human acute myoca rdial infarction.