Sinkiewicz W, Romański B, Bartuzi Z, Zbikowska M, Staszyńska M
Katedry i Kliniki Alergologii i Chorób Wewnetrznych, Akademii Medycznej w Bydgoszczy.
Przegl Lek. 1998;55(10):512-5.
Increased activation of polymorphonuclear neutrophils in the wideness of irreversible myocardial injury was described by many authors. Released proteolytic enzymes may cause deliquescence of necrotic muscle tissue and attenuate collagenic structure of myocardium, lead to endothelium damage and generate free oxygen radicals. Eosinophilic leucocytes reveal also enhanced proinflammatory activation. They take participation in inflammatory and immunologic reactions, among others, by producing and releasing many biologic mediators. One of the most important and powerful mediators is eosinophil cationic protein (ECP), the specific marker of eosinophil activation in vivo. We studied 17 patients (pts) with acute myocardial infarction (MI) and 21 pts with angina pectoris (AP). The plasma concentrations of ECP and the number of eosinophils in peripheral blood were measured 3 times-near before beginning of the treatment, and on the 4-th and 8-th day of MI. During the first 4 days measurements of CK-MB every 6 hours were made. We observed the significant increase of eosinophils and ECP correspondingly on the 8-th and 4-th day, when compared to the first day of MI (p < 0.05) and the patients with AP (p < 0.01). Despite tendency, the significant correlation of eosinophils and ECP values was not obtained (r = 0.36). In the group of patients with AP the eosinophil and ECP values were significantly higher at the pts with unstable angina, when compared to pts with stable angina (p < 0.001).