In-stent restenosis after revascularization of myocardium with drug-eluting stents is accompanied by elevated level of blood plasma eosinophil cationic protein.

The aim of this study was to assess the involvement of eosinophil cationic protein, a marker of eosinophil activation, in the development of in-stent restenosis after drug-eluting stent implantation. Follow-up angiography at 6 to 12 months was performed in 32 patients who were treated with percutaneous coronary intervention and implantation of sirolimus-eluting stents. Blood plasma levels of eosinophil cationic protein (ECP) and total immunoglobulin E (IgE) were measured by enzyme-linked immunosorbent assay and the level of C-reactive protein (hs-CRP) by high-sensitivity nephelometry. According to angiography data, in-stent restenosis occurred in 13 patients, while 19 patients did not develop it. There were no differences between the hs-CRP and IgE levels in patients with or without restenosis. In contrast, ECP level was higher in patients with restenosis compared with that in patients without restenosis [17.7 ng/mL (11.2-24.0) vs. 9.0 ng/mL (6.4-12.9), p = 0.017]. The incidence of in-stent restenoses was 63% in patients with ECP level higher than or equal to 11 ng/mL, and 19% in patients with an ECP level lower than 11 ng/mL (p = 0.019). These findings suggest that elevated eosinophil activation may play an important role in the pathogenesis of in-stent restenosis after implantation of drug-eluting stents.

CD4(+)CD25(high)CD127(low) regulatory T cells in patients with stable angina and their dynamics after intracoronary sirolimus-eluting stent implantation.

Rapamycin contributes to the expansion of regulatory T cells (Tregs) in vitro. We investigated CD4(+)CD25(high)CD127(low) Treg level dynamics as well as the major parameters of cell immunity and sCD25 and highly sensitive C-reactive protein (hsCRP) concentrations in the blood of patients after coronary stenting (CS) with sirolimus (rapamycin)-eluting stents (SES; n = 43). The relation between initial Treg values and the severity of coronary atherosclerosis was observed. Treg and sCD25 levels were increased 1 month after CS versus baseline values and versus data in the control group (coronary angiography [CA], n = 20). A positive correlation between Treg and sCD25 levels was reported, whereas no relation was observed with the length of SES implanted. HsCRP level was increased during the first 7 days and returned to baseline values 1 month after CS/CA. Treg content is lower in patients with multivessel CAD. Elevated levels of Tregs and sCD25 after SES implantation might occur because of the immunomodulating effect of rapamycin.

Eptifibatide does not suppress the increase of inflammatory markers in patients with non-ST-segment elevation acute coronary syndrome.

BACKGROUND: Platelets are involved in inflammatory reactions which play an important role in the development of atherosclerosis and its acute complications. The objective of this study was to test the ability of glycoprotein (GP) IIb-IIIa antagonist eptifibatide to suppress the increase of inflammatory markers in non-ST-segment elevation acute coronary syndrome (ACS). METHODS: Twenty-five patients with unstable angina and non-ST-segment elevation myocardial infarction received eptifibatide on admission (two 180 microg/kg boluses followed by infusion at 2.0 and 1.3 microg/kg/min for 24 and 48 h, respectively) and 25 were treated without GP IIb-IIIa antagonists. Plasma von Willebrand factor (vWF) and soluble P-selectin were determined at baseline, 48 h and 2 weeks after onset of ACS, and were also measured in a group of healthy volunteers. Serum C-reactive protein (CRP), tumor necrosis factor alpha (TNFalpha), and interleukin 6 (IL6) were measured at baseline, 48 h, 2 weeks and 6 months. RESULTS: P-selectin was increased at baseline and vWF at baseline, 48 h and 2 weeks in comparison with healthy donors. CRP, TNFalpha, but not IL6 were increased at baseline, 48 h and 2 weeks in comparison with their levels at 6 months. Maximal values of CRP, TNFalpha and vWF were detected at 48 h. At any time point eptifibatide failed to decrease the levels of all tested markers. CONCLUSION: Eptifibatide does not suppress elevated levels of inflammatory markers in patients with non-ST-segment elevation ACS.