Treg/Th17 balance in stable CAD patients with different stages of coronary atherosclerosis.

Objective. Immune processes play a significant role in atherosclerosis plaque progression. Regulatory T cells and T helpers 17 were shown to possess anti- and pro-atherogenic activity, respectively.

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.

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.

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.