Background/Aim. Inflammation as a consequence of vascular injury after percutaneous coronary intervention (PCI) is a pathological substrate of restenosis and of its complications. The aim of the study was to examine perprocedural inflammatory response expressed by soluble CD40 ligand (sCD40L) and C-reactive protein (CRP) in patients treated with PCI and dual antiplatelet therapy. Methods. The experimental group included 52 patients (80.8% men, age 60 ± 9 years) with angina pectoris treated by PCI (22 urgent PCI) with stent implantation, and dual antiplatelet therapy (tienopiridins and aspirin), according to the current recommendations for the execution of the intervention. The control group consisted of 8 patients (70.5% men, age 59 ± 7 years) with angina pectoris, who had undergone coronarography taking aspirin 3 days prior to it. In all the patients 24 hours before and after the PCI concentrations of CRP and sCD40L in the blood were determined. Results. In the experimental group, the concentration of sCD40L was lower as compared to the control (p < 0.02). In 34 (65%) patients postprocedural decrease in sCD40L was recorded, in 18 (34.6%) of them increase, while in 50 (96%) patients there was a rise in CRP. The patients with postprocedural fall in sCD40L hod greater preprocedural concentration of sCD40L (p < 0.001), and less postprocedural concentration of sCD40L (p < 0.001), compared to the group with an increase in sCD40L after the PCI, while CRP levels tients treated with emergency PCI compared to elective patietns had a postprocedural decrease in sCD40L (p = 0.02). Increase in the level of CRP was higher in the group with emergency PCI in relation to elective PCI (p < 0.01). Conclusion. Emergency PCI procedures in the treatment of patients with unstable angina pectoris lead to a postprocedural fall in the serum concentration of sCD40L. Dual antiplate therapy with tienopiridins and aspirin inhibits the release of sCD40L. Regardless a clinical presentation of coronary disease PCI leads to an postprocedural increase in concentrations of CRP in the serum.