Background. Inflammation is involved in all stages of development of atherosclerotic plaques. Currently, percutaneous coronary intervention (PCI) is a widely used method of treatment of coronary artery disease (CAD) when combined with optimal medical therapy (OMT). However, there is still controversy over invasive versus optimal pharmacological treatment in stable CAD (SCAD). Systemic inflammatory response triggered by PCI may limit its effectiveness in patients with SCAD. Objectives. We aimed to evaluate plasma CRP and its relation to thrombin generation and platelet reactivity both early after the procedure and in a one-month observation following successful PCI with stent implantation, in patients with SCAD and OMT, including statins. Material and Methods. We conducted a prospective study, in which CRP, platelet activation, thrombin generation and time course of prothrombin activation were determined at baseline, 3-5 days and 30 days after successful PCI with stent implantation, in 50 consecutive patients with SCAD, on chronic statin therapy. Results. Early after PCI CRP increased by 176% as compared with baseline (p < 0.001) and one-month after angioplasty CRP was still 54% higher than before the procedure (p = 0.002). In multivariate model prolonged increase in CRP 1 month after PCI was independently associated with P2Y12-reactivity index (PRI) (p = 0.04) and maximum concentration of thrombin (p = 0.003), both measured 30 days after the procedure. Conclusions. Post-procedural CRP increase, which persists at least one month in patients with SCAD, after elective PCI with stent implantation, is one of the main finding of our study. We demonstrated the relationship between prolonged post-PCI inflammatory reaction, reflected by elevated CRP, and increased thrombin generation and low platelets' response to clopidogrel, which may account for limited benefits of PCI in stable coronary patients. It may be advisable to assay post-procedural CRP in each patient with SCAD, who underwent PCI to predict those, with potentially low response to clopidogrel (Adv Clin Exp Med 2015, 24, 6, 979-985).