Plasma pentraxin 3 may be a more sensitive marker of inflammatory response than high-sensitivity C-reactive protein after bare-metal stent compared to drug-eluting stent implantation.

C-reactive protein (CRP) and pentraxin 3 (PTX3) are members of a highly conserved pentraxin superfamily. CRP is synthesized in the liver and may represent a systemic response to local inflammation. PTX3 is synthesized locally at the inflammatory sites and may represent a marker for local inflammation at sites of vessel injury. We compared plasma high-sensitivity CRP (hsCRP) and PTX3 concentrations after bare-metal stent (BMS) and drug-eluting stent (DES) implantation. Fifty-three patients with stable coronary artery disease who underwent percutaneous coronary intervention were divided into 2 groups: 1-24 patients (BMS group) and 2-29 patients (DES group). Patients were scheduled for an elective, 6-month clinical follow-up. Major adverse cardiovascular events (MACEs) (death, myocardial infarction, target vessel revascularization) were assessed. Baseline clinical characteristics were similar in both groups. Patients after BMS implantation had a higher median PTX3 concentration 1.02 ng/mL compared to patients after DES implantation 0.80 ng/mL, P=0.045. Median hsCRP concentrations were similar in both groups: 0.9 mg/L versus 0.89 mg/L, respectively. Six-month follow-up was available in 33 patients. Four out of 33 patients had MACEs during follow-up. The cut-off value to predict MACEs for PTX3 was >1.16 ng/mL (P=0.004) and for hsCRP was >0.95 mg/L (P<0.001). Patients after DES implantation showed significantly lower plasma PTX3 levels compared with patients after BMS implantation. hsCRP showed no difference between the study groups. PTX3 may be a more sensitive marker of local inflammatory response due to vessel injury by BMS than hsCRP. DES implantation may attenuate the early inflammatory response. Lower PTX3 levels may reflect potent anti-inflammatory properties of DES.