C-Reactive protein, clinical outcome, and restenosis rates after implantation of different drug-eluting stents.

Sirolimus-eluting stents (SESs), paclitaxel-eluting stents (PESs), and dexamethasone-eluting stents (DEXs) have anti-inflammatory properties; thus, the decreased in-segment restenosis rate observed with the use of these stents might be related to a weaker postprocedural inflammatory response. One hundred sixty consecutive patients with stable coronary artery disease who underwent successful single-vessel/lesion coronary artery stenting were prospectively studied. Thin-strut bare metal stents were deployed in 39 patients, SESs in 30, PESs in 61, and DEXs in 30. The 4 groups were similar with respect to demographic and angiographic variables and prevalence of risk factors. C-reactive protein (CRP) was measured at baseline and 24 and 48 hours after the procedure. Maximal increase in CRP was calculated as the increase in CRP at 48 hours/CRP compared with baseline. Angiographic follow-up was performed after 12.9 +/- 1.3 months or sooner, if needed, on the basis of clinical evidence. All patients presented a postprocedural increase in CRP that peaked at 48 hours (median 10.0 mg/L). Maximal CRP increase was similar across the 4 groups (medians 3.5 mg/L in the bare metal stent group, 3.6 mg/L in the SES group, 4.0 mg/L in the PES group, 3.5 mg/L in the DEX group, p = 0.45). Incidences of angiographic binary restenosis (>50% lumen diameter decrease) were 20.5% in the bare metal stent group, 3.3% in the SES group, 4.9% in the PES group, and 36.6% in the DEX group (p = 0.0004 for SES and PES groups vs bare metal stent and DEX groups). Postprocedural increase in CRP was significantly correlated with clinical and angiographic outcomes. In conclusion, the acute postprocedural systemic inflammatory response induced by drug-eluting stent implantation appears to be similar to that induced by bare metal stents. However, the restenosis rate is lower for SESs and PESs than for DEXs and bare metal stents. Thus, the decreased incidence of stent restenosis that was observed after SES and PES deployment is unlikely to be related to a decreased acute systemic inflammatory response, but rather to an increased local resistance to inflammatory mediators.