Plasma levels of C-reactive protein and interleukin-10 predict late coronary in-stent restenosis 6 months after elective stenting

Background: In-stent restenosis (ISR) is one of the major limitations of percutaneous coronary intervention (PCI). Aim: To evaluate the relationship between the levels of hs-CRP, IL-6, IL-10 and intimal hyperplasia six months after coronary bare metal stent (EMS) implantation. Methods: The study population consisted of 73 consecutive patients who underwent bare metal stent implantation into narrowed coronary segments. A total of 74 stents were implanted. Angiographic study after six months, together with evaluation of serum level of IL-6 (pg/ml), IL-10 (pg/ml), hs-CRP (mu g/ml), fasting insulin (mu IU/ml) and glucose (mg%) was performed. Insulin sensitivity was calculated using the HOMA-IR formula The QCA analysis of stented segments was performed at baseline, after intervention and at six-month follow-up. Results: Restenosis at six months occurred in 10 patients (13.7%). The mean % diameter stenosis at follow-up was 27.8 +/- 19% and late loss was 0.81 +/- 0.6 mm. We found a correlation between late loss and serum hs-CRP, IL-6 and IL-10 concentration. There was no correlation between the lipid profiles, insulin levels and HOMA-IR and re-narrowing of the stented segments. Patients with restenosis were characterised by significantly higher serum concentration of CRP (2.04 +/- 3.4 vs. 10.38 +/- 6.7 mu g/ml, p = 0.0036), IL-6 (14.98 +/- 8.3 vs. 5.70 +/- 5.5 pg/ml, p = 00062), and fasting glucose (184.0 +/- 50.5 vs. 107.5 +/- 40.4 mg%, p = 0.0051), as well as lower IL-10 levels (1.25 +/- 0.6 vs. 4.85 +/- 4.9 pg/ml, p = 0.0000). The ROC analysis indicated that CRP (> 2.86 mu g/ml), IL-6 (> 6.24 pg/ml) and IL-10 (< 1.7 pg/ml) values predicted the restenosis with reasonable accuracy. A multiple logistic regression model identified CRP and IL-10 levels as independent predictors of restenosis. Conclusion: We demonstrated that elevated inflammatory markers 6 months after PCI are associated with late angiographic in-stent restenosis.