A persistent increase in C-reactive protein is a risk factor for restenosis in patients with stable angina who are not receiving statins


      Inflammation has been postulated to be a major contributor to restenosis after angioplasty. We examined the correlation between inflammatory and coagulatory reactions and the occurrence of restenosis, and how treatment with statins influences this correlation. A total of 243 patients with stable angina who were scheduled for a percutaneous coronary intervention (PCI) and follow-up coronary angiography were enrolled in the study. Eighty-one of these patients were treated with statins for at least 1 month before their PCI and throughout the study period. Blood was withdrawn on the day of the PCI and on the day of the follow-up catheterization. Patients with the highest hs-CRP at the time of the initial PCI maintained elevated hs-CRP levels over time and showed significantly higher rates of restenosis or TLR after 6±1 months than subjects with low initial hs-CRP. Statin treatment abolished this difference. Fibrinogen levels were also increased in subjects with high initial hs-CRP, both at the time of the initial PCI and at follow-up. In an univariate analysis, both initial and follow-up levels of hs-CRP and fibrinogen correlated with restenosis. However, both the initial and follow-up levels of hs-CRP only were independent predictors of increased restenosis in a multivariate analysis, except in the statin-treated subgroup. In conclusions, the persistent increase in CRP is a risk factor for restenosis in patients with stable angina who have not been treated with statins.


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