An increasing amount of basic scientific data indicates that adhesion molecules may be involved in the pathogenesis of vessel re-narrowing in patients undergoing coronary angioplasty. Furthermore, inflammation is suggested to be a pivotal mechanism linking atherosclerosis and restenosis. The aim of this study was to assess if periprocedural evaluation of soluble P-selectin (sP-selectin) and E-selectin (sE-selectin) possesses any additive value in the restenosis prediction to C-reactive protein (CRP) measurement. One hundred and nine stable angina patients were consecutively enrolled into the prospective cohort study. All participants were treated with single vessel coronary bare metal stenting. sP-selectin, sE-selectin and CRP were measured in peripheral venous blood samples collected before and 6, 24 h and 1 month after the procedure. Clinical follow-up visits were held 7 days*, 1*, 3, 6*, and 12 months (*with an exercise test) after stenting. Any symptoms of restenosis were verified angiographically. Clinical restenosis occurred in 18 subjects. Concentrations of sP-selectin and sE-selectin did not differ between patients with and without clinical restenosis at any measuring point. In the latter group a decrease in sP-selectin and sE-selectin levels was observed 6 h after stenting. These findings when considered in all of the investigated subjects had no impact on the subsequent incidence of restenosis. An inflammatory response assessed as an increase in CRP level with the peak values at 24 h was noted in the whole population. However, it was significantly more pronounced in the restenosis group. Application of the Cox's proportional hazard model revealed a high CRP level 24 h after stenting and the history of coronary angioplasty concerning a nontarget lesion to be the only independent predictors of clinical restenosis. To conclude, the periprocedural evaluation of sP-selectin and sE-selectin in peripheral venous blood in patients undergoing elective coronary stenting provides no prognostic information in terms of clinical restenosis prediction, and the magnitude of the systemic inflammatory response triggered by coronary angioplasty assessed as an increase in CRP level and the history of coronary angioplasty concerning nontarget stenosis remain independent predictors of lesion re-narrowing.

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