Periprocedural soluble P- and E-selectin levels fail as predictors of clinical restenosis in patients treated with elective coronary stenting.

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.

Combined periprocedural evaluation of CRP and TNF-alpha enhances the prediction of clinical restenosis and major adverse cardiac events in patients undergoing percutaneous coronary interventions.

To assess the value of serial C-reactive protein (CRP), serum amyloid A (SAA), tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) evaluation in the risk stratification in patients undergoing percutaneous coronary intervention. The study was designed as a prospective cohort trial with a 1-year follow-up. Eighty patients (70 with stable angina, 10 with unstable angina) were enrolled. Blood samples were collected before the procedure and after 6 and 24 h, and 1 month. Clinical follow-up visits were performed (*with exercise test) 7 days* and 1*, 3, 6* and 12 months after the procedure. Any symptoms of restenosis were verified angiographically. Multivariate logistic regression analysis identified increased preprocedural TNF-alpha and CRP levels and elevated CRP concentrations evaluated 24 h after the procedure as significant predictors of both clinical restenosis and major adverse cardiac events (MACE), while high SAA values at 24 h accurately predicted clinical restenosis. Patients, who were in the highest tertile of, either, baseline TNF-alpha and/or baseline CRP/CRP at 24 h, were more prone to develop restenosis and MACE than stratified only on the basis of a single marker. Our data indicate that combined analysis of CRP and TNF-alpha might be an effective approach to the clinical restenosis and MACE prediction. Additionally, long-term outcome is markedly influenced by the periprocedural activation of inflammation.