Tertiles of CRP, SAA and fibrinogen levels before PTCA, multivessel disease and residual diameter stenosis were associated with increased risk of clinical restenosis at the univariate analysis. However, CRP (RR = 6.2, CI = 2.0 to 18.7, III tertile vs. I tertile, p = 0.001) and residual stenosis (RR = 3.2, CI = 1.3 to 7.5, >30% vs. ≤30% stenosis, p = 0.007) were the only independent predictors of restenosis (chi-square model = 23.6, df = 3, p < 0.001) (Table le6). The risk predicted by our multivariate logistic analysis was closely correlated with observed events (percentage of correct classification = 70%; Hosmer-Lemeshow Goodness-of-Fit, p = 0.968). Of note is that elevated CRP levels, compared with low levels, increased the restenosis rate from 18% to 44% in patients with ≤30% residual stenosis and from 37% to 77% in patients with >30% residual stenosis (Figure 3). When acute-phase proteins and residual stenosis were analyzed as continuous variables, SAA levels (RR for log [SAA] = 6.0, CI = 2.3 to 16.2, p < 0.001), acute gain (RR = 0.3, CI = 0.1 to 0.8, p = 0.011) and multivessel disease (RR = 2.7, CI = 1.0 to 7.0, p = 0.042) were the only independent predictors of clinical restenosis (chi-square model = 25.6, df = 3, p < 0.001); after exclusion of other inflammatory markers, CRP [RR for log [CRP] = 2.9, CI = 1.4 to 6.3, p = 0.004], but not fibrinogen levels, were also independent predictors of restenosis. Preprocedural CRP levels (RR = 4.9, CI = 1.6 to 14.4, III tertile vs. I tertile, p = 0.008) were also the most powerful predictor of major adverse cardiac events (e.g., death, MI or need for repeat revascularization) at follow-up.