The impact of admission C-reactive protein levels on the development of poor myocardial perfusion after primary percutaneous intervention in patients with acute myocardial infarction

Abstract

Increased preprocedural C-reactive protein (CRP) levels in patients with acute myocardial infarction (MI) undergoing primary percutaneous coronary intervention (PCI) may affect myocardial perfusion. Accordingly, this study was designed to investigate the impact of admission CRP levels on the development of poor myocardial perfusion after PCI in patients with acute MI. The study population consisted of 75 patients (62 men, mean age, 61.6+/-6.68 years), who were admitted to our hospital with acute anterior MI and who underwent primary PCI in the left anterior descending coronary artery. All patients underwent stenting following balloon angioplasty. Myocardial perfusion was evaluated by using Thrombolysis In Myocardial Infarction (TIMI) myocardial perfusion grade (TMPG). Patients were divided into two groups according to TMPG after PCI. Group 1 consisted of 25 patients with TMPG 0-1 and group 2 comprised 50 patients with TMPG 2-3. Admission serum high sensitive CRP (hs-CRP) levels were analysed by using nephelometric method. Admission hs-CRP levels, pain to balloon time and white blood cell count (WBC) of patients in group 1 were significantly higher than those of the patients in group 2 (P<0.001; P<0.001; P=0.002, respectively). Univariate analysis identified ejection fraction, pain to balloon time, WBC and hs-CRP levels as the predictors of poor myocardial perfusion. In multivariate logistic regression analysis, hs-CRP levels and pain to balloon time were found to have statistically significant independent association with poor myocardial perfusion. Adjusted odds ratios were calculated as 1.85 for hs-CRP [P=0.003; 95% confidence interval (CI), 1.23-2.80] and 5.49 for pain to balloon time (P=0.04; 95% CI, 1.08-27.84). On admission, high CRP level in patients with acute MI undergoing primary PCI is likely to be in the causal pathway leading to the development of poor myocardial perfusion, especially when combined with prolonged pain to balloon time.