The relation between exercise- induced myocardial ischemia and high-sensitive C-reactive protein and neopterin levels

Objective: High sensitivity C-reactive protein (hsCRP) and neopterin are associated with atherosclerosis. We aimed to evaluate the association between hsCRP and neopterin, and myocardial ischemia during exercise stress test (EST) in patients with stable angina pectoris (SAP) and to assess the predictive value of these mediators in obstructive coronary artery disease. Methods: Forty-five patients with SAP were included in this prospective observational study. EST- positive group included 23 patients (15 males, mean age 54 +/- 10 years) and EST-negative group-22 patients (14 males, mean age 52 +/- 9 years). In each patient, blood samples were obtained 1 hour before and 30 minutes after EST. In EST-positive group, coronary angiography was performed to determine the presence and severity of coronary artery lesions as assessed by Gensini score. Statistical analysis was performed using Chi-square, unpaired t, Mann-Whitney U and Wilcoxon rank tests. Logistic regression analysis was used to establish the predictive value of tests. Results: Before EST, hsCRP and neopterin levels were similar between the two groups, however, hsCRP levels were higher in EST-positive group after EST (p=0.03). There was no significant difference between the two groups with respect to neopterin levels after EST (p=0.4). In EST-positive group, EST resulted in significant increases in both hsCRP and neopterin levels (from 3.8 +/- 2.8 mg/L to 4.3 +/- 3.1 mg/L, p=0.001; from 8.7 +/- 4.0 nmol/L to 13.1 +/- 10.0 nmol/L, p=0.001, respectively). In EST-negative group only neopterin levels significantly increased after EST (from 6.9 +/- 1.8 nmol/L to 9.0 +/- 3.9 nmol/L, p=0.001). No relation was observed between the obstructive coronary lesions and the levels of hsCRP or neopterin at any point. Conclusion: In SAP patients, independent with the existence of obstructive coronary lesion, elevated levels of hsCRP after EST might be an indicator of immune activation caused by myocardial ischemia. (Anadolu Kardiyol Derg 2010; 10: 502-7)