Inflammatory markers in a 2-year follow-up of coronary artery disease

Our study was designed in an attempt to determine the dynamics of changes in serum tumor necrosis factor (TNF)-α, soluble forms of its receptors (sTNFR 1, sTNFR 2), and adhesion molecules (sE-selectin, sP-selectin, sVCAM-1, sICAM-1) over a 2-year follow-up of patients with coronary artery disease (CAD). The study involved 70 patients with stable CAD (stable angina class II/III according to the Canadian Cardiovascular Society) and 20 apparently healthy subjects. Over the follow-up period a marked attenuation of angina (P < 0.001) was observed. Interventional treatment (percutaneous coronary intervention, coronary artery bypass grafting) was used in 53 CAD patients. Laboratory analysis revealed a significant decrease of serum TNF-α and sTNFR1 at 2 years (TNF-α: 12.1 ± 0.7 pg/ml; sTNFR 1: 1306 ± 46 pg/ml) as compared to baseline levels (16.5 ± 0.7 pg/ml, P = 0.030; 1551 ± 82 pg/ml, P = 0.048, respectively). The levels of sP-selectin (159 ± 7 vs 201 ± 14 ng/ml, P < 0.01) and sICAM-1 (133 ± 4 vs 153 ± 6 ng/ml, P < 0.05) were found to be significantly increased as compared to the baseline. Interventional procedures resulted in suppression of both cytokine (TNF-α, sTNFR 2) and adhesion molecule (sE-selectin, sP-selectin) activation in the CAD group. The baseline and post-follow-up TNF-α and sTNFR 1 levels showed persistent elevation in CAD patients as compared to the controls (9.0, 956.3 pg/ml, respectively; P < 0.01). There were no differences between baseline and final cytokines and adhesion molecules in healthy subjects. The course of CAD as modified by a clinically effective therapy is characterized by changes of immune markers activation. Revascularization seems to be an important factor suppressing both cytokine and adhesion molecule activation in CAD patients.