Increased peripheral circulating inflammatory cells and plasma inflammatory markers in patients with variant angina

Background Emerging data suggest that inflammation may play an important role in the pathogenesis of coronary artery disease. However, the relation of inflammatory status to coronary vasospasm has been less investigated in patients with variant angina (VA). Purpose The aim of this study, therefore, was to determine peripheral circulating white blood cells as well as monocyte cells and plasma C-reactive protein (CRP) and interleukin-6 (IL-6) levels in patients with VA, and to compare patients with VA, stable coronary artery disease, and controls with angiographically normal coronary arteries. Method Thirty-three consecutive patients with documented VA, 26 with stable coronary artery disease, and 22 normal controls (with angiographically normal coronary arteries) were involved in this study. The peripheral blood was taken, and white blood cells and monocyte cells were counted. The plasma concentrations of CRP and IL-6 were also evaluated by enzyme-linked immunosorbent assay (ELISA). Results The data showed that white blood cell counts and monocyte cell counts were significantly higher in patients of the VA group than in the other two groups (white blood cell counts: 7340 +/- 1893/mm(3) vs. 6187 +/- 1748/mm(3) VS. 5244 +/- 1532/mm(3), P < 0.05, respectively; monocyte cell counts: 510 +/- 213/mm(3) vs. 425 +/- 209/mm(3) vs. 383 +/- 192/3 mm, P < 0.05, respectively). Similarly, levels of plasma CRP and IL-6 were also significantly higher in patients of the VA group than in patients with stable coronary artery disease (CRP: 0.42 +/- 0.21 mg/l vs. 0.27 +/- 0.14 mg/l; IL-6: 10.4 +/- 1.0 pg/dl vs. 6.2 +/- 0.7 pg/dl, P < 0.01, respectively), and patients with normal controls (CRP: 0.42 +/- 0.21 mg/l vs. 0.17 +/- 0.10 mg/l; IL-6: 10.4 1.0 pd/dl vs. 3.0 +/- 0.7 pg/dl, P < 0.01, respectively). The multivariate analysis showed that CRP was the independent variable most strongly associated with VA. Conclusion Taken together, these findings suggested that more chronic, severe inflammation might be involved in the pathogenesis of VA, manifested by increased counts of circulating inflammatory cells and elevated plasma levels of CRP and IL-6.