BACKGROUND: Aneurysm and ectasia have similar pathological pathways. TH2-associated cytokines are stimulated by aneurismal tissue and correspondingly lack mediators associated with TH1 response. In this study, we measured serum TNF-alpha and IL-18 levels which are strong TH1 stimulating cytokines and also investigated the expression of CD11a, CD11b, CD18 adhesion molecules and CD45 on leukocytes in patients with coronary artery ectasia (CAE) and controls with normal coronary arteries (NCA). METHODS: A total of 51 isolated CAE patients free of atherosclerosis and 37 NCA controls were included in the study. Cell counts and cell surface adhesion molecules were detected by flow cytometry using fluorescence conjugated monoclonal antibodies. Serum TNF-alpha, IL-18 levels, and Chlamydophila pneumoniae IgG and IgM and Helicobacter pylori IgG levels were detected by ELISA methods. RESULTS: The mean fluorescence intensities of CD11a on granulocytes, monocytes and lymphocytes and CD45 on granulocytes and monocytes were significantly higher in CAE patients when compared with the NCA group (10.01 +/- 8.2 vs. 6.79 +/- 3.49, p = 0.04; 15.84 +/- 8.64 vs. 11.56 +/- 5.27, p = 0.016; 29.58 +/- 9.98 vs. 20.02 +/- 9.66, p < 0.001; 7.58 +/- 5.03 vs. 4.57 +/- 3.05, p = 0.003; 18.73 +/- 1238 vs. 10.74 +/- 738, p = 0.004; respectively) detected by flow cytometry. TNF-alpha levels were significantly lower in the patient group (18.76 +/- 7.07 vs. 24.29 +/- 8.46; p < 0.001) when compared with controls. The percentage of granulocytes was higher in the CAE group when compared with the NCA group (65.52 +/- 14.91 vs. 52.28 +/- 1537; p = 0.002). Contrarily, the percentage of monocytes was higher in the control group when compared with the CAE group (18.12 +/- 15.69 vs. 934 +/- 733 p = 0.008). Among the infection markers studied, only C. pneumoniae IgG levels were significantly higher in patients when compared with controls (81.62 +/- 48.53 RU/mL vs. 63.79 +/- 33.83 RU/mL; p = 0.045). In CAE patients, TNF-alpha levels significantly correlated with mean fluorescence intensity levels of CD45+ granulocyte (0.525, p < 0.001), monocyte (0.469, p = 0.001) and lymphocytes (0376, p = 0.013). CONCLUSIONS: The decreased levels of TNF-alpha may indicate predominance of TH2 and lack of TH1 type immunity in CAE patients, similar to patients with aortic aneurysms. Increased levels of cell surface adhesion molecules in CAE are an indicator of activation of leukocytes for adherence and transmigration through the vessels for the initiation of inflammation.
BACKGROUND:Aneurysm and ectasia have similar pathological pathways. TH2-associated cytokines are stimulated by aneurismal tissue and correspondingly lack mediators associated with TH1 response. In this study, we measured serum TNF-alpha and IL-18 levels which are strong TH1 stimulating cytokines and also investigated the expression of CD11a, CD11b, CD18 adhesion molecules and CD45 on leukocytes in patients with coronary artery ectasia (CAE) and controls with normal coronary arteries (NCA). METHODS: A total of 51 isolated CAE patients free of atherosclerosis and 37 NCA controls were included in the study. Cell counts and cell surface adhesion molecules were detected by flow cytometry using fluorescence conjugated monoclonal antibodies. Serum TNF-alpha, IL-18 levels, and Chlamydophila pneumoniae IgG and IgM and Helicobacter pylori IgG levels were detected by ELISA methods. RESULTS: The mean fluorescence intensities of CD11a on granulocytes, monocytes and lymphocytes and CD45 on granulocytes and monocytes were significantly higher in CAE patients when compared with the NCA group (10.01 +/- 8.2 vs. 6.79 +/- 3.49, p = 0.04; 15.84 +/- 8.64 vs. 11.56 +/- 5.27, p = 0.016; 29.58 +/- 9.98 vs. 20.02 +/- 9.66, p < 0.001; 7.58 +/- 5.03 vs. 4.57 +/- 3.05, p = 0.003; 18.73 +/- 1238 vs. 10.74 +/- 738, p = 0.004; respectively) detected by flow cytometry. TNF-alpha levels were significantly lower in the patient group (18.76 +/- 7.07 vs. 24.29 +/- 8.46; p < 0.001) when compared with controls. The percentage of granulocytes was higher in the CAE group when compared with the NCA group (65.52 +/- 14.91 vs. 52.28 +/- 1537; p = 0.002). Contrarily, the percentage of monocytes was higher in the control group when compared with the CAE group (18.12 +/- 15.69 vs. 934 +/- 733 p = 0.008). Among the infection markers studied, only C. pneumoniae IgG levels were significantly higher in patients when compared with controls (81.62 +/- 48.53 RU/mL vs. 63.79 +/- 33.83 RU/mL; p = 0.045). In CAE patients, TNF-alpha levels significantly correlated with mean fluorescence intensity levels of CD45+ granulocyte (0.525, p < 0.001), monocyte (0.469, p = 0.001) and lymphocytes (0376, p = 0.013). CONCLUSIONS: The decreased levels of TNF-alpha may indicate predominance of TH2 and lack of TH1 type immunity in CAE patients, similar to patients with aortic aneurysms. Increased levels of cell surface adhesion molecules in CAE are an indicator of activation of leukocytes for adherence and transmigration through the vessels for the initiation of inflammation.