BACKGROUND: Coronary artery ectasia is defined as localized or diffuse dilation of the coronary arteries exceeding the 1.5-fold of normal adjacent segment. Scarce data are available about the role of inflammation in coronary artery ectasia. In the present study, we aimed to evaluate the expression of CD11b and CD45 adhesion molecules in peripheral blood granulocytes, monocytes and lymphocytes from the patients with coronary artery ectasia as possible indicators of inflammation. METHOD: The study consisted of 14 patients who had angiographically normal coronary arteries with coronary artery ectasia and 13 age and sex-matched controls without coronary artery ectasia. Cell surface adhesion molecules were detected by direct immunofluorescence evaluated by flow cytometry using monoclonal antibodies tagged with fluorescent markers. Venous blood samples were taken after coronary angiography. RESULTS: Mean fluorescence intensity of CD45 (33.8+/-3.1 vs. 13.0+/-0.7, P<0.001) and CD11b (39.1+/-13.5 vs. 19.5+/-1.32, P<0.001) on the monocyte surface of patients with coronary artery ectasia were higher than those of controls. Similarly in patients with coronary artery ectasia, the expression of CD11b (7.5+/-0.61 vs. 5.6+/-0.2, P=0.009) and CD45 (47.5+/-3.6 vs. 36.2+/-2.5, P=0.02) on lymphocytes was also significantly higher than those of controls. CONCLUSION: Increased levels of cellular adhesion molecules in patients with coronary artery ectasia may be an indicator of endothelial activation and inflammation and are likely to be in the causal pathway leading to coronary artery ectasia.
BACKGROUND:Coronary artery ectasia is defined as localized or diffuse dilation of the coronary arteries exceeding the 1.5-fold of normal adjacent segment. Scarce data are available about the role of inflammation in coronary artery ectasia. In the present study, we aimed to evaluate the expression of CD11b and CD45 adhesion molecules in peripheral blood granulocytes, monocytes and lymphocytes from the patients with coronary artery ectasia as possible indicators of inflammation. METHOD: The study consisted of 14 patients who had angiographically normal coronary arteries with coronary artery ectasia and 13 age and sex-matched controls without coronary artery ectasia. Cell surface adhesion molecules were detected by direct immunofluorescence evaluated by flow cytometry using monoclonal antibodies tagged with fluorescent markers. Venous blood samples were taken after coronary angiography. RESULTS: Mean fluorescence intensity of CD45 (33.8+/-3.1 vs. 13.0+/-0.7, P<0.001) and CD11b (39.1+/-13.5 vs. 19.5+/-1.32, P<0.001) on the monocyte surface of patients with coronary artery ectasia were higher than those of controls. Similarly in patients with coronary artery ectasia, the expression of CD11b (7.5+/-0.61 vs. 5.6+/-0.2, P=0.009) and CD45 (47.5+/-3.6 vs. 36.2+/-2.5, P=0.02) on lymphocytes was also significantly higher than those of controls. CONCLUSION: Increased levels of cellular adhesion molecules in patients with coronary artery ectasia may be an indicator of endothelial activation and inflammation and are likely to be in the causal pathway leading to coronary artery ectasia.