AIM: To evaluate possible links between coronary flow anomalies, inflammatory activation and coronary artery ectasia (CAE). METHODS: Fourteen consecutive patients with CAE diagnosed at coronary angiography were enrolled in the study and compared with 17 patients with coronary atherosclerosis without CAE and 15 controls with normal coronary angiography. All patients underwent blood assay with evaluation of circulating levels of interleukin (IL)-1b, IL-2, IL-8, IL-10 and tumor-necrosis-factor(TNF)-α. The number of coronary segments showing CAE at coronary angiography, the Markis class, and coronary flow assessed with TIMI frame count (TFC) were also assessed. RESULTS: Subjects with CAE showed higher levels of IL-1b, TNF-α, and IL-10 (p<0.05). The number of coronary segments showing CAE was related to TFC both in left anterior descending (LAD) coronary artery (p<0.01) and in right coronary artery (RCA) (p<0.001), and to circulating levels of IL-1b and IL-10 (p<0.01). TFC on LAD (p<0.05) and on RCA (p<0.001), circulating IL-1b levels (p<0.01), IL-8 (p<0.05), and IL-10 (p<0.01) were proportionally increased comparing controls, subjects with coronary atherosclerosis without CAE, and with decreasing Markis class. In subjects with CAE involving LAD, TFC on LAD was related to IL-8 and TNF-α levels (p<0.05); subjects with IL-1b levels above median showed higher TFC values on LAD (p<0.01), CONCLUSIONS: In subjects with CAE, the extension of disease is related to the impairment of coronary circulation and to inflammatory activation. The inflammatory response is also related to an impaired coronary circulation.
AIM: To evaluate possible links between coronary flow anomalies, inflammatory activation and coronary artery ectasia (CAE). METHODS: Fourteen consecutive patients with CAE diagnosed at coronary angiography were enrolled in the study and compared with 17 patients with coronary atherosclerosis without CAE and 15 controls with normal coronary angiography. All patients underwent blood assay with evaluation of circulating levels of interleukin (IL)-1b, IL-2, IL-8, IL-10 and tumor-necrosis-factor(TNF)-α. The number of coronary segments showing CAE at coronary angiography, the Markis class, and coronary flow assessed with TIMI frame count (TFC) were also assessed. RESULTS: Subjects with CAE showed higher levels of IL-1b, TNF-α, and IL-10 (p<0.05). The number of coronary segments showing CAE was related to TFC both in left anterior descending (LAD) coronary artery (p<0.01) and in right coronary artery (RCA) (p<0.001), and to circulating levels of IL-1b and IL-10 (p<0.01). TFC on LAD (p<0.05) and on RCA (p<0.001), circulating IL-1b levels (p<0.01), IL-8 (p<0.05), and IL-10 (p<0.01) were proportionally increased comparing controls, subjects with coronary atherosclerosis without CAE, and with decreasing Markis class. In subjects with CAE involving LAD, TFC on LAD was related to IL-8 and TNF-α levels (p<0.05); subjects with IL-1b levels above median showed higher TFC values on LAD (p<0.01), CONCLUSIONS: In subjects with CAE, the extension of disease is related to the impairment of coronary circulation and to inflammatory activation. The inflammatory response is also related to an impaired coronary circulation.