title: Coronary artery ectasia is related to coronary slow flow and inflammatory activation.
abstract: OBJECTIVE
  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.
authors.affiliation: University of Foggia, Cardiology Department, Viale Pinto 1, 71100 Foggia, Italy. Electronic address: natale.brunetti@unifg.it.
authors.forename: Natale Daniele
authors.initials: ND
authors.lastname: Brunetti
authors.affiliation: University of Foggia, Cardiology Department, Viale Pinto 1, 71100 Foggia, Italy.
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Salvemini
authors.affiliation: University of Foggia, Cardiology Department, Viale Pinto 1, 71100 Foggia, Italy.
authors.forename: Andrea
authors.initials: A
authors.lastname: Cuculo
authors.affiliation: University of Foggia, Cardiology Department, Viale Pinto 1, 71100 Foggia, Italy.
authors.forename: Antonio
authors.initials: A
authors.lastname: Ruggiero
authors.affiliation: University of Foggia, Cardiology Department, Viale Pinto 1, 71100 Foggia, Italy.
authors.forename: Luisa
authors.initials: L
authors.lastname: De Gennaro
authors.affiliation: University of Foggia, Cardiology Department, Viale Pinto 1, 71100 Foggia, Italy.
authors.forename: Antonio
authors.initials: A
authors.lastname: Gaglione
authors.affiliation: University of Foggia, Cardiology Department, Viale Pinto 1, 71100 Foggia, Italy.
authors.forename: Matteo
authors.initials: M
authors.lastname: Di Biase
mesh_terms: D000368:Aged; D015415:Biomarkers; D001783:Blood Flow Velocity; D015897:Comorbidity; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000473:pathology* / Q000503:physiopathology; D003920:Diabetes Mellitus / Q000453:epidemiology; D004108:Dilatation, Pathologic / Q000503:physiopathology; D050171:Dyslipidemias / Q000453:epidemiology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000453:epidemiology; D007249:Inflammation; D007378:Interleukins / Q000097:blood; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D018487:Ventricular Dysfunction, Left / Q000453:epidemiology
chemical_list: D015415:Biomarkers; D007378:Interleukins; D014409:Tumor Necrosis Factor-alpha
keywords: Coronary artery ectasia; Coronary flow; Cytokines; Inflammation