title: Mild inflammatory activation of mammary arteries in patients with acute coronary syndromes.
abstract: Acute coronary syndromes (ACS) are characterized by multiple unstable coronary plaques and elevated circulating levels of inflammatory biomarkers. The endothelium of internal mammary arteries (IMA), which are atherosclerosis resistant, is exposed to proinflammatory stimuli as vessels that develop atherosclerosis. Our study investigated the IMA endothelial expression of inflammatory molecules in patients with ACS or chronic stable angina (CSA). IMA demonstrated normal morphology, intact endothelial lining, and strong immunoreactivity for glucose transporter 1. E-selectin expression was observed more frequently in IMA of ACS patiention than CSA patients (ACS 61% vs. CSA 14%, P = 0.01). High fluorescence for major histocompatibility complex (MHC) was significantly more frequent on the luminal endothelium (ACS 66.7% vs. CSA 17.6%, P = 0.001 for class I; and ACS 66.7% vs. CSA 6.2%, P = 0.0003 for class II-DR) and on the vasa vasorum (ACS 92.9% vs. CSA 33.3% and 7.7%, P = 0.0007 and P < 0.0001 for class I and class II-DR, respectively) of ACS patients than CSA patients. ICAM-1, VCAM-1, Toll-like receptor 4, tissue factor, IL-6, inducible nitric oxide synthase, and TNF-alpha expression were not significantly different in ACS and CSA. Circulating C-reactive protein [ACS 4.8 (2.6-7.3) mg/l vs. CSA 1.8 (0.6-3.5) mg/l, P = 0.01] and IL-6 [ACS 4.0 (2.6-5.5) pg/ml vs. CSA 1.7 (1.4-4.0) pg/ml, P = 0.02] were higher in ACS than CSA, without a correlation with IMA inflammation. The higher E-selectin, MHC class I and MHC class II-DR on the endothelium and vasa vasorum of IMA from ACS patients suggests a mild, endothelial inflammatory activation in ACS, which can be unrelated to the presence of atherosclerotic coronary lesions. These findings indicated IMA as active vessels in coronary syndromes.
authors.affiliation: Clinical Cardiovascular Biology Laboratory and Cardiac Surgery Unit, Cardiothoracic and Vascular Department, University Vita-Salute, San Raffaele Scientific Institute, Milano, Italy. foglieni.chiara@hsr.it
authors.forename: Chiara
authors.initials: C
authors.lastname: Foglieni
authors.forename: Francesco
authors.initials: F
authors.lastname: Maisano
authors.forename: Lorella
authors.initials: L
authors.lastname: Dreas
authors.forename: Alessio
authors.initials: A
authors.lastname: Giazzon
authors.forename: Giacomo
authors.initials: G
authors.lastname: Ruotolo
authors.forename: Elisabetta
authors.initials: E
authors.lastname: Ferrero
authors.forename: Laura
authors.initials: L
authors.lastname: Li Volsi
authors.forename: Stefano
authors.initials: S
authors.lastname: Coli
authors.forename: Gianfranco
authors.initials: G
authors.lastname: Sinagra
authors.forename: Bartolo
authors.initials: B
authors.lastname: Zingone
authors.forename: Ottavio
authors.initials: O
authors.lastname: Alfieri
authors.forename: Anton E
authors.initials: AE
authors.lastname: Becker
authors.forename: Attilio
authors.initials: A
authors.lastname: Maseri
mesh_terms: D054058:Acute Coronary Syndrome / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000787:Angina Pectoris / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D001167:Arteritis / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D019040:E-Selectin / Q000032:analysis; D004730:Endothelium, Vascular / Q000737:chemistry; D005260:Female; D006684:HLA-DR Antigens / Q000032:analysis; D015395:Histocompatibility Antigens Class I / Q000032:analysis; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis*; D008297:Male; D008323:Mammary Arteries / Q000737:chemistry* / Q000276:immunology / Q000473:pathology; D018613:Microscopy, Confocal; D008875:Middle Aged; D015854:Up-Regulation; D014651:Vasa Vasorum / Q000737:chemistry
chemical_list: D019040:E-Selectin; D006684:HLA-DR Antigens; D015395:Histocompatibility Antigens Class I; D018836:Inflammation Mediators