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This Article Full Text Full Text (PDF) All Versions of this Article: 294/6/H2831    most recent 91428.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Foglieni, C. Articles by Maseri, A. Search for Related Content PubMed PubMed Citation Articles by Foglieni, C. Articles by Maseri, A.

Mild inflammatory activation of mammary arteries in patients with acute coronary syndromes

¹Clinical Cardiovascular Biology Laboratory and Cardiac Surgery Unit, Cardiothoracic and Vascular Department, University Vita-Salute, San Raffaele Scientific Institute, Milano; ²Cardiac Surgery Unit, Ospedali Riuniti, Trieste, Italy; and ³Laboratory of Tumor Immunology and Department of Oncology, San Raffaele Scientific Institute, Milano, Italy

Submitted 10 December 2007 ; accepted in final form 23 April 2008

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- 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.

endothelium; E-selectin; major histocompatibility complex class I; major histocompatibility complex class II-DR

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