title: Pentraxin 3, a novel cardiovascular biomarker, is expressed in aortic specimens of patients with coronary artery disease with and without rheumatoid arthritis.
abstract: BACKGROUND
  The aims were to evaluate the presence and extent of pentraxin 3 depositions in specimens from the outer layers of the aorta and from the internal thoracic artery of patients with coronary artery disease with and without rheumatoid arthritis and to search for relationships between pentraxin 3 and vascular inflammation.
  
  
  METHODS
  Using histochemistry and immunohistochemistry, we examined biopsies from the aortic adventitia and from the internal thoracic artery (both with adjacent perivascular tissue), removed during coronary artery bypass grafting in 19 rheumatoid arthritis and 20 non-rheumatoid-arthritis patients, for presence/extent of pentraxin 3 depositions, inflammatory cell infiltrates, and fibrosis.
  
  
  RESULTS
  In the aorta, pentraxin 3 deposition occurred in all specimens, mostly at sites with inflammatory cell infiltrates or fibrosis, and their extent was related to the extent of inflammatory cell infiltrates (rho=0.43, 95% confidence interval: 0.13-0.66, P=.007). The extent of pentraxin 3 and inflammatory cell infiltrates in the aorta was similar in rheumatoid arthritis and non-rheumatoid-arthritis patients, but rheumatoid arthritis patients had more fibrosis and a lower proportion of T-cells in inflammatory cell infiltrates. In the internal thoracic artery, pentraxin 3 occurred only in 36% patients, and inflammatory cell infiltrates and fibrosis occurred in none.
  
  
  CONCLUSIONS
  Pentraxin 3 depositions in the outer aortic layers are common and are related to the local inflammation. On the other hand, they occur less frequently in the internal thoracic artery, i.e., a vessel highly resistant to atherosclerosis. Rheumatoid arthritis patients had more pronounced fibrosis in the aortic specimens and a different leukocytic response than non-rheumatoid-arthritis patients. In theory, pentraxin 3 might modulate the inflammatory process involved in the pathogenesis of cardiovascular disease and represent a target for new therapies.
authors: Department of Cardiac Surgery, Feiring Heart Clinic, Feiring, Norway; Hospital for Rheumatic Diseases, Lillehammer, Norway. Electronic address: ivana.hollan@revmatismesykehuset.no.
authors: Ivana
authors: I
authors: Hollan
authors: Manuela
authors: M
authors: Nebuloni
authors: Barbara
authors: B
authors: Bottazzi
authors: Knut
authors: K
authors: Mikkelsen
authors: Oystein T
authors: OT
authors: Førre
authors: Sven Martin
authors: SM
authors: Almdahl
authors: Alberto
authors: A
authors: Mantovani
authors: Morten Wang
authors: MW
authors: Fagerland
authors: Pål
authors: P
authors: Aukrust
authors: Pier Luigi
authors: PL
authors: Meroni
mesh_terms: D063194:Adventitia / Q000378:metabolism / Q000473:pathology; D000368:Aged; D001011:Aorta / Q000378:metabolism* / Q000473:pathology; D001172:Arthritis, Rheumatoid / Q000150:complications* / Q000378:metabolism* / Q000473:pathology; D015415:Biomarkers / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism*; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000150:complications* / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005355:Fibrosis; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D000683:Serum Amyloid P-Component / Q000378:metabolism*; D013601:T-Lymphocytes / Q000473:pathology; D000099153:Pentraxins
chemical_list: D015415:Biomarkers; D002097:C-Reactive Protein; D000683:Serum Amyloid P-Component; D000099153:Pentraxins
keywords: Atherosclerosis; Inflammation; Pentraxin 3; Rheumatoid arthritis