title: Inflammation and Carotid Artery--Risk for Atherosclerosis Study (ICARAS).
abstract: BACKGROUND
  Compelling evidence suggests that inflammation is fundamentally involved in the pathogenesis of atherosclerosis; however, temporal correlation between inflammation and morphological features of atherosclerosis progression has not been demonstrated unequivocally.
  
  
  RESULTS
  We prospectively studied 1268 consecutive patients who were initially asymptomatic with respect to carotid artery disease. Patients underwent serial carotid ultrasound investigations at baseline and after a follow-up interval of a median of 7.5 months (range 6 to 9 months), with measurement of carotid flow velocities and categorization of carotid arteries as 0% to 29%, 30% to 49%, 50% to 69%, 70% to 89%, or 90% to 99% stenosed or occluded. High-sensitivity C-reactive protein (hs-CRP) and serum amyloid A (SAA) were measured at baseline and follow-up. Progression of carotid atherosclerosis was found in 103 (8.1%) of 1268 patients. Hs-CRP and SAA, respectively, at baseline (P=0.004 and P=0.014) and follow-up (P<0.001 and P<0.001) and the change from baseline to follow-up (P<0.001 and P<0.001) were significantly associated with progressive atherosclerosis. Adjusted ORs (95% CI) for atherosclerosis progression with increasing quintiles of baseline hs-CRP were 1.65 (0.71 to 3.84), 1.87 (0.8 to 4.37), 3.32 (1.49 to 7.39), and 3.65 (1.65 to 8.08), and with increasing quintiles of baseline SAA, they were 0.86 (0.38 to 1.92), 0.99 (0.49 to 1.99), 1.72 (0.91 to 3.28), and 2.28 (1.24 to 4.20), respectively, compared with the lowest quintiles.
  
  
  CONCLUSIONS
  These findings supply evidence for a close temporal correlation between inflammation and morphological features of rapidly progressive carotid atherosclerosis, which suggests that elevation or increase of the inflammatory biomarkers hs-CRP and SAA identifies the presence of active atherosclerotic disease.
authors.affiliation: Department of Angiology, of Vienna, Medical School, Vienna, Austria. martin.schillinger@meduniwien.ac.at
authors.forename: Martin
authors.initials: M
authors.lastname: Schillinger
authors.forename: Markus
authors.initials: M
authors.lastname: Exner
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Mlekusch
authors.forename: Schila
authors.initials: S
authors.lastname: Sabeti
authors.forename: Jasmin
authors.initials: J
authors.lastname: Amighi
authors.forename: Robert
authors.initials: R
authors.lastname: Nikowitsch
authors.forename: Ewald
authors.initials: E
authors.lastname: Timmel
authors.forename: Bernhard
authors.initials: B
authors.lastname: Kickinger
authors.forename: Christoph
authors.initials: C
authors.lastname: Minar
authors.forename: Matthias
authors.initials: M
authors.lastname: Pones
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Lalouschek
authors.forename: Helmut
authors.initials: H
authors.lastname: Rumpold
authors.forename: Gerald
authors.initials: G
authors.lastname: Maurer
authors.forename: Oswald
authors.initials: O
authors.lastname: Wagner
authors.forename: Erich
authors.initials: E
authors.lastname: Minar
mesh_terms: D000368:Aged; D050197:Atherosclerosis / Q000000981:diagnostic imaging / Q000209:etiology*; D002097:C-Reactive Protein / Q000032:analysis; D002340:Carotid Artery Diseases / Q000000981:diagnostic imaging / Q000209:etiology* / Q000473:pathology; D016893:Carotid Stenosis; D018450:Disease Progression; D005260:Female; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000000981:diagnostic imaging; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012307:Risk Factors; D000685:Serum Amyloid A Protein / Q000032:analysis; D014463:Ultrasonography
chemical_list: D000685:Serum Amyloid A Protein; D002097:C-Reactive Protein