title: Relationship of circulating biomarkers of inflammation and hemostasis with preclinical atherosclerotic burden in nonsmoking hypercholesterolemic men.
abstract: BACKGROUND
  Relations of mediators of inflammation and hemostasis with preclinical atherosclerosis have been poorly analyzed. The aim of this study was to test potential associations of these blood markers with indicators of cardiovascular risk and atherosclerotic burden in asymptomatic, nonsmoking, hypercholesterolemic men.
  
  
  METHODS
  A total of 87 men underwent cardiovascular risk assessment by means of 10-year Framingham risk calculation (median 9%) and atherosclerotic burden evaluation by means of ultrasonographic measurement of common carotid intima-media thickness and assessment of atherosclerotic plaques at three arterial sites (three-site plaques).
  
  
  RESULTS
  Of the markers C-reactive protein, tumor necrosis factor-alpha, interleukin-10, factor VIIc, fibrinogen, plasminogen activator inhibitor-activator, soluble intercellular adhesion molecule-1, soluble P-selectin (sP-selectin), and von Willebrand factor, only sP-selectin was positively and independently associated with high Framingham risk score (>9%) (71.7 +/- 3.6 ng/mL, n = 33 v 59.6 +/- 2.8, n = 54; mean +/- SEM; P < .05) and with three-site plaques (75.4 +/- 5.7 ng/mL, n = 14 v 62.0 +/- 2.5, n = 73; P < .05). After adjustment for all of the above markers and for cardiovascular risk factors, odd ratios of having high Framingham risk and three-site plaques were 3.38 (1.43 to 10.21) and 5.23 (1.74 to 23.52) respectively, per 1-standard deviation increase in sP-selectin.
  
  
  CONCLUSIONS
  These results confirm that among several hemostasis and inflammation mediators, only sP-selectin blood level was associated with preclinical atherosclerosis. It might confer to sP-selectin measurement a clinical usefulness for detecting and managing high cardiovascular risk in primary prevention.
authors.affiliation: Centre de Médecine Préventive Cardiovasculaire, Hôpital Broussais, Groupe HEGP Broussais, AP-HP and Université René Descartes-Faculté de Médecine, Paris, France.
authors.forename: Gilles
authors.initials: G
authors.lastname: Chironi
authors.forename: Christine
authors.initials: C
authors.lastname: Dosquet
authors.forename: Muriel
authors.initials: M
authors.lastname: Del-Pino
authors.forename: Nicolas
authors.initials: N
authors.lastname: Denarie
authors.forename: Jean-Louis
authors.initials: JL
authors.lastname: Megnien
authors.forename: Ludovic
authors.initials: L
authors.lastname: Drouet
authors.forename: Claire
authors.initials: C
authors.lastname: Bal dit Sollier
authors.forename: Jaime
authors.initials: J
authors.lastname: Levenson
authors.forename: Alain
authors.initials: A
authors.lastname: Simon
mesh_terms: D000328:Adult; D050197:Atherosclerosis / Q000097:blood* / Q000209:etiology* / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D003430:Cross-Sectional Studies; D005169:Factor VIII / Q000378:metabolism; D005340:Fibrinogen / Q000378:metabolism; D006487:Hemostasis / Q000502:physiology*; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood* / Q000503:physiopathology; D007249:Inflammation / Q000097:blood*; D016753:Interleukin-10 / Q000097:blood; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000097:blood*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D018570:Risk Assessment; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D017539:Tunica Intima / Q000000981:diagnostic imaging / Q000473:pathology; D014463:Ultrasonography; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D015415:Biomarkers; D019007:P-Selectin; D017395:Plasminogen Activator Inhibitor 1; C051321:SERPINE1 protein, human; D014409:Tumor Necrosis Factor-alpha; D014841:von Willebrand Factor; D016753:Interleukin-10; D005169:Factor VIII; D005340:Fibrinogen; D002097:C-Reactive Protein