title: Association between inflammation, lipid and hemostatic factors in patients with stable angina.
abstract: BACKGROUND
  Dyslipidemia and thrombotic processes are both clearly involved in atherogenesis and its secondary complications. Moreover, inflammation has also been shown to play an important role in the pathophysiology of atherosclerosis. Our objective was to determine the association between inflammation, lipids and thrombosis in a group of patients with stable angina.
  
  
  METHODS
  295 patients (217 males and 78 females) with a mean age of 65.69+/-11.24 years. Levels of C-reactive protein, total cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, lipoprotein(a), apolipoproteins A1 and B100, fibrinogen and D-dimer were determined for each.
  
  
  RESULTS
  Arithmetic and geometric means of C-reactive protein in the sample were 10.7 and 1.4 mg/l, respectively. Distributing the sample by quartiles of C-reactive protein, we found a positive correlation between C-reactive protein, fibrinogen and D-dimer levels (p<0.000), and an inverse correlation for HDL cholesterol and apolipoprotein A1 (p<0.000). In multivariate analysis, fibrinogen (p<0.000) and D-dimer (p<0.01) levels were independently associated with high levels of C-reactive protein. Of the lipid factors, only apolipoprotein A1 (p<0.000) was independently and inversely associated with high levels of C-reactive protein.
  
  
  CONCLUSIONS
  These data confirm the association between prothrombotic and inflammatory states and suggest the anti-inflammatory effect of apolipoprotein A1.
authors.affiliation: Servicio de Cardiología, Hospital de Basurto, Departamento Medicina, Universidad del País Vasco UPV/EHU, Bilbao, Spain.
authors.forename: José D
authors.initials: JD
authors.lastname: Sagastagoitia
authors.forename: Yolanda
authors.initials: Y
authors.lastname: Sáez
authors.forename: Marta
authors.initials: M
authors.lastname: Vacas
authors.forename: Idoia
authors.initials: I
authors.lastname: Narváez
authors.forename: Jesús P
authors.initials: JP
authors.lastname: Sáez de Lafuente
authors.forename: Enrique
authors.initials: E
authors.lastname: Molinero
authors.forename: Ana
authors.initials: A
authors.lastname: Magro
authors.forename: Manuel
authors.initials: M
authors.lastname: Lafita
authors.forename: Mónica
authors.initials: M
authors.lastname: Santos
authors.forename: Antonio
authors.initials: A
authors.lastname: Escobar
authors.forename: José A
authors.initials: JA
authors.lastname: Iriarte
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000097:blood* / Q000209:etiology*; D016632:Apolipoprotein A-I / Q000097:blood; D053299:Apolipoprotein B-100 / Q000097:blood; D050197:Atherosclerosis / Q000209:etiology*; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005340:Fibrinogen / Q000378:metabolism; D006801:Humans; D017270:Lipoprotein(a) / Q000097:blood; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D016632:Apolipoprotein A-I; D053299:Apolipoprotein B-100; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D005338:Fibrin Fibrinogen Degradation Products; D017270:Lipoprotein(a); D014280:Triglycerides; C036309:fibrin fragment D; D005340:Fibrinogen; D002097:C-Reactive Protein; D002784:Cholesterol