title: Lipoprotein(a) and asymptomatic carotid artery disease. Evidence of a prominent role in the evolution of advanced carotid plaques: the Bruneck Study.
abstract: OBJECTIVE
  Elevated levels of lipoprotein(a) [Lp(a)] have been reported in association with symptomatic coronary and carotid artery disease. Relevancy of Lp(a) as a risk predictor of presymptomatic atherosclerosis in general populations is not well established.
  
  
  METHODS
  Serum Lp(a) distribution and its relation to sonographically assessed carotid atherosclerosis were examined in a random sample of 885 men and women aged 40 to 79 years (Bruneck Study).
  
  
  RESULTS
  Logistic regression analysis revealed a binary-type association between Lp(a) and carotid artery disease, with the threshold level of Lp(a) for an enhanced atherosclerosis risk defined at 32 mg/dL. The strength of relation increased with advancing severity of carotid atherosclerosis (odds ratios for Lp(a), 1.8 for nonstenotic and 4.7 for stenotic carotid artery disease; P < .001). Lp(a) was unaffected by environmental factors except for a significant decrease in women taking hormone replacement therapy (P < .05). In a multivariate approach, Lp(a) turned out to be an independently significant predictor of carotid atherosclerosis (P < .001). No differential effect of Lp(a) on atherosclerosis (effect modification) was observed for sex, age, low-density lipoprotein cholesterol, apolipoprotein A-I and B, fasting glucose, diabetes, or hypertension. However, the Lp(a)-atherosclerosis relation was significantly modified by fibrinogen (P < .01) and antithrombin III (P < .05).
  
  
  CONCLUSIONS
  The present study demonstrates a strong and independent association between elevated Lp(a) levels and carotid atherosclerosis in a large randomized population and provides evidence of a potential role of Lp(a) in the evolution of carotid stenosis. Apart from atherogenicity of Lp(a) cholesterol, interference with fibrinolysis of atheroma-associated clots and fibrin deposits in the arterial wall may achieve pathophysiological significance.
authors.affiliation: Department of Neurology, University Clinic Innsbruck, Austria.
authors.forename: J
authors.initials: J
authors.lastname: Willeit
authors.forename: S
authors.initials: S
authors.lastname: Kiechl
authors.forename: P
authors.initials: P
authors.lastname: Santer
authors.forename: F
authors.initials: F
authors.lastname: Oberhollenzer
authors.forename: G
authors.initials: G
authors.lastname: Egger
authors.forename: E
authors.initials: E
authors.lastname: Jarosch
authors.forename: A
authors.initials: A
authors.lastname: Mair
mesh_terms: D000328:Adult; D000368:Aged; D000428:Alcohol Drinking; D000990:Antithrombin III / Q000032:analysis; D001161:Arteriosclerosis / Q000097:blood / Q000000981:diagnostic imaging*; D002340:Carotid Artery Diseases / Q000097:blood / Q000000981:diagnostic imaging*; D016893:Carotid Stenosis / Q000097:blood / Q000000981:diagnostic imaging; D018450:Disease Progression; D015914:Estrogen Replacement Therapy; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D005544:Forecasting; D006801:Humans; D007558:Italy; D017270:Lipoprotein(a) / Q000097:blood*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D016017:Odds Ratio; D012307:Risk Factors; D014463:Ultrasonography
chemical_list: D017270:Lipoprotein(a); D000990:Antithrombin III; D005340:Fibrinogen