(Stroke. 1995;26:1582-1587.)
© 1995 American Heart Association, Inc.
Articles |
Lipoprotein(a) and Asymptomatic Carotid Artery Disease
Evidence of a Prominent Role in the Evolution of Advanced Carotid Plaques: The Bruneck Study
From the Departments of Neurology (J.W., S.K.) and Laboratory Medicine (E.J.), University Clinic Innsbruck (Austria); and the Departments of Laboratory Medicine (P.S., A.M.) and Internal Medicine (F.O., G.E.), Hospital of Bruneck (Italy).
Correspondence to Johann Willeit, MD, Department of Neurology, University Clinic of Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria.
Background and Purpose 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.
Key Words: atherosclerosis • carotid arteries • epidemiology • lipoproteins • ultrasonics
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