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Clinical Chemistry 0: clinchem.2006.079947v2, 2007; 10.1373/clinchem.2006.079947
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Received on September 11, 2007
Accepted on January 15, 2007

Lipids, Lipoproteins, and Cardiovascular Risk Factors

Plasma Lipoprotein(a) Indicates Risk for 4 Distinct Forms of Vascular Disease

Gregory T. Jones 1*, Andre M. van Rij 1, Jennifer Cole 2, Michael J.A. Williams 1, Emma H. Bateman 1, Santica M. Marcovina 3, Meiying Deng 1, Sally P.A. McCormick 2

1 Department of Medical and Surgical Sciences, University of Otago, Dunedin, New Zealand
2 Department of Biochemistry, University of Otago, Dunedin, New Zealand
3 New Zealand and the Department of Medicine (SMM), Northwest Lipid Research Laboratories, University of Washington, Seattle, WA

* To whom correspondence should be addressed. E-mail: greg.jones{at}otago.ac.nz.

Background: Increased lipoprotein(a) [Lp(a)] concentrations are predictive for coronary artery disease (CAD). The risk conferred by Lp(a) for other types of vascular disease compared with CAD has not been investigated within a single population. This study aimed to investigate Lp(a) risk association for 4 different types of vascular disease (including CAD) within a predominantly white population.

Methods: We used an Lp(a) ELISA that measures Lp(a) independently of apo(a) size to measure plasma Lp(a) in patients [384 CAD, 262 peripheral vascular disease, 184 ischemic stroke (stroke), 425 abdominal aortic aneurysm] and 230 disease-free controls. We then conducted association studies with logistic regression, integrating the potential confounding effects of age, sex, diabetes, plasma lipids, and a history of previous hypertension, hypercholesterolemia, and smoking.

Results: Multivariate analyses with Lp(a) concentrations of >45 nmol/L (the 75th percentile value for controls) as the clinical cutoff showed increased Lp(a) concentrations to be a risk factor for all disease groups, with adjusted odds ratios ranging from 1.96 [95% confidence interval (CI) 1.24-3.08] for CAD to 2.33 (95% CI 1.39-3.89) for PVD. The risk conferred by Lp(a) appeared to be independent of other confounders, including exposure to statin/fibrate therapies. Similar odds ratios and confidence intervals between disease groups indicated that increased Lp(a) conferred a similar risk for all groups studied.

Conclusions: Lp(a) constitutes a stable risk factor of similar magnitude for 4 major forms of vascular disease. This association was not altered by exposure to standard lipid-lowering therapy.




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