Racial variation in lipoprotein-associated phospholipase A2 in older adults
- Equal contributors
1 Department of Health Research and Policy, Stanford University School of Medicine, HRP Redwood Building, Stanford, CA 94305-5405 USA
2 Kaiser Santa Clara Cardiology, Department 348, Kaiser Permanente of Northern California, 710 Lawrence Expressway, Santa Clara, CA 95051 USA
3 Center for Health Research, Kaiser Permanente Northwest, 3800 N. Interstate Avenue, Portland, OR 97227 USA
4 Stanford Prevention Research Center, Stanford University School of Medicine, Medical School Office Building, 251 Campus Drive, Stanford, CA 94305-5411 USA
5 Division of Research, Kaiser Permanente of Northern California, 2000 Broadway, Oakland, CA 94612 USA
6 Department of Epidemiology, Biostatistics, and Medicine, University of California, San Francisco, 185 Berry Street, Lobby 5, Suite 5700, San Francisco, CA 94107 USA
7 Cardiovascular Medicine, Stanford University School of Medicine, 300 Pasteur Drive, Falk Cardiovascular Research Center, Stanford, CA 94305-5406 USA
Citation and License
BMC Cardiovascular Disorders 2011, 11:38 doi:10.1186/1471-2261-11-38Published: 29 June 2011
Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a predictor of cardiovascular events that has been shown to vary with race. The objective of this study was to examine factors associated with this racial variation.
We measured Lp-PLA2 mass and activity in 714 healthy older adults with no clinical coronary heart disease and not taking dyslipidemia medication. We evaluated the association between race and Lp-PLA2 mass and activity levels after adjustment for various covariates using multivariable linear regression. These covariates included age, sex, diabetes, hypertension, body mass index, lipid measurements, C-reactive protein, smoking status, physical activity, diet, income, and education level. We further examined genetic covariates that included three single nucleotide polymorphisms shown to be associated with Lp-PLA2 activity levels.
The mean age was 66 years. Whites had the highest Lp-PLA2 mass and activity levels, followed by Hispanics and Asians, and then African-Americans; in age and sex adjusted analyses, these differences were significant for each non-White race as compared to Whites (p < 0.0001). For example, African-Americans were predicted to have a 55.0 ng/ml lower Lp-PLA2 mass and 24.7 nmol/ml-min lower activity, compared with Whites, independent of age and sex (p < 0.0001). After adjustment for all covariates, race remained significantly correlated with Lp-PLA2 mass and activity levels (p < 0.001) with African-Americans having 44.8 ng/ml lower Lp-PLA2 mass and 17.3 nmol/ml-min lower activity compared with Whites (p < 0.0001).
Biological, lifestyle, demographic, and select genetic factors do not appear to explain variations in Lp-PLA2 mass and activity levels between Whites and non-Whites, suggesting that Lp-PLA2 mass and activity levels may need to be interpreted differently for various races.