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(Stroke. 2009;40:3466.)
© 2009 American Heart Association, Inc.

Original Contributions

Inflammatory Biomarkers of Vascular Risk as Correlates of Leukoariosis

Clinton B. Wright, MD, MS; Yeseon Moon, MS; Myunghee C. Paik, PhD; Truman R. Brown, PhD; LeRoy Rabbani, MD; Mitsuhiro Yoshita, MD, PhD; Charles DeCarli, MD; Ralph Sacco, MD, MS Mitchell S.V. Elkind, MD, MS

From Evelyn F. McKnight Center for Age-Related Memory Loss and the Department of Neurology (C.B.W., R.S.), Miller School of Medicine, University of Miami, Miami, Fla; Department of Biostatistics (Y.M., M.C.P.), Mailman School of Public Health, Columbia University, New York, NY; Department of Radiology (T.R.B.), Columbia University, New York, NY; Department of Medicine (L.R.), College of Physicians and Surgeons, Columbia University, New York, NY; Department of Neurology (M.Y.), Kanazawa University Graduate School of Medical Science, Takara-machi, Kanazawa, Japan; Department of Neurology and Center for Neuroscience (C.D.), University of California-Davis, Sacramento, Calif; Department of Neurology (M.S.V.E.), College of Physicians and Surgeons, Columbia University, New York, NY.

Correspondence to Clinton Wright, MD, MS, Evelyn F. McKnight Center for Age-related Memory Loss, Department of Neurology, Miller School of Medicine, University of Miami, 1120 NW 14th Street, Room 1349, Miami, FL 33136. E-mail cwright{at}med.miami.edu

Background and Purpose— Inflammatory biomarkers, including lipoprotein-associated phospholipase A2 (Lp-PLA2), myeloperoxidase (MPO), and high-sensitivity C-reactive protein (hsCRP) are associated with ischemic stroke risk. White matter hyperintensities (WMH) seen on brain MRI scans are associated with vascular risk factors and an increased risk of incident stroke, but their relation to inflammatory biomarkers is unclear.

Methods— The Northern Manhattan Study includes a stroke-free community-based sample of Hispanic, black, and white participants with quantitative measurement of WMH volume (WMHV) and inflammatory biomarkers. We measured the association between Lp-PLA2, MPO, and hsCRP levels, and log-transformed WMHV after adjusting for sociodemographic and vascular risk factors.

Results— The hsCRP (median, 2.42 mg/L; IQR, 1.04, 5.19), Lp-PLA2 (median, 220.97 ng/mL; IQR, 185.77, 268.05), and MPO (median, 15.14 ng/mL; IQR, 12.32, 19.69) levels were available in 527 The Northern Manhattan Study participants with WMHV data but no subclinical infarcts. Those with hsCRP in the upper quartile (Q4 >4.92 mg/L or >3 mg/L), Lp-PLA2 in Q4 (264.9 ng/mL), or MPO levels in Q3 (15.04–19.39 ng/mL) or Q4 (>19.39 ng/mL) each had greater WMHV, adjusting for sociodemographic and vascular risk factors. Adjusting for all biomarkers simultaneously, WMHV was 1.3-fold greater for Lp-PLA2 levels in Q4 compared to Q1 (β=0.28; P=0.008) and 1.25-fold greater for MPO levels above the median compared to below (β=0.22; P=0.02), but hsCRP was not associated with WMHV.

Conclusions— Relative elevations of the inflammatory markers Lp-PLA2 and MPO were associated with a greater burden of WMH independent of hsCRP.

Key Words: C-reactive protein • leukoariosis • lipoprotein-associated phospholipase A₂ • myeloperoxidase • white matter disease