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(Stroke. 2006;37:2910.)
© 2006 American Heart Association, Inc.

Original Contributions

C-Reactive Protein, Carotid Atherosclerosis, and Cerebral Small-Vessel Disease

Results of the Austrian Stroke Prevention Study

Reinhold Schmidt, MD; Helena Schmidt, MD, PhD; Martin Pichler, MD; Christian Enzinger, MD; Katja Petrovic, PhD, MSc; Kurt Niederkorn, MD; Susanna Horner, MD; Stefan Ropele, PhD; Norbert Watzinger, MD; Martin Schumacher, MD; Andrea Berghold, PhD; Gerhard M. Kostner, PhD Franz Fazekas, MD

From the Departments of Neurology (R.S., M.P., C.E., K.P., K.N., S.H., S.R., F.F.) and Radiology (R.S., C.E.); the Institute of Medical Molecular Biology and Medical Biochemistry (H.S., G.M.K.); the Department of Cardiology (N.W., M.S.); and the Institute for Medical Informatics, Statistics and Documentation (A.B.), Medical University of Graz, Graz, Austria.

Correspondence to Reinhold Schmidt, MD, Department of Neurology, Medical University of Graz, Auenbruggerplatz 22, 8036 Graz, Austria. E-mail reinhold.schmidt{at}meduni-graz.at

Background and Purpose— C-reactive protein (CRP) is an inflammatory marker known to be a risk factor for stroke. We examined the associations between CRP, carotid atherosclerosis, white matter lesions, and lacunes as manifestations of cerebral large- and small-vessel disease.

Methods— In the community-based Austrian Stroke Prevention Study, CRP concentrations were measured by a highly sensitive assay in 700 participants at baseline. All underwent carotid duplex scanning, and a subset of 505 subjects underwent brain magnetic resonance imaging. Imaging was repeated after 3 and 6 years. We graded carotid atherosclerosis in both common and internal carotid arteries on a 5-point scale and calculated the sum of scores as an index of the severity of carotid atherosclerosis. The volume of white matter lesions and the number of lacunes were considered small vessel disease–related brain abnormalities.

Results— After adjustment for vascular risk factors, the severity and progression of extracranial carotid atherosclerosis increased with increasing quintiles of CRP. Only study participants in the fourth and fifth quintile (>2.50 mg/L) had significantly more baseline atherosclerosis and greater progression when we used the first quintile (<0.80 mg/L) as a reference. No interactions were seen between CRP quintiles and vascular risk factors for carotid atherosclerosis. The associations between severity and progression of small vessel disease–related brain abnormalities and CRP were nonsignificant.

Conclusions— We found evidence for differential effects of CRP in different beds of the arterial brain supply. CRP was a marker for active carotid atherosclerosis but not for small vessel disease–related brain lesions.

Key Words: carotid atherosclerosis • cerebral small-vessel disease • lacunes • risk factors • white matter lesions

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