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Published online before print March 19, 2008, doi:10.1212/01.wnl.0000303969.63165.34)
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NEUROLOGY 2008;70:1200-1207
© 2008 American Academy of Neurology

Carotid plaque, a subclinical precursor of vascular events

The Northern Manhattan Study

T. Rundek, MD, PhD, H. Arif, MD, B. Boden-Albala, DrPH, M. S. Elkind, MD, MS, M. C. Paik, PhD and R. L. Sacco, MD, MS

From the Departments of Neurology (T.R., R.L.S.) and Epidemiology and Human Genetics (R.L.S.), University of Miami, Miller School of Medicine, FL; Department of Neurology (H.A., B.B.-A., M.S.E.), Columbia University College of Physicians and Surgeons, New York, NY; and Departments of Sociomedical Sciences (B.B.-A.) and Biostatistics (M.C.P.), Joseph Mailman School of Public Health, and Gertrude H. Sergievsky Center (M.S.E.), Columbia University, New York, NY.

Address correspondence and reprint requests to Dr. Tatjana Rundek, Department of Neurology, Miller School of Medicine, University of Miami, Clinical Research Bldg. (CRB), Suite 1348, 1120 NW 14th Street, Miami, FL 33136 trundek{at}med.miami.edu

Background: Carotid atherosclerosis is a known biomarker associated with future vascular disease. The risk associated with small, nonstenotic carotid plaques is less clear. The objective of this study was to examine the association between maximum carotid plaque thickness and risk of vascular events in an urban multiethnic cohort.

Methods: As part of the population-based Northern Manhattan Study, carotid plaque was analyzed among 2,189 subjects. Maximum carotid plaque thickness was evaluated at the cutoff level of 1.9 mm, a prespecified value of the 75th percentile of the plaque thickness distribution. The primary outcome measure was combined vascular events (ischemic stroke, myocardial infarction, or vascular death).

Results: Carotid plaque was present in 1,263 (58%) subjects. After a mean follow-up of 6.9 years, vascular events occurred among 319 subjects; 121 had fatal or nonfatal ischemic stroke, 118 had fatal or nonfatal myocardial infarction, and 166 died of vascular causes. Subjects with maximum carotid plaque thickness greater than 1.9 mm had a 2.8-fold increased risk of combined vascular events in comparison to the subjects without carotid plaque (hazard ratio, 2.80; 95% CI, 2.04–3.84). In fully adjusted models, this association was significant only among Hispanics. Approximately 44% of the low-risk individuals by Framingham risk score had a 10-year vascular risk of 18.3% if having carotid plaque.

Conclusions: Maximum carotid plaque thickness is a simple and noninvasive marker of subclinical atherosclerosis associated with increased risk of vascular outcomes in a multiethnic cohort. Maximum carotid plaque thickness may be a simple and nonexpensive tool to assist with vascular risk stratification in preventive strategies and a surrogate endpoint in clinical trials.

Abbreviations: ARIC = Atherosclerosis Risk in Communities; FRS = Framingham risk score; IMT = intima-media thickness; MCPT = maximum carotid plaque thickness; MI = myocardial infarct; NOMAS = Northern Manhattan Study.


Supplemental data at www.neurology.org

e-Pub ahead of print on March 19, 2008, at www.neurology.org.

Supported in part by the Gilbert Baum Memorial Grant and the Goddess Fund for Stroke Research in Women (TR) and by grants from the National Institute of Neurological Disorders and Stroke, R01 29993 (TR, RLS), K23 NS42912 (MSVE), AHA (Kathleen Scott Research Fellowship, MSVE), and the General Clinical Research Center (2 M01 RR00645).

Disclosure: The authors report no conflicts of interest.

Received July 20, 2007. Accepted in final form November 14, 2007.




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