Published Online
on March 3, 2005

A more recent version of this article appeared on April 1, 2005

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Submitted on November 3, 2004
Revised on January 5, 2005
Accepted on January 12, 2005

Monocyte Count Is a Predictor of Novel Plaque Formation. A 7-Year Follow-up Study of 2610 Persons Without Carotid Plaque at Baseline. The Tromsø Study

Stein Harald Johnsen MD^*; Einar Fosse MD; Oddmund Joakimsen MD, PhD; Ellisiv B. Mathiesen MD, PhD; Eva Stensland-Bugge MD, PhD; Inger Njølstad MD, PhD; and Egil Arnesen MD

From the Institute of Community Medicine (S.H.J., E.F., E.B.M., I.N., E.A.), University of Tromsø; and the Department of Neurology (O.J., E.B.M., E.S.-B.), University Hospital of Northern Norway, Tromsø, Norway.

^* To whom correspondence should be addressed. E-mail: Stein.Johnsen{at}ism.uit.no.

Background and Purpose--Activation of monocytes and differentiation into lipid-laden macrophages are fundamental events in generation of atherosclerotic lesions. There exist few data on monocyte activity and the risk for atherosclerosis. In this prospective population-based study, we examined whether monocyte count in blood is a predictor of future plaque formation in persons without pre-existing carotid atherosclerosis.

Methods--At baseline, we measured monocyte count, white cell count (WCC), fibrinogen, intima-media thickness (IMT), and traditional cardiovascular risk factors in 2610 men and women aged 25 to 82 years who on ultrasound had no plaque in their right carotid artery. After 7 years of follow-up, a new ultrasound screening was performed and the number of novel plaques was grouped as none, 1 plaque, and 2 or more plaques.

Results--In multivariate analysis, monocyte count, age, sex, total cholesterol, current smoking, systolic blood pressure, and IMT were independent predictors of novel plaque formation. No significant association was found between plaque formation and either WCC or fibrinogen. For 1 standard deviation (0.17x10⁹) increase in monocyte count, the risk of being in a higher plaque category increased by 18% (OR, 1.18; 95% CI, 1.08 to 1.29). In the highest monocyte quartile, the risk for having plaque compared with the lowest quartile was 1.85 (OR) (95% confidence interval, 1.41 to 2.43). Repeating the analysis without IMT did not change the monocyte estimate. Excluding subjects with cardiovascular disease and diabetes mellitus from analysis neither changed the monocyte estimate.

Conclusion--Monocyte count is an independent predictor of future plaque formation in subjects without pre-existing carotid atherosclerosis.

Key words: atherosclerosis • inflammation • intima-media thickness • risk factors • ultrasonography

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