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. 2002 Nov;33(11):2587-92.
doi: 10.1161/01.str.0000034400.71491.10.

Leukocyte count is associated with aortic arch plaque thickness

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Leukocyte count is associated with aortic arch plaque thickness

Mitchell S V Elkind et al. Stroke. 2002 Nov.

Abstract

Background and purpose: Leukocyte count has been associated with cardiovascular and cerebrovascular disease, including carotid plaque thickness, in several studies. We hypothesized that white blood cell count is associated with aortic arch plaque thickness (AAPT).

Methods: Leukocyte count was measured in randomly selected stroke-free community participants undergoing transesophageal echocardiography. AAPT was measured for each subject and dichotomized into <4 and > or =4 mm (thick plaque). Multivariate linear and logistic regression was used to calculate the effect of leukocyte count on AAPT after adjustment for potential confounding factors. Mean age of the 145 participants was 68.5+/-8.3 years; 43.5% were women; 15.9% were white; 31.7% were black; and 49.0% were Hispanic.

Results: Mean leukocyte count was 5.88+/-1.76x10(9)/L. Each unit increase in leukocyte count was associated with a mean 0.28-mm increase in AAPT (P=0.0036). After adjustment for other atherosclerosis risk factors, including age, sex, hypertension, diabetes, hyperlipidemia, and smoking, the relationship persisted (mean increase in AAPT, 0.24 mm; P=0.0064). Thirty-five participants (24.1%) had AAPT > or =4 mm. Mean leukocyte count among those with thick plaque was significantly higher than among those with plaque <4 mm (6.54+/-1.60 versus 5.65+/-1.76x10(9)/L, respectively; P=0.009). Each unit increase in leukocyte count was associated with an increased risk of thick plaque (adjusted odds ratio, 1.38; 95% CI, 1.05 to 1.79). The relationships were similar for men and women and for those <70 or > or =70 years of age.

Conclusions: Leukocyte count is associated with AAPT and is specifically correlated with AAPT > or =4 mm, a degree of thickening associated with increased stroke risk. These findings are consistent with current hypotheses regarding the inflammatory or infectious etiology of risk of atherosclerosis and stroke.

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