Elevated CRP levels are associated with increased carotid atherosclerosis independent of visceral obesity
Received 22 August 2007; received in revised form 18 November 2007; accepted 21 December 2007. published online 20 February 2008.
Abstract
Background
Visceral obesity (VO) is associated with an increased risk of cardiovascular disease. Elevated C-reactive protein (CRP) levels are associated with VO and cardiovascular disease. After exploring the relation between CRP and VO, we aimed to evaluate the VO independent relation between CRP and carotid atherosclerosis.
Methods and results
The prevalence of inflammation was evaluated in 439 male subjects with VO without type 2 diabetes and manifest cardiovascular disease. Waist circumference significantly correlated with CRP (r: 0.20, p<0.001). However, 18.2% of patients in the waist circumference group 94–102 had elevated CRP levels while 9.6% of patients in the waist circumference group >118cm had low CRP levels. From the 439 subjects, 40 subjects were prospectively selected for MRI assessment of carotid atherosclerosis and visceral and subcutaneous adipose tissue distribution in a case–control setting matching for age and waist circumference. Twenty male subjects with age >50 years with CRP levels >2.5mg/L (CRP+) were compared to 20 controls with CRP levels <1.8mg/L (CRP−). Maximum vessel wall thickness in CRP+ was significantly higher both in the common carotid artery (15%, p<0.01) and the bulb region (18%, p<0.01). The distribution of fat in visceral and subcutaneous deposits was not significantly different between CRP+ and CRP−.
Conclusion
Elevated CRP levels are associated with significantly increased maximum vessel wall thickness independent of VO and of MRI measured adipose tissue distribution, both in the common carotid artery and the carotid bulb.
aVascular Medicine, Department of General Internal Medicine & Endocrinology, Leiden University Medical Centre, Leiden, The Netherlands
bDepartment of Radiology, Leiden University Medical Centre, Leiden, The Netherlands
cDepartment of Nephrology & Einthoven Laboratory, Leiden University Medical Centre, Leiden, The Netherlands
dDepartment of Clinical Chemistry, Leiden University Medical Centre, Leiden, The Netherlands
Corresponding author at: Vascular Medicine, Department of General Internal Medicine & Endocrinology, Leiden University Medical Centre, P.O. Box 9600, 2300RC Leiden, The Netherlands. Tel.: +31 71 5262085; fax: +31 71 5248140.
ABSTRACT