European Heart Journal Advance Access originally published online on November 30, 2004
European Heart Journal 2005 26(2):153-158; doi:10.1093/eurheartj/ehi016
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European Heart Journal vol. 26 no. 2 © The European Society of Cardiology 2004; all rights reserved.
Monocyte cyclooxygenase-2 overactivity: a new marker of subclinical atherosclerosis in asymptomatic subjects with cardiovascular risk factors?
1Department of Internal Medicine, University Clinic, Clínica Universitaria, Avenida de Pío XII 36, 31008 Pamplona, Spain
2Area of Cardiovascular Pathophysiology, Centre for Applied Medical Research, School of Medicine, Pamplona, Spain
3Department of Radiology, University Clinic, University of Navarra, Pamplona, Spain
Received 1 March 2004; revised 27 August 2004; accepted 8 September 2004; online publish-ahead-of-print 30 November 2004.
* Corresponding author. Tel: +34 948 296784; fax: +34 948 296500. E-mail address: obeloqui{at}unav.es
Aims Cyclooxygenase-2 (COX-2)-mediated prostaglandin production by activated macrophages is associated with inflammation and atherosclerosis. We investigated the relationship between COX-2-mediated prostaglandin-E2 (PGE2) release, cardiovascular risk factors, and carotid atherosclerosis in apparently healthy subjects.
Methods and results PGE2 release by lipopolysaccharide-stimulated blood monocytes was measured by ELISA in 291 subjects (76.5% men, mean age 58) who underwent global vascular risk assessment and carotid ultrasonography. COX-2 expression (real-time RT–PCR) was analysed in a subgroup of 100 subjects (76% men, mean age 59). Inducible PGE2 production was associated with smoking and diabetes (P<0.05), but not with arterial hypertension, dyslipidaemia, or obesity. Subjects in the highest tertile of PGE2 (>8.1 ng/mL) had significantly higher mean carotid intima–media thickness (IMT) than those in the lowest tertile (P<0.01). No significant differences among tertiles were observed in the levels of inflammatory markers (C-reactive protein, fibrinogen, and von Willebrand factor). The association between PGE2 and carotid IMT remained statistically significant (P=0.012) after adjustment for a number of cardiovascular and inflammatory risk factors. A correlation between COX-2 expression and PGE2 production was observed (P<0.005).
Conclusions COX-2-mediated PGE2 overproduction by stimulated monocytes might provide a new marker of subclinical atherosclerosis in asymptomatic subjects exposed to cardiovascular risk factors.
Key Words: Cyclooxygenase • Inflammation • Atherosclerosis • Cardiovascular risk • Carotid ultrasonography
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