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Circulation. 2005;111:1660-1665
Published online before print March 28, 2005, doi: 10.1161/01.CIR.0000160365.18879.1C
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(Circulation. 2005;111:1660-1665.)
© 2005 American Heart Association, Inc.


Pediatric Cardiology

Endothelial Dysfunction in Childhood Infection

Marietta Charakida, MD; Ann E. Donald, AVS; Mari Terese, BSc (Hons), AVS; Sam Leary, PhD; Julian P. Halcox, MB, MA, MRCP; Andy Ness, PhD, MFPH; George Davey Smith, MD, DSc, FFPH; Jean Golding, PhD, DSc, FMedSci; Peter Friberg, MD, PhD; Nigel J. Klein, PhD, FRCPCH; John E. Deanfield, BA, BCh, MB, FRCP, for the ALSPAC (Avon Longitudinal Study of Parents and Children) Study Team

From the Vascular Physiology Unit (M.C., A.E.D., J.P.H., P.F., J.E.D.) and Infectious Diseases and Microbiology Unit (N.J.K.), Institute of Child Health, UCL University, London, United Kingdom; and the Unit of Paediatric and Perinatal Epidemiology (M.T., S.L., A.N., G.D.S., J.G.), Department of Community Based Medicine, University of Bristol, Bristol, United Kingdom.

Correspondence to Marietta Charakida, Vascular Physiology Unit, 30 Guilford St, London WC1N 1EH, United Kingdom. E-mail charakidadoc{at}hotmail.com

Received July 25, 2004; revision received December 13, 2004; accepted January 25, 2005.

Background— Atherosclerosis begins in early life, and endothelial dysfunction is recognized as a key initiating event in the development of atherosclerosis. Although infection has been implicated in endothelial dysfunction and atherogenesis, the impact of acute common childhood infections on the vascular endothelium is unknown.

Methods and Results— We studied 600 children aged 10 years drawn from the Avon Longitudinal Study of Parents and Children. The children were divided into 3 groups: those with current acute infection (AI; n=135; 73 boys and 62 girls); a convalescent group with infection in the past 2 weeks (n=166; 78 boys and 88 girls), and a healthy control group (n=299; 131 boys and 168 girls). Endothelial function was determined in all subjects by high-resolution ultrasound to measure brachial artery flow-mediated dilation (FMD) and was expressed as the percentage change in diameter from baseline after reactive hyperemia. FMD was repeated in 40 children in the AI group and 50 in the control group after a mean interval of 1 year. FMD was lower in both the AI group (6.3±2.7%, mean±SD) and the convalescent group (8.1±3.1%) than in the control group (9.7±2.5%; P<0.001 for both). The observed differences in FMD remained after adjustment for potential confounding variables. At the repeat visit, FMD was unchanged in controls (P=0.85) but improved in the AI group (P<0.001).

Conclusions— Acute infection in childhood is associated with impaired endothelium-dependent vasodilation. These findings support a potential role for previously unsuspected extrinsic inflammatory stimuli in the pathogenesis of early atherosclerosis.


Key Words: infection • endothelium • risk factors • population


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