(Circulation. 2001;103:1064.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Chronic Infections and the Risk of Carotid Atherosclerosis
Prospective Results From a Large Population Study
From the Departments of Neurology (S.K., W.P., J.W.) and Internal Medicine (C.J.W.), University Clinic Innsbruck, the Institute for Biomedical Aging Research, Austrian Academy of Science (M. Mayr, Q.X., G.W.), and the Institute of General and Experimental Pathology, University of Innsbruck (G.W.), Innsbruck, Austria; the Department of Internal Medicine, Bruneck Hospital, Bruneck (G.E., F.O.), and the Department of Endocrinology and Metabolism, University of Verona, Verona (E.B., M. Muggeo), Italy; and the Department of Cardiological Sciences, St George’s Hospital Medical School, London, UK (Q.X.).
Correspondence to Dr S. Kiechl, Department of Neurology, Innsbruck University Clinic, Anichstraße 35, A-6020 Innsbruck, Austria.
Background—Chronic infections have been implicated in the pathogenesis of atherosclerosis, yet from an epidemiological perspective, this concept remains controversial.
Methods and Results—The Bruneck Study is a prospective population-based survey on the pathogenesis of atherosclerosis. In 826 men and women 40 to 79 years old (1990 baseline), 5-year changes in carotid atherosclerosis were thoroughly assessed by high-resolution duplex scanning. The presence of chronic respiratory, urinary tract, dental, and other infections was ascertained by standard diagnostic criteria. Chronic infections amplified the risk of atherosclerosis development in the carotid arteries. The association was most pronounced in subjects free of carotid atherosclerosis at baseline (age-/sex-adjusted odds ratio [95% CI] for any chronic infection versus none, 4.08 [2.42 to 6.85]; P<0.0001) and applied to all types of chronic (bacterial) infections. It remained independently significant after adjustment for classic vascular risk attributes and extended to low-risk individuals free of conventional risk factors. Among subjects with chronic infections, atherosclerosis risk was highest in those with a prominent inflammatory response. Markers of systemic inflammation, such as soluble adhesion molecules and circulating bacterial endotoxin, and levels of soluble human heat-shock protein 60 and antibodies to mycobacterial heat-shock protein 65 were elevated in subjects with chronic infections and predictive of an increased risk of atherosclerosis.
Conclusions—The present study provides solid evidence for a role of common chronic infections in human atherogenesis. Induction of systemic inflammation and autoimmunity may be potential pathophysiological links.
Key Words: atherosclerosis • inflammation • infection • carotid arteries • cardiovascular disease
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 J. K. Kiecolt-Glaser, L. McGuire, T. F. Robles, and R. Glaser Psychoneuroimmunology and Psychosomatic Medicine: Back to the Future Psychosom Med, January 1, 2002; 64(1): 15 - 28. [Abstract] [Full Text] [PDF]
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 E. Lutgens and M. J.A.P. Daemen Transforming Growth Factor-{beta}: A Local or Systemic Mediator of Plaque Stability? Circ. Res., November 9, 2001; 89(10): 853 - 855. [Full Text] [PDF]
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C. J. Wiedermann, S. Kiechl, P. Schratzberger, S. Dunzendorfer, G. Weiss, and J. Willeit The role of immune activation in endotoxin-induced atherogenesis Innate Immunity, August 1, 2001; 7(4): 322 - 326. [Abstract] [PDF]
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L. Li, E. Messas, E. L. Batista Jr, R. A. Levine, and S. Amar Porphyromonas gingivalis Infection Accelerates the Progression of Atherosclerosis in a Heterozygous Apolipoprotein E-Deficient Murine Model Circulation, February 19, 2002; 105(7): 861 - 867. [Abstract] [Full Text] [PDF]
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