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(Stroke. 2005;36:2571.)
© 2005 American Heart Association, Inc.

Original Contributions

Association of Serum-Soluble Heat Shock Protein 60 With Carotid Atherosclerosis

Clinical Significance Determined in a Follow-Up Study

Qingzhong Xiao, MD; Kaushik Mandal, MD; Georg Schett, MD; Manuel Mayr, MD, PhD; Georg Wick, MD; Friedrich Oberhollenzer, MD; Johann Willeit, MD; Stefan Kiechl, MD Qingbo Xu, MD, PhD

From the Department of Cardiac and Vascular Sciences (Q.X., K.M., M.M., Q.X.), St George’s University of London, United Kingdom; Department of Internal Medicine (G.S.), University of Vienna, Austria; Department of Internal Medicine (F.O.), Hospital of Brunneck, Italy; Division of Experimental Pathology and Immunology (G.W.), Medical University Innsbruck, Austria; and Department of Neurology (J.W., S.K.), Medical University Innsbruck, Austria

Correspondence to Qingbo Xu, MD, PhD, Department of Cardiological Sciences, St George’s University of London, Cranmer Terrace, London SW17 0RE, United Kingdom. E-mail q.xu{at}sghms.ac.uk

Background and Purpose— Previous work has shown that soluble heat shock protein 60 (HSP60; sHSP60), present in circulating blood, is associated with carotid atherosclerosis. In the current evaluation, we tested the hypothesis that sHSP60 levels are associated with the progression of carotid arteriosclerosis, prospectively.

Methods— The association of sHSP60 with early atherogenesis (5-year development and progression of nonstenotic carotid plaques) was investigated as part of the population-based prospective Bruneck Study. The current study focused on the follow-up period between 1995 and 2000 and, thus, included 684 subjects.

Results— sHSP60 levels measured in 1995 and 2000 were highly correlated (r=0.40; P<0.001), indicating consistency over a 5-year period. Circulating HSP60 levels were significantly correlated with antilipopolysaccharide and anti-HSP60 antibodies. It was also elevated in subjects with chronic infection (top quintile group of HSP60, among subjects with and without chronic infection: 23.8% versus 17.0%; P=0.003 after adjustment for age and sex). HSP60 levels were significantly associated with early atherogenesis, both in the entire population (multivariate odds ratio, for a comparison between quintile group V versus I+II: 2.0 [1.2 to 3.5] and the subgroup free of atherosclerosis at the 1995 baseline: 3.8 [1.6 to 8.9]). The risk of early atherogenesis was additionally amplified when high-sHSP60 and chronic infection were present together.

Conclusions— Our study provides the first prospective data confirming an association between high levels of sHSP60 and early carotid atherosclerosis. This possibly indicates an involvement of sHSP60 in activating proinflammatory processes associated with early vessel pathology.

Key Words: heat shock protein • atherosclerosis • progression • follow-up

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