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Cardiovascular Research 2002 56(2):178-180; doi:10.1016/S0008-6363(02)00652-1
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Chlamydia pneumoniae inside the atherosclerotic plaque—does it affect plaque inflammation and plaque progression?

Allard C van der Wal*

Department of Cardiovascular Pathology, Academic Medical Centre, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands

* Tel.: +31-20-566-5633; fax: +31-20-691-4738. a.c.vanderwal@amc.uva.nl

Received 27 August 2002; accepted 28 August 2002

The first 10% of the full text of this article appears below.

See article by Ezzahiri et al. [5] (pages 269–276) in this issue.


    1. Introduction
 
Exposure to Chlamydia pneumoniae (Cp) is very common among the human population world-wide. Circa 50% of adults bear antibodies to Cp and re-infections occur frequently: most people have 2–3 infections in a lifetime [1]. In Cardiovascular Medicine, interest for such a common opportunistic agent was initiated by insights in seroepidemiologic associations between Cp infection and the risk of atherosclerotic vascular disease, myocardial infarction and stroke [2]. Atherosclerosis has recently been classified as a chronic inflammatory disease [3], so potentially the disease could indeed be initiated or modulated by infectious agents. Still, despite numerous clinical and pathological observations . . . [Full Text of this Article]


    2. Chlamydia pneumoniae infection and plaque inflammation
 

    3. Chlamydia pneumoniae infection and plaque progression
 

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M. D. de Kruif, E. C.M. van Gorp, T. T. Keller, J. M. Ossewaarde, and H. ten Cate
Chlamydia pneumoniae infections in mouse models: relevance for atherosclerosis research
Cardiovasc Res, February 1, 2005; 65(2): 317 - 327.
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