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Dilated cardiomyopathy andChlamydia pneumoniaeinfection
  1. H SONG,
  2. H TASAKI,
  3. A YASHIRO,
  4. K YAMASHITA,
  5. T TOYOKAWA,
  6. Y NAGAI,
  7. H TAKATSU,
  8. H TANIGUCHI*,
  9. Y NAKASHIMA
  1. 2nd Department of Internal Medicine
  2. *Department of Microbiology
  3. School of Medicine
  4. University of Occupational and Environmental Health
  5. Kitakyushu, Japan
  1. Dr Hiromi Tasaki, 2nd Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan: h-tasaki{at}med.uoeh-u.ac.jp

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Dilated cardiomyopathy (DCM), characterised by a severe dysfunction of the heart muscle, often results from a myocarditis, which could be caused by a variety of organisms or mediated by autoimmune responses to the exposure of cardiac specific antigen, such as myosin, after cardiomyocyte damage. DCM of humans can be experimentally reproduced in susceptible mouse strains by immunisation with purified cardiac myosin.1 Moreover, chlamydia infection may mediate heart disease through an antigenic mimicry between the chlamydia outer membrane protein and muscle specific α myosin of the heart.2 The aim of this study was to investigate the prevalence of Chlamydia pneumoniae infection by measuring the serum IgG and IgA antibodies against C pneumoniae in patients with DCM.

Twenty six consecutive patients with DCM, aged 56.9 (15.5) years, diagnosed according to the World Health Organization/International Society and Federation of Cardiology criteria,3 were enrolled. Twenty eight healthy subjects, mean (SD) age 57.4 (13.7) years, matched for age and sex, were used as the controls; they were chosen from the subjects undergoing coronary angiography during the same period and not showing any significant coronary stenosis, valvar disease or other cardiovascular diseases. None of the patients had a clinical history of specific heart muscle disease that may have caused left ventricular …

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