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Lack of association between infectious burden and carotid atherosclerosis in Japanese patients

Noriko Hagiwara1, Kazunori Toyoda, Tooru Inoue

  • 1Department of Cerebrovascular Disease, Cerebrovascular Center and Clinical Research Institute, National Hospital Organization Kyushu Medical Center, Fukuoka, Japan. hagiwara@intmed2.med.kyushu-u.ac.jp <hagiwara@intmed2.med.kyushu-u.ac.jp>

Journal of Stroke and Cerebrovascular Diseases : the Official Journal of National Stroke Association
|August 11, 2007
PubMed

Insights

Infectious agents like cytomegalovirus (CMV) and herpes simplex virus (HSV) were investigated for their role in carotid atherosclerosis among Japanese patients. Detection rates of these pathogens in plaques and blood were low and did not correlate with disease severity.

Area of Science:

  • Cardiovascular Medicine
  • Infectious Diseases
  • Pathogenesis Research

Background:

  • Infectious agents including Chlamydia pneumoniae, cytomegalovirus (CMV), herpes simplex virus (HSV), and Helicobacter pylori are suspected contributors to atherosclerosis.
  • The role of infection in atherosclerosis pathogenesis may differ across racial and geographic populations.
  • Understanding the infectious burden in atherogenesis is crucial, particularly in diverse patient groups.

Purpose of the Study:

  • To investigate the association between specific pathogens (C. pneumoniae, CMV, HSV, H. pylori) and carotid atherosclerosis in Japanese patients.
  • To evaluate the relevance of infectious agents in the development of atherosclerosis in patients undergoing carotid endarterectomy.
  • To determine if the presence of pathogens or serological markers correlates with plaque characteristics and clinical symptoms.

Main Methods:

  • Polymerase chain reaction (PCR) was used to detect DNA of C. pneumoniae, CMV, HSV, and H. pylori in 50 carotid atherosclerotic plaques.
  • Immunocytochemistry (ICC) was employed to detect C. pneumoniae in plaque samples.
  • Serum IgG and/or IgA antibodies for each pathogen were analyzed, alongside PCR and ICC results, to assess infectious burden.

Main Results:

  • Herpes simplex virus (HSV) DNA was detected in 4% of specimens, and Chlamydia pneumoniae (C. pneumoniae) was identified by ICC in 16% of plaques.
  • No significant correlation was found between the presence of detected pathogens (via PCR, ICC) or serum antibodies and plaque severity (stenosis, ulceration) or symptoms.
  • The detection rates of infectious agents within atherosclerotic plaques were notably lower in this Japanese cohort compared to previous international studies.

Conclusions:

  • The low detection rates suggest that common infectious agents may play a limited role in the pathogenesis of severe carotid atherosclerosis among the studied Japanese population.
  • An inflammatory mechanism driven by these specific infections might not be a primary factor in atherogenesis for Japanese patients with severe carotid artery stenosis.
  • Further research is needed to explore potential ethnic or geographic variations in the relationship between infectious agents and atherosclerosis.

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