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Correlation between rises in Chlamydia pneumoniae-specific antibodies, platelet activation and lipid peroxidation

H Kälvegren1, J Fridfeldt, P Garvin

  • 1Department of Medicine and Health, Faculty of Health Sciences, Linköping University, 581 85, Linköping, Sweden. hanka@imv.liu.se

European Journal of Clinical Microbiology & Infectious Diseases : Official Publication of the European Society of Clinical Microbiology
|March 20, 2008
PubMed

Insights

Percutaneous coronary intervention (PCI) may release Chlamydia pneumoniae from atherosclerotic lesions, activating platelets and causing lipid peroxidation. This study investigated the link between PCI, C. pneumoniae infection, and cardiovascular risk markers.

Area of Science:

  • Cardiovascular Medicine
  • Infectious Diseases
  • Biochemistry

Background:

  • Chlamydia pneumoniae (C. pneumoniae) is known to activate platelets and oxidize low-density lipoproteins in vitro.
  • The potential release of C. pneumoniae during percutaneous coronary intervention (PCI) and its subsequent effects on platelet activation and lipid peroxidation remain under investigation.

Purpose of the Study:

  • To determine if C. pneumoniae is released during PCI.
  • To investigate the association between C. pneumoniae release, platelet activation, and lipid peroxidation following PCI.

Main Methods:

  • Serum C. pneumoniae IgA and IgG antibodies, serotonin, and lipid peroxidation were measured in 73 patients undergoing PCI/CABG and 57 controls.
  • Measurements were taken before and at 24 hours, 1 month, and 6 months after angiography.

Main Results:

  • Patients undergoing PCI/CABG showed significantly higher serum C. pneumoniae IgA concentrations than controls.
  • In 38% of C. pneumoniae IgG-positive patients, IgG levels increased 1 month post-PCI.
  • Elevated C. pneumoniae IgG 1 month post-PCI correlated strongly with increased plasma lipid peroxidation (r=0.91) and platelet-derived serotonin (r=0.62).

Conclusions:

  • PCI treatment for coronary stenosis appears to release C. pneumoniae from atherosclerotic lesions.
  • This release is associated with subsequent platelet activation and lipid peroxidation, suggesting a potential mechanism for cardiovascular events post-PCI.

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