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Published on: May 6, 2014

Impact of intimal pathogen burden in acute coronary syndromes--correlation with inflammation, thrombosis, and

René P Andrié1, Gerhard Bauriedel, Izabela Tuleta

  • 1Department of Internal Medicine II/Cardiology, University of Bonn, Bonn, Germany. rene.andrie@ukb.uni-bonn.de

Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology
|November 17, 2009
PubMed

Insights

Pathogen burden (PB) in atheroma is linked to cardiovascular events. This study found increased PB and inflammation markers in acute coronary syndrome lesions, suggesting infectious agents contribute to plaque instability.

Area of Science:

  • Cardiovascular pathology
  • Infectious disease research
  • Immunology

Background:

  • Growing evidence links pathogen burden (PB) to cardiovascular event risk.
  • Atheroma, associated with acute coronary syndromes (ACS) and stable angina (SA), was investigated for intimal pathogen presence.
  • The study examined the effect of pathogens on intimal C-reactive protein (CRP), tissue factor (TF), and human heat-shock protein 60 (hHSP60) expression.

Purpose of the Study:

  • To evaluate the intimal presence of four specific pathogens in atheroma.
  • To assess the correlation between pathogen burden and cardiovascular events.
  • To determine the impact of pathogens on inflammatory and prothrombotic markers within atherosclerotic plaques.

Main Methods:

  • Coronary atherectomy specimens from 60 patients (35 ACS, 25 SA) were analyzed.
  • Immunohistochemistry was used to detect Chlamydia pneumoniae (Cpn), Helicobacter pylori (HP), Cytomegalovirus (CMV), and Epstein–Barr Virus (EBV).
  • Expression levels of CRP, TF, and hHSP60 were quantified in the intimal tissue.

Main Results:

  • Pathogens were detected in 92% of lesions, with Cpn (73%), HP (31%), EBV (40%), and CMV (16%) being most prevalent.
  • Higher pathogen burden was observed in ACS lesions compared to SA lesions.
  • Significantly elevated expressions of CRP, TF, and hHSP60 were found in ACS lesions, correlating with the number of detected pathogens.

Conclusions:

  • Pathogen burden significantly impacts atheroma plaque instability.
  • Infectious agents within plaques may promote local inflammation, thrombosis, and immune responses.
  • These findings highlight a potential role for pathogens in the pathogenesis of acute coronary syndromes.
Abstract

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