C-reactive protein levels and viable Chlamydia pneumoniae in carotid artery atherosclerosis

S C Johnston1, L M Messina, W S Browner

  • 1Neurovascular Service, Department of Neurology, University of California, San Francisco, USA. clayj@itsa.ucsf.edu

Stroke
|December 12, 2001
PubMed

Insights

Chronic Chlamydia pneumoniae infection in carotid artery plaques is linked to higher C-reactive protein levels, a marker for cardiovascular disease risk. This suggests a potential mechanism explaining the association between inflammation and stroke.

Area of Science:

  • Cardiovascular Science
  • Infectious Disease Epidemiology
  • Inflammation Research

Background:

  • Elevated C-reactive protein (CRP) is a known predictor of stroke and coronary artery disease.
  • Chlamydia pneumoniae infection has been detected in atherosclerotic plaques.
  • The role of chronic C. pneumoniae infection in systemic inflammation remains unclear.

Purpose of the Study:

  • To investigate the association between serum C-reactive protein levels and the presence of viable Chlamydia pneumoniae in carotid artery atherosclerotic plaques.
  • To determine if C. pneumoniae infection contributes to systemic inflammation indicated by CRP.

Main Methods:

  • Serum CRP levels were measured in patients undergoing carotid endarterectomy.
  • Carotid plaques were analyzed for C. pneumoniae using polymerase chain reaction (PCR) to detect DNA and mRNA (indicating viability).

Main Results:

  • Viable C. pneumoniae (detected by mRNA) was found in 38% of the 48 studied plaques.
  • Patients with viable C. pneumoniae in their plaques had significantly higher serum CRP levels (median 8 mg/L vs. undetectable).
  • Detectable CRP levels were an independent predictor of viable C. pneumoniae infection (OR, 4.2; P=0.04).

Conclusions:

  • Viable Chlamydia pneumoniae is present in a significant proportion of carotid atherosclerotic plaques.
  • This infection is associated with elevated serum C-reactive protein levels.
  • These findings may elucidate the link between CRP, inflammation, and cardiovascular disease risk, warranting further investigation in larger cohorts.
Abstract

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