Presence of Chlamydia pneumoniae in human symptomatic and asymptomatic carotid atherosclerotic plaque.
BACKGROUND
Chlamydia pneumoniae has been identified in atherosclerotic plaques of patients with cerebrovascular and cardiovascular disease. However, the direct causative effect of C pneumoniae infection in the activation of atherosclerotic plaque to a prothrombotic state remains to be established. The aim of the present study is to examine the correlation between intraplaque presence of chlamydiae and symptomatic carotid disease in humans.


METHODS
Plaques from 37 symptomatic and 57 asymptomatic consenting patients undergoing carotid endarterectomy were snap-frozen, and the tissue was prepared for polymerase chain reaction analysis for Chlamydia pneumoniae per Institutional Review Board-approved protocol. Blood was drawn from each patient at the time of surgery for serological analysis.


RESULTS
The overall rate of plaques positive for C pneumoniae was 14.82%, with 5 of 37 (13.5%) plaques from symptomatic patients and 9 of 57 (15.8%) from asymptomatic patients, which revealed a definitive presence of the organism. No association existed between C pneumoniae presence and symptomatic disease (P:=1.0). Also, no association existed between presence of C pneumoniae and severity of stenosis. Finally, seropositivity for anti-chlamydial IgG, IgA, and IgM anti-chlamydial antibodies did not correlate with identification of C pneumoniae in the plaques. However, high-serum anti-chlamydial IgA levels (>/=1:128) were associated with occurrence of symptomatic disease (P=0.03; odds ratio, 2.86; 95% CI, 1.12 to 7.28).


CONCLUSIONS
Presence of C pneumoniae as a single factor does not appear to be sufficient to explain the occurrence of cerebrovascular symptoms. Low sensitivity of seropositivity for IgG, IgA, or IgM associated with PCR-identified C pneumoniae presence in the plaque makes it unlikely to be valuable as the single determining factor for actively infected plaque. Association of high-level anti-chlamydial IgA with symptomatic disease suggests that chronic or acute chlamydial infection anywhere in the body could play a role in atherosclerotic plaque activation and be used as a marker to target populations in future stroke prevention trials.
LaBiche
R
R
Stroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.
Koziol
D
D
Quinn
T C
TC
Gaydos
C
C
Azhar
S
S
Ketron
G
G
Sood
S
S
DeGraba
T J
TJ
D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood; D001161:Arteriosclerosis / Q000150:complications / Q000382:microbiology* / Q000473:pathology / Q000601:surgery; D002339:Carotid Arteries / Q000382:microbiology / Q000473:pathology / Q000601:surgery; D016893:Carotid Stenosis / Q000150:complications / Q000382:microbiology* / Q000473:pathology / Q000601:surgery; D016993:Chlamydophila pneumoniae / Q000235:genetics / Q000276:immunology / Q000302:isolation & purification*; D016894:Endarterectomy, Carotid; D005260:Female; D005455:Fluorescent Antibody Technique; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood; D008297:Male; D015999:Multivariate Analysis; D016133:Polymerase Chain Reaction; D012307:Risk Factors; D012698:Serologic Tests
D000907:Antibodies, Bacterial; D007070:Immunoglobulin A