OBJECTIVE: We evaluated the correlation between the presence of Chlamydia pneumoniae in atherosclerotic carotid plaques, lymph nodes, and peripheral blood mononuclear cells (PBMCs), and symptomatic carotid atherosclerotic disease. METHODS: Fifty-one consecutive patients undergoing carotid endarterectomy were enrolled; 18 of the 51 patients had symptomatic disease, whereas 33 had asymptomatic disease. Detection of C pneumoniae DNA in atherosclerotic carotid plaques, lymph nodes, and PBMCs was performed with polymerase chain reaction (PCR). C pneumoniae antibodies were measured with a microimmunofluorescence test. RESULTS: C pneumoniae DNA in atherosclerotic carotid plaques was detected in 44.4% of patients with symptomatic disease and in 30.3% of those with asymptomatic disease (P =.48). C pneumoniae DNA in lymph nodes was detected in 33.3% of patients with symptomatic disease and 18.2% of those with asymptomatic disease (P =.19). Prevalence of C pneumoniae DNA in PBMCs was significantly higher in patients with symptomatic disease (72.2%) compared with those with asymptomatic disease (30.3%) (P =.01). Serologic results support the association between C pneumoniae DNA in PBMCs and symptomatic carotid atherosclerotic disease, because seropositivity for anti-chlamydial immunoglobulin (Ig) A antibodies was significantly higher in PCR-positive PBMCs in patients with symptomatic disease compared with patients with asymptomatic disease (P =.02). CONCLUSIONS: Detection of C pneumoniae in PBMCs shows that C pneumoniae may be associated with symptomatic carotid atherosclerotic disease. Although we believe there is need for standardization of PCR methods and for assessing sensitivity, specificity, and predictive values of the tests, we suggest that presence of C pneumoniae DNA in PBMCs is a valid surrogate marker of risk for endovascular chlamydial infection. Only long-term cohort studies and interventional trials will clarify the etiopathogenic role of C pneumoniae.
OBJECTIVE: We evaluated the correlation between the presence of Chlamydia pneumoniae in atherosclerotic carotid plaques, lymph nodes, and peripheral blood mononuclear cells (PBMCs), and symptomatic carotid atherosclerotic disease. METHODS: Fifty-one consecutive patients undergoing carotid endarterectomy were enrolled; 18 of the 51 patients had symptomatic disease, whereas 33 had asymptomatic disease. Detection of C pneumoniae DNA in atherosclerotic carotid plaques, lymph nodes, and PBMCs was performed with polymerase chain reaction (PCR). C pneumoniae antibodies were measured with a microimmunofluorescence test. RESULTS: C pneumoniae DNA in atherosclerotic carotid plaques was detected in 44.4% of patients with symptomatic disease and in 30.3% of those with asymptomatic disease (P =.48). C pneumoniae DNA in lymph nodes was detected in 33.3% of patients with symptomatic disease and 18.2% of those with asymptomatic disease (P =.19). Prevalence of C pneumoniae DNA in PBMCs was significantly higher in patients with symptomatic disease (72.2%) compared with those with asymptomatic disease (30.3%) (P =.01). Serologic results support the association between C pneumoniae DNA in PBMCs and symptomatic carotid atherosclerotic disease, because seropositivity for anti-chlamydial immunoglobulin (Ig) A antibodies was significantly higher in PCR-positive PBMCs in patients with symptomatic disease compared with patients with asymptomatic disease (P =.02). CONCLUSIONS: Detection of C pneumoniae in PBMCs shows that C pneumoniae may be associated with symptomatic carotid atherosclerotic disease. Although we believe there is need for standardization of PCR methods and for assessing sensitivity, specificity, and predictive values of the tests, we suggest that presence of C pneumoniae DNA in PBMCs is a valid surrogate marker of risk for endovascular chlamydial infection. Only long-term cohort studies and interventional trials will clarify the etiopathogenic role of C pneumoniae.