Endovascular Presence of Chlamydia pneumoniae in Patients with Hemodynamically Effective Carotid Artery Stenosis

Abstract

The bacterial pathogen Chlamydia pneumoniae has been associated with atherosclerosis. Recent studies have reported chlamydial antigen to be present in atherosclerotic coronary arteries, but this relation has not yet been widely accepted. In order to verify an endovascular presence of potentially viable chlamydiae by detection of genomic DNA, the authors examined atherosclerotic carotid arteries by using a C. pneumoniae-specific nested polymerase chain reaction. Chlamydial DNA was detected in 9 of 61 (15%) arterial samples obtained from therapy of hemodynamically effective cervical vascular stenosis. Chlamydial presence was limited to advanced atherosclerotic lesions (P < or = 0.02): tissues from the same arteries with early subendothelial lesions did not harbor the pathogen. Thus, an etiologic role of C. pneumoniae is more plausible for progression than for initiation of atherosclerotic lesions. Histomorphologic discrimination of infected and noninfected samples was not possible and serology was unrewarding in detecting the infected patients. Chlamydial occurrence in atheromatous plaques is apparently a general phenomenon of atherosclerosis not limited to coronary arteries. Endovascular presence of genomic DNA of a bacterial pathogen susceptible to antimicrobial agents encourages thought on a new approach to prevent progression of atherosclerosis in a substantial proportion of patients. However, an etiologic contribution of C. pneumoniae in the multifactorial process of atherogenesis yet remains to be demonstrated.

Primary Prevention of Ischemic Stroke

“…Chlamydia pneumoniae, a Gram-negative obligate intracellular bacterium, has been identified in atherosclerotic carotid plaques [261][262][263][264][265] and localizes to regions of altered plaque morphology. 263,264 The fact that seropositivity to Chlamydia does not seem to correlate to carotid atherosclerosis, as measured by duplex ultrasonography, 265,266 supports the notion that Chlamydia may participate in plaque progression and destabilization as opposed to initiation of atherosclerosis, which may be why there appears to be a relationship between serum antibody titers to C pneumoniae and stroke. [267][268][269][270] The benefit of eradicating C pneumoniae from carotid plaques with antibiotic therapy remains unclear.…”

Chlamydial Heat Shock Protein 60 Localizes in Human Atheroma and Regulates Macrophage Tumor Necrosis Factor-α and Matrix Metalloproteinase Expression

“…9 Atheromatous lesions of the carotid arteries 10 and of the lower extremities 11 also contain C pneumoniae. Preliminary reports show that short courses of macrolide antibiotic therapy can reduce recurrent coronary events in patients with recent myocardial infarction or unstable angina and elevated anti-C pneumoniae antibody titers.…”

Chronic perivascular inoculation with Chlamydophila pneumoniae results in plaque formation in vivo

“…However, plaque progression following chronic CPN infection may result from the vasculotropism and the ability of CPN to persist in VSMCs and atheromatous plaques, 4,40,41 whereas other bacteria such as E. coli or C. trachomatis have never been detected in plaque tissues. The vasculotropism of CPN was recently demonstrated in an ex vivo human renal artery model, where LPS from CPN could be detected broadly in arteries following local infection; however, in this study, recultivation of viable organisms failed in all cases.…”