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Review
. 2003 Jul;12(4):447-53.

Pathogenetic role of Chlamydia pneumoniae in calcific aortic stenosis: immunohistochemistry study and review of the literature

Affiliations
  • PMID: 12918845
Review

Pathogenetic role of Chlamydia pneumoniae in calcific aortic stenosis: immunohistochemistry study and review of the literature

Jens J Kaden et al. J Heart Valve Dis. 2003 Jul.

Abstract

Background and aim of the study: Non-rheumatic, calcific aortic stenosis (AS) is the most prevalent heart valve disease in the elderly. It is based on a chronic inflammatory process with infiltration and activation of leukocytes, and a rise in systemic inflammatory markers. An association with Chlamydia pneumoniae infection has been discussed, but previous studies have yielded divergent results.

Methods: Tricuspid aortic valves with calcific AS were obtained from patients undergoing aortic valve replacement. Control valves from patients matched for age and cardiovascular risk factors were obtained at autopsy. Immunohistochemistry was performed using monoclonal antibodies directed against C. pneumoniae and against leukocyte common antigen. Cultured HEp-2 cells infected with C. pneumoniae were used as positive controls.

Results: Positive immunostaining for C. pneumoniae was demonstrated in 12 of 14 (86%) stenotic valves and in six of nine (67%) control valves. Immunostained cells were located mainly in cell- and leukocyte-rich areas. Although stenotic valves showed a higher staining intensity as assessed by semiquantitative scoring (1.8 +/- 0.4 versus 0.8 +/- 0.2 units, p < 0.05), there was no statistically significant difference between stenotic and control valves regarding the presence of C. pneumoniae (p = 0.90).

Conclusion: Positive immunostaining for C. pneumoniae was not associated with the presence of calcific AS. As in previous serologic and molecular biology studies, a high prevalence of C. pneumoniae in the adult population was demonstrated, irrespective of heart valve disease. Thus, C. pneumoniae is most likely not involved in the pathogenesis of calcific aortic stenosis.

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