Detection of Chlamydia pneumoniaein Human Nonrheumatic Stenotic Aortic Valves

AbstractObjectives. We sought to study the possible presence of Chlamydia pneumoniaein aortic valve stenosis (AVS).Background. Inflammation and immune mechanisms are considered important for the pathogenesis of nonrheumatic AVS. All chlamydial species are able to cause heart infections, and seroepidemiologic studies have indicated an association between chronic C. pneumoniaeinfection and coronary artery disease. Furthermore, the organism has been demonstrated in atherosclerotic lesions.Methods. Aortic valve specimens with varying degrees of macroscopic disease were obtained from 35 subjects—17 consecutive patients undergoing aortic valve replacement for treatment of nonrheumatic AVS and 18 age-matched subjects at autopsy. The possible presence of C. pneumoniaein aortic valves was studied by immunohistochemical analysis, polymerase chain reaction or transmission electron microscopy, or a combination of these.Results. Positive immunohistochemical staining with C. pneumoniaespecific antibody was found in 9 (53%) of 17 patients with advanced aortic valve disease requiring surgical treatment (group A), 8 (80%) of 10 cadavers with clearly macroscopic aortic valve pathology (group B) and 1 (12%) of 8 grossly normal cadaver control subjects (group C). Statistical significance with regard to the presence of C. pneumoniaewas found when combined diseased subjects (groups A and B: total 17 of 27 subjects) were compared with group C (p = 0.018). However, when group A was compared with group C, there was only marginal statistical significance (p = 0.088). Finally, there was a strong statistical significance (p = 0.015) when groups B and C were compared. Chlamydia pneumoniaeDNA was also found in three stenotic valves, and in two of the three tested valve specimens chlamydia-like particles were seen by electron microscopy.Conclusions. Chlamydia pneumoniaeis frequently present in nonrheumatic AVS. Similarly, the high number of C. pneumoniaeinfections detected in the early lesions of “degenerative” AVS suggest that this pathogen may play an etiologic role in the development of this disease. The validity of this relation requires additional study.(J Am Coll Cardiol 1997;29:1054–9)© 1997 by the American College of Cardiolog