Microorgansims and valve tissue/ Demonstration of Chlamydophila pneumoniae, Mycoplasma pneumoniae, Cytomegalovirus, and Epstein-Barr virus in atherosclerotic coronary arteries, nonrheumatic calcific aortic and rheumatic stenotic mitral valves by polymerase chain reaction

Abstract

Editöre Mektuplar Letter to Editor 564The authors sought to evaluate the presence of two bacterial (C. pneumoniae and M. pneumoniae) and two viral (CMV and EBV) pathogens in heart valves extracted during surgery. They found out that C. pneumoniae, M. pneumoniae, and CMV were detected in patients with stenotic aortic and mitral valves and in patients with coronary atherosclerosis with similar frequencies. The most striking findings for us are the relatively high frequency of C. pneumoniae, M. pneumoniae and CMV in mitral valve tissue (21%, 7%, and 12% respectively). The underlying mechanism and the progression of chronic rheumatic valve disease are remained to be a dilemma in regard to pathophysiologic insight. At least but not last, we know that the chronic phase of rheumatic valve involvement is strongly associated with ongoing release of serum inflammatory mediators, which correlate with the severity of valve involvement, valve scarring and subsequent valve calcification (2, 3). However, the most intriguing question so far, remained to be as an unknown triggering factor for progression and ongoing inflammation. Now according to Bayram et al. (1) we can speculate that one of the triggering mechanisms for valve scarring and ongoing inflammation might be a coexistence of some bacteria or viral microorganism? Alternatively, is there a proactive role of those organisms in terms of fibrotic tissue progression? Although the study by Bayram et al. (1) is too preliminary and needs to be clarified with respect to a cause-effect relationship, the results excite us for shedding more information about what presence of in micro word of valve.We thank authors for whipping us for a little more questioning the etiology of rheumatic valve.