Microorganisms 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/Mikroorganizmalar ve kapak dokusu/aterosklerotik....
We read with great interest the article by Bayram et al. (1) regarding the presence of bacterial and viral pathogens in coronary and valve specimens determined by means of polymerase chain reaction method. The 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.
(1.) Bayram A, Erdogan MB, Eksi F, Yamak B. 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. Anadolu Kardiyol Derg 2011; 11: 237-43.
(2.) Sari I, Davutoglu V. Association of chronic subclinical inflammation with severity and progression of rheumatic valve disease. Int J Cardiol 2008; 124: 263.
(3.) Davutoglu V, Qelik A, Aksoy M. Contribution of selected serum inflammatory mediators to the progression of chronic rheumatic valve disease, subsequent valve calcification and NYHA functional class. J Heart Valve Dis 2005; 14: 251-6.
Vedat Davutoglu, Suleyman Ercan, Muhammed Oylumlu 
Department of Cardiology, Faculty of Medicine, Gaziantep University, Gaziantep
 Clinic of Cardiology, Sehitkamil State Hospital, Gaziantep-Turkey
Address for Correspondence/Yazisma Adresi: Dr. Vedat Davutoglu Department of Cardiology, Faculty of Medicine, Gaziantep University, 27310, Gaziantep-Turkey Phone: + 90 342 360 60 60/76290 Fax: + 90 342 360 39 28 E-mail: email@example.com Available Online Date/Cevrimici Yayin Tarihi: 11.08.2011
We agree with the information that authors of the letter have shared with us. We are thankful for their interest in our study (1). Additionally, we want to answer their questions about the potential role of microorganisms in the pathogenesis of atherosclerosis.
The hypothesis that several bacterial and viral agents may induce the progression of atherosclerosis has been extensively studied for two decades. Several studies have suggested an association between infectious agents and atherosclerosis (2,3).
These microorganisms not only bear triggering mechanisms for ongoing inflammations, they also have proactive roles in fibrotic tissue progression. They may comprise triggering factors for the initiation and/ or acceleration of an ongoing inflammatory process by increased expression of adhesion molecules and inflammatory cytokines, procoagulant effects, increased receptor expression and activity, enhanced uptake of cholesterol and of modified low-density lipoprotein, increased smooth muscle cell migration and proliferation, anti-apoptotic effects, and autoimmune response to infection (4).
The question whether microorganisms have proactive role in fibrotic tissue progression is answered partly by Tang et al. (5), who detected viral DNA in the lungs of patients with idiopathic pulmonary fibrosis (IPF) in their study. Similar to the lung pathology in patients with I PR another study supported the concept that viral infection of renal epithelial cells contributed to the pathogenesis of chronic interstitial nephritis with characteristic interstitial fibrosis (6). According to data obtained from these studies, we can conclude that chronic viral infection of epithelial cells may be a trigger for fibrogenesis in several organs, as well as in vessel wall.
(1.) Bayram A, Erdogan MB, Eksj F, Yamak B. 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. Anadolu Kardiyol Derg. 2011; 11: 237-43.
(2.) Kaplan M, Yavuz SS, Qmar B, Kbksal V, Kut MS, Yapici F, et al. Detection of Chlamydia pneumoniae and Helicobacter pylori DNA in atherosclerotic plaques of carotid artery by polimerase chain reaction. Int J Infect Dis 2006; 10: 116-23.
(3.) Ibrahim Al, Obeid MT, Jouma MJ, Moasis GA, Al-Richane WL, Kindermann I, et al. Detection of herpes simplex virus, cytomegalovirus and Epstein-Barr virus DNA in atherosclerotic plaques and in unaffected bypass grafts. J Clin Virol 2005; 32: 29-32.
(4.) Shi Y, Tokunaga 0. Herpes virus (HSV-1, EBV and CMV) infections in atherosclerotic compared with non-atherosclerotic aortic tissue. Pathol Int 2002;52:31-9.
(5.) Tang YW, Johnson JE, Browning PJ, Cruz-Gervis RA, Davis A, Graham BS. Herpes virus DNA is consistently detected in lungs of patients with idiopathic pulmonary fibrosis. J Clin Microbiol 2003; 41: 2633-40.
(6.) Becker JL, Miller E Nuovo GJ, Josepovitz C, Schubach WH, Nord ER Epstein-Barr virus infection of renal proximal tubule cells: possible role in chronic interstitial nephritis. J Clin Invest 1999; 104:1673-81.
Aysen Bayram, Mustafa B. Erdogan , Fahriye Eksi, Birol Yamak 
Department of Microbiology and Clinical Microbiology, Faculty of
Medicine, Gaziantep University
 Clinic of Cardiovascular Surgery, Sanko Hospital, Gaziantep-Turkey
Address for Correspondence/Yazisma Adresi: Dr. Aysen Bayram Department of Microbiology and Clinical Microbiology, Faculty of Medicine, Gaziantep University, Gaziantep-7ur/cey Phone: +90 342 360 60 60/77533 E-mail: firstname.lastname@example.org Available Online Date/Cevrimici Yaym Tarihi: 11.08.2011
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|Author:||Davutoglu, Vedat; Ercan, Suleyman; Oylumlu, Muhammed|
|Publication:||The Anatolian Journal of Cardiology (Anadolu Kardiyoloji Dergisi)|
|Article Type:||Letter to the editor|
|Date:||Sep 1, 2011|
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