Original Article Detection of infectious agents by polymerase chain reaction in human aortic wall Edyta Reszka a , Bogdan Jegier b, ⁎ , Wojciech Wasowicz a , Malgorzata Lelonek c , Maciej Banach c , Ryszard Jaszewski b a Department of Toxicology and Carcinogenesis, Nofer Institute of Occupational Medicine, Lodz, Poland b Department of Cardiac Surgery, 1st Chairof Cardiology and Cardiac Surgery, Medical University of Lodz, Poland c Department of Cardiology, 1st Chairof Cardiology and Cardiac Surgery, Medical University of Lodz, Poland Received 19 June 2007; received in revised form 8 October 2007; accepted 5 November 2007 Abstract Introduction: Several studies have been suggested that infectious agents may induce or progress the process of atherosclerosis in humans. In the present study, the samples of visually healthy human aortic wall were examined for the presence of Chlamydia pneumoniae, Mycoplasma pneumoniae, Helicobacter pylori, herpes simplex virus (HSV), and cytomegalovirus (CMV). Methods: Bacterial DNA of C. pneumoniae, M. pneumoniae, and H. pylori and viral DNA of HSV and CMV were analyzed by polymerase chain reaction. The specimens were obtained from 40 patients with atherosclerotic three-vessel stable coronary artery disease referred to surgical revascularization (coronary group) and 20 controls referred to aortic valve replacement (valve group). Results: C. pneumoniae was detected in 11 of 40 samples of aorta in coronary group (27.5%) and 5 of 20 in valve group (25%). M. pneumoniae was found in 6 of 40 (15%) and 5 of 20 (25%) samples, and CMV was found in 22 of 40 (55%) and 10 of 20 (50%) samples. The most frequent detected pathogens were H. pylori and HSV. H. pylori was found in 32 of 40 samples of aortic wall in coronary group (80%) and 17 of 20 samples in valve group (85%), whereas HSV was found in 27 of 40 (67.5%) and 17 of 20 (85%) aortic wall specimens. Conclusion: Results demonstrate that C. pneumoniae, M. pneumoniae, H. pylori, CMV, and HSV can be detected in macroscopically healthy aortic wall of coronary and valve patients in similar frequency, which do not support hypothesis concerning the role of microorganisms in atherosclerosis etiology. © 2008 Elsevier Inc. All rights reserved. Keywords: Atherosclerosis; Aortic wall; PCR; C. pneumoniae; M. pneumoniae; H. pylori; HSV; CMV 1. Introduction The hypothesis that the most popular infectious agents may induce or progress the process of atherosclerosis in humans has been extensively tested in epidemiologic, clinical, and experimental in vivo and in vitro studies. Animal model study, in which infection of herpes simplex virus (HSV) caused induction of atherosclerotic lesions [1], and human study, in which association between acute myocardial infarctions and Chlamydia pneumoniae anti- bodies was found [2], indicate that both viral and bacterial infectious agents are worth to consider in atherosclerosis development. The most investigated initiators of atherosclerotic injury include C. pneumoniae, Mycoplasma pneumoniae, Helico- bacter pylori, cytomegalovirus (CMV), HSV-1 and HSV-2, and common human pathogens. However, seroepidemiolo- gic reports have not confirmed well the association between infectious agents and atherosclerosis risk [3,4]. More direct analysis for atheroma formation in coronary vessels, caused by viral and/or bacterial infections, has been given when polymerase chain reaction, in situ hybridization, and electron microscopy techniques were applied, but also with conflict- ing results. In tested aortic tissues from 33 autopsies, 10 atherosclerotic aortic tissues were positive for HSV-1 in 80% and for CMV in 40%, whereas 23 nonatherosclerotic tissue samples were positive for HSV-1 in 13% and for CMV Cardiovascular Pathology 17 (2008) 297 – 302 ⁎ Corresponding author. Department of Cardiac Surgery, 1st Chair of Cardiology and Cardiac Surgery, Medical University of Lodz, Poland, Sterlinga St. 1/3, 91-425 Lodz, Poland. Tel.: +48 42 633 15 58; fax: +48 42 633 15 58. E-mail address: bjegier@op.pl (B. Jegier). 1054-8807/08/$ – see front matter © 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.carpath.2007.11.002