C. pneumoniae DNA in 12% of thoracic aortic aneu- rysm and in 0% of aortic dissection tissue (12), whereas another group of investigators failed to dem- onstrate the presence of C. pneumoniae in this kind of tissue, as well as in abdominal aortic aneurysm (17). Furthermore, another study failed to demonstrate the presence of C. pneumoniae in Type A aortic dissection tissue (18). In the present study C. pneumoniae DNA was found in 26% of the thoracic aortic aneurysm patients (13) and in 11% of the aortic dissection patients but in none of the control aortic biopsies. The higher prevalence in this new study than in our previous one (12) may be due partly to the use of a more sensitive PCR method and partly to a potential patchy distribution of the bacteria (5). In contrast to abdominal aortic aneurysm, athero- sclerosis is believed to be an infrequent cause of thoracic aortic aneurysm and of aortic dissection (19). The aneurysm patients in this study had a rather low degree of coronary artery stenosis, as veriﬁed by coronary angiography. On the other hand, atheroscle- rotic changes in the aneurysm were demonstrated by histology in 9/23 patients; however, these changes were not more prevalent in C. pneumoniae-positive patients than in C. pneumoniae-negative patients. Regarding presence of inﬂammatory cells, no differ- ence was noted between aneurysm and dissection biopsies. However, among the aneurysm biopsies, inﬂammatory cells were signiﬁcantly more frequent in C. pneumoniae-positive aneurysms than in C. pneumoniae-negative aneurysms. No such differ- ence existed among the dissection biopsies. Presence of C. pneumoniae in circulating PBMC may be associated with cardiovascular disease (11). However, detection rates in different studies on such patients vary between 0% (20) and 59%, and detec- tion rates in healthy blood donors vary from 0% to 46% (11). Such wide variation can probably be explained by differences in sampling, nucleic acid extraction methods, and PCR techniques. To our knowledge, this is the ﬁrst study of C. pneumoniae in PBMC of thoracic aortic aneurysm. One study has investigated the presence of C. pneumoniae in PBMC in aortic dissection patients, and all patients with Type A aortic dissection were negative for C. pneumoniae DNA (18). All patients in this study tested negative for C. pneumoniae in PBMC, indicat- ing that the bacteria probably had disseminated to the aorta long before the patient was in need of surgery. Isolation of C. pneumoniae from atherosclerotic tissue has only been successful in a few studies (7,16), and then only after several passages. This work is time-consuming, with a high risk of contam- ination. Instead, viable and metabolically active C. pneumoniae can be demonstrated by the presence C. pneumoniae in aortic aneurysm and dissection 185 of bacterial mRNA. We have previously shown that patients undergoing CABG have C. pneumoniae mRNA coding for the major outer membrane protein in macroscopically normal thoracic aorta (10). How- ever, in that study samples that were positive for C. pneumoniae DNA were not always positive for C. pneumoniae mRNA. Most of the aortic samples in the present study were altered by advanced disease, including ﬁbrosis and calciﬁcation, and they were all negative for C. pneumoniae mRNA. All samples con- tained rather low amounts of RNA but were, however, positive for human cDNA, indicating that the mRNA extraction had worked. This suggests that the bacteria have entered into a persistent and non-active state in the disease-altered tissue and are thus not producing measurable amounts of mRNA. C. pneumoniae antibodies were determined with the micro-immunoﬂuorescence method. Considering the age of the patients, antibody titres seemed to be in the normal range (6), with 56% of the aneurysm patients and 43% of the dissection patients having IgG against C. pneumoniae. Inﬂammatory cells have previously been demon- strated in thoracic aortic aneurysms (21), and it has been suggested that different antigens may be involved in the formation of the aneurysms (3). These antigens could possibly be micro-organisms, as we have demonstrated the presence of C. pneumoniae in the aneurysms and others have demonstrated other bacteria in the aneurysms (22). Moreover, in vitro studies have demonstrated that C. pneumoniae is able to degrade elastin, a load-bearing protein in the aortic wall (23), and these mechanisms may contribute to the pathogenesis of the rupture of the aortic wall. Certain changes in trace element concentrations can be used as markers of infection/inﬂammation (24). We have previously demonstrated such markers in sera of patients undergoing surgery because of aortic valve stenosis, where a large number of the patients were positive for C. pneumoniae in the valve (25). In a more recent study of sera and aortic biopsies of the thoracic aortic aneurysm patients in the present study we demonstrated trace element changes, indi- cating on-going infection/inﬂammation in the patients compared to healthy controls (13). In conclusion, the results in the present study demonstrate that C. pneumoniae may be found in the aortic wall in thoracic aortic aneurysm patients and aortic dissection patients though not in a meta- bolically active state. Dissemination of C. pneumoniae from the respiratory tract to the aortic wall may have occurred long before the patient was in need of thoracic surgery as no C. pneumoniae could be found in the PBMC. This indicates that the C. pneumoniae infection in the patients is not in an active state but has