OBJECTIVE: Atherosclerotic inflammation, with a possible role of infectious agents, could contribute to the pathogenesis of abdominal aortic aneurysms (AAA). Finding of Chlamydia pneumoniae (CP) in these lesions in previous, non-quantifying studies ranged from 0-100%. The objective is to quantify the presence of CP and Mycoplasma pneumoniae (MP) in AAA. METHODS: Thickness, number of cells positive for CP by immunohistochemistry and percent area occupied by MP, detected by "in situ" hybridization in the three layers of the aorta, were measured in the three aortic layers using an image-analysis system in 10 necropsy abdominal aneurysmatic aortas. Three groups of controls were used: 1) samples of the same aortas, outside the aneurysms, except if the dilatation took the whole sub-renal portion of the artery (n=7); 2) aortas with severe atherosclerosis but without aneurysms (n=10); 3) aortas with no or mild atherosclerosis (n=10). All specimens were obtained at necropsies. Wald's test was used to compare groups; significance level was established at 5%. RESULTS: The intima was thinner and the media thicker in the normal cases than in the other groups (p<0.01). Positive cells for CP were found in all groups, more frequently at the adventitia; no significant difference was detected between them (p>0.05). MP was also detect in all groups. This agent predominated in the group of patients with atherosclerosis, but no aneurysms at both intima and adventitia; nevertheless, differences between the groups were not significant (p>0.05). CONCLUSIONS: our data suggest that the bacteria we focused have not an important role in the pathogenesis of AAA.
Aorta; Aortic aneurysm, abdominal; Chlamydophila pneumoniae; Mycoplasma pneumoniae; Atherosclerosis; Autopsy
