A Five-Year Experience of Sparing Treatment of Descending Aortic Atherosclerotic Aneurysms

A growing number of specialists are now beginning to ascertain that treatment of individuals with descending aortic atherosclerotic aneurysms must be provided by cardiologists on a scheduled basis. Surgery is feasible when there is a risk of aneurysm rupture. It requires for the development of conservative treatments and elaboration of indications for surgery. A total of 97 patients with thoracic aortic atherosclerotic aneurysms (TAAA) and abdominal aortic aneurysms (AAA) have been examined over a 5-year period. They received multifaceted anti-inflammatory medical treatment to strengthen the aortic wall and control its possible expansion. Operative treatment was offered only if there was a risk of aneurysm rupture. One of the principal factors adversely affecting mortality is the presence of co-morbidities requiring permanent medical corrective treatment irrespective of surgical or medical treatment provided. It is also important to outline the indications for surgery based on multifactorial pathogenetic manifestations. Treatment aiming at the reversal of ethiopathogenic mechanisms of disease progression contributes to a significant longer survival in DAA patients.

Involvement of TLR2 and TLR4,Chlamydophila pneumoniae and Mycoplasma pneumoniae in adventitial inflammation of aortic atherosclerotic aneurysm

Aortic atherosclerotic aneurysm (AAA) is associated with adventitial inflammation where infection is suggested to have a role. Co-infection with Chlamydophila pneumoniae (Cp) and Mycoplasma pneumoniae (Mp) was linked with coronary plaque rupture, in association with vessel dilatation and adventitial inflammation. Pathogens are recognized by Toll-like receptors (TLRs) development of the inflammatory process. Objective: Here, we studied whether co-infection by Cp and Mp was involved in the increased inflammation present in AAA and if it could be associated with deficient expression of TLRs. We compared human samples of AAA with non-dilated human aortic atherosclerotic lesions, regarding the amount of Cp and Mp antigens, and expression of TLR2 and TLR4. Methods: Two groups of aorta fragments were analyzed: G1 (n = 13) moderate atherosclerosis and G2 (n = 14) AAA samples, through immunohisto-chemistry and in situ hybridization methods. Results: Mp and Cp antigens in intima/medial layer were greater in G2 than G1, with no difference in adventitia. TLR2 and TLR4 were higher in G2 than G1 adventitia fat. There was a correlation between Mp versus TLR2 and of TLR4 in intima/medial layer and in adventitia of G1, but there was a lack of correlation in G2. In Cp adventitia, the correlation in G1 was high with TLR2 but not with TLR4, and in G2 the correlation was positive for both TLRs. Conclusion: This study favors the concept that symbiotic co-infection by Cp and Mp participates in the pathogenesis of AAA. It also emphasizes that adventitial fat is the initial site for colonization of these bacteria that probably reach the tissue through vasa vasorum. An exacerbated immune reaction is not efficient to control the infection that reaches and proliferates in high levels at the medial and intimal layer, contributing to the development of vessel dilatation.