RESUMO
BACKGROUND: We searched for any relationship between Chlamydophila pneumoniae, Mycoplasma pneumoniae, matrix metalloproteinase 9 (MMP-9), and tissue inhibitor of metalloproteinase 1 (TIMP-1) in aneurysmatic atherosclerotic lesions, and whether this relationship differed from that in atherosclerotic nonaneurysmatic lesions. METHODS: Twenty-eight tissue samples paired by age and sex were grouped as follows: group 1 included 14 nonaneurysmal atherosclerotic fragments obtained from abdominal aortas collected from necropsies; group 2 included 14 aneurysmatic atherosclerotic aortic fragments obtained from patients during corrective surgery. Immunohistochemistry reactions were evaluated for C pneumoniae, M pneumoniae, MMP-9, and TIMP-1 antigens. Both groups were compared using the Mann-Whitney test, and the correlations among variables were obtained using the Spearman correlation test. P ≤ 0.05 was considered statistically significant. RESULTS: C pneumoniae and M pneumoniae antigens were detected in 100% of cases. A higher amount of C pneumoniae (P = 0.005), M pneumoniae (P = 0.002), and MMP-9 (P = 0.021) was found in adventitia of group 2 with aneurysm. A positive correlation was found in the aneurysm group, as follows: intima C pneumoniae versus adventitia thickness (r = 0.70; P = 0.01), media C pneumoniae versus adventitia C pneumoniae (r = 0.75; P = 0.002), intima C pneumoniae versus media C pneumoniae (r = 0.8; P = 0.00), and adventitia C pneumoniae versus intima M pneumoniae (r = 0.54; P = 0.05); negative correlations were as follows: adventitia thickness and adventitia M pneumoniae (r = -0.65; P = 0.01), media MMP-9 and media thickness (r = -0.55; P = 0.04), TIMP-1 media versus adventitia C pneumoniae (r = -0.86; P = 0.00), and TIMP-1 media versus M pneumoniae intima (r = -0.67; P = 0.03). Nonaneurysmal atherosclerotic group 1 results are as follows: adventitia C pneumoniae versus TIMP-1 media (r = 0.75; P = 0.01) and media C pneumoniae and adventitia C pneumoniae (r = 0.59; P = 0.03). CONCLUSIONS: The present work favors a role for coinfection of both M pneumoniae and C pneumoniae in the development of aortic atherosclerotic aneurysm, with increased adventitial inflammation, inhibition of TIMP-1 activity, and increased collagen degradation.
Assuntos
Aneurisma Infectado/enzimologia , Aorta/enzimologia , Aneurisma Aórtico/enzimologia , Aterosclerose/enzimologia , Infecções por Chlamydophila/enzimologia , Coinfecção , Metaloproteinase 9 da Matriz/análise , Pneumonia por Mycoplasma/enzimologia , Inibidor Tecidual de Metaloproteinase-1/análise , Túnica Adventícia/enzimologia , Túnica Adventícia/microbiologia , Idoso , Aneurisma Infectado/diagnóstico , Aneurisma Infectado/microbiologia , Aneurisma Infectado/cirurgia , Aorta/microbiologia , Aorta/patologia , Aneurisma Aórtico/diagnóstico , Aneurisma Aórtico/microbiologia , Aneurisma Aórtico/cirurgia , Aterosclerose/diagnóstico , Infecções por Chlamydophila/diagnóstico , Infecções por Chlamydophila/microbiologia , Infecções por Chlamydophila/cirurgia , Chlamydophila pneumoniae/isolamento & purificação , Dilatação Patológica , Feminino , Humanos , Imuno-Histoquímica , Masculino , Pessoa de Meia-Idade , Mycoplasma pneumoniae/isolamento & purificação , Pneumonia por Mycoplasma/diagnóstico , Pneumonia por Mycoplasma/microbiologia , Pneumonia por Mycoplasma/cirurgiaRESUMO
The etiology of the artherosclerotic abdominal aortic aneurysm is still controversial. Different theories developed in independent ways. Probably therefore thedifferent concepts developed independently, and were not considered together to explain the different aspects of the etiology of this peculiar vascular pathology. Recently a tendency appeared to try to put together the different theories since it became clear that etiology of the aneurysm could not be explained by a single ideia. The biomecanical is based upon the fact that the infra-renal abdominal aorta has a tapered fashion, is more rigid than the thoracic aorta and is more prone to suffer the influence of the reflection waves caused by the branches. It has also fewer elastic lamelae in its wall and fewer vessels arising from its vasa vasorum. It seems possible that the artherosclerotic disease contributes to impar the nutrition of the vessel wall. Although the growing rate of an aneurysm is determined by Laplace's law, the ultimate stability of the aneurysm can beexplained by recruitment of collagen fibers, by the progressive rigidity of the wall and by the modification of the geometry of the wall. Mural trombi and smooth muscle fibers do add very little to the wall strength. The theory of the influence of metals in the development of the aneurysm is based upon the clinical and experimental evidences of a participation of the copper metabolism upon the development of aneurysms of the aorta. The genetic theory is based upon the fact that there is probably a familiar tendency for the appearance by an aortic aneurysms. The proteolytic theory explains the aneurysm by an imbalance between proteolysis and anti-proteolysis although the findings of diminishment of elastin and collagen in theaortic wall were not considered to be primary. The most important risc factors such as hipertension and cigarette smoking do probably act as mechanical and metabolic factors. Is is very likely that thete abdominal aortic aneurysm should be explained by an association of a proteolytic and anti-proteolytic imbalance, a genetic predisposition, a structural pesisposition and hemodynamic factors related to the aorto-iliac geometry. HYpertension yn and cigarette smoking doact as worsening factors