Medline ® Abstracts for References 19,33

Cellular immunity may play a role in the pathogenesis of atherosclerosis. In this report the potential role of these cells in the formation of abdominal aortic aneurysms by immunohistochemistry was investigated. Aortic tissues from 32 patients were examined: 4 normal aortas, 6 aortas with occlusive atherosclerotic disease, 17 abdominal aortic aneurysms, and 5 inflammatory abdominal aneurysms. Using monoclonal anti-CD3 (T cells), anti-CD19 (B cells), anti-CD11c (macrophages), anti-CD4 (T helper cells), and anti-CD8 (T suppressor cells), several distinctions among these groups were found. The amount of inflammatory cell infiltrate was as follows: inflammatory aneurysms more than abdominal aortic aneurysms more than occlusive aortas more than normal aortas. CD3-positive T lymphocytes rarely were found in the adventitia of normal or occlusive aortas. In contrast, abdominal aortic aneurysms and inflammatory aneurysms exhibited most of the CD3-positive infiltrates in the adventitia. CD19-positive B lymphocytes were present mainly in the adventitia of all pathologic tissues. The CD4-positive:CD8-positive ratio was greater in abdominal aortic aneurysms and inflammatory aneurysms than in the other groups, both in the adventitia and in the media of the aortas. CD11c-positive macrophages were present throughout the diseased tissues, often surrounded by lymphoid aggregates; the greatest numbers of macrophages were found in the inflammatory aneurysm group. Our data suggests that the aneurysmal disease may progress from occlusive disease and is accompanied by an increase in chronic inflammatory cells as well as a redistribution of these cell types. Therefore it is suggested that aneurysmal disease may represent an immune-mediated event.

BACKGROUND: Early elective surgery may prevent rupture of abdominal aortic aneurysms, but mortality is 5-6%. The risk of rupture seems to be low for aneurysms smaller than 5 cm. We investigated whether prophylactic open surgery decreased long-term mortality risks for small aneurysms.

METHODS: We randomly assigned 1090 patients aged 60-76 years, with symptomless abdominal aortic aneurysms 4.0-5.5 cm in diameter to undergo early elective open surgery (n=563) or ultrasonographic surveillance (n=527). Patients were followed up for a mean of 4.6 years. If the diameter of aneurysms in the surveillance group exceeded 5.5 cm, surgical repair was recommended. The primary endpoint was death. Mortality analyses were done by intention to treat.

FINDINGS: The two groups had similar cardiovascular risk factors at baseline. 93% of patients adhered to the assigned treatment. 309 patients died during follow-up. The overall hazard ratio for all-cause mortality in the early-surgery group compared with the surveillance group was 0.94 (95% CI 0.75-1.17, p=0.56). The 30-day operative mortality in the early-surgery group was 5.8%, which led to a survival disadvantage for these patients early in the trial. Mortality did not differ significantly between groups at 2 years, 4 years, or 6 years. Age, sex, or initial aneurysm size did not modify the overall hazard ratio.

INTERPRETATION: Ultrasonographic surveillance for small abdominal aortic aneurysms is safe, and early surgery does not provide a long-term survival advantage. Our results do not support a policy of open surgical repair for abdominal aortic aneurysms of 4.0-5.5 cm in diameter.