[Natural history of abdominal aortic aneurysm with and without concomitant chronic obstructive pulmonary disease]

The relationship between abdominal aortic aneurysms (AAA) and chronical obstructive pulmonary disease (COPD), and in particular the suggested common elastin degradation caused by elastase and smoking was analysed by a cross sectional population mass screening study for AAA, and a prospective cohort study of small AAA. All previous computer-hospital-recorded diagnoses were received concerning 4,404 men invited to screening for AAA. One hundred and forty-one had AAA (4.2%). They were asked for an interview, a clinical examination, and a blood sample. Men with an AAA of 3-5 cm were offered annual control-scans to check for expansion. Of COPD-patients, 7.7% had AAA (crude OR = 2.05), however the adjusted OR was only 1.53 after adjusting for other co-existing diseases (p = 0.13). The mean annual expansion was 2.74 mm per year in COPD patients and 2.72 in non-COPD patients, and 4.7 mm in oral steroid-users compared to 2.6 in non-steroid-users (p < 0.05). S-elastin-peptides (SEP) and P-elastase-alpha1-antitrypsin-complexes (PEAC) were negatively correlated to FEV1 in COPD-patients. However, SEP, beta-agonist-treatment, and FEV1 was positively correlated to expansion by multivariate regression analysis, while PEAC and S-alpha1-antitrypsin did not influence expansion, suggesting elastase plays a major role in the pathogenesis of COPD but not in AAA. The high prevalence of AAA among patients with COPD is more likely to be caused by medication and coexisting diseases rather than a common pathway of pathogenesis.