Natural history of abdominal aortic aneurysm with and without coexisting chronic obstructive pulmonary disease

Abstract Purpose: To study the relation between abdominal aortic aneurysms and chronical obstructive pulmonary disease (COPD), in particular the suggested common elastin degradation caused by elastase and smoking. Methods: A cross-sectional population study and a prospective cohort study of small abdominal aortic aneurysms was performed in a community setting. All previous diagnoses recorded in a hospital computer database were received for 4404 men 65 to 73 years of age who had been invited to a population screening for abdominal aortic aneurysm. One hundred forty-one men had AAA (4.2%). They were asked to participate in an interview, a clinical examination, and collection of blood sample. Men with an abdominal aortic aneurysm 3 to 5 cm in diameter were offered annual ultrasound scans to check for expansion. Results: Among patients with COPD 7.7% had abdominal aortic aneurysms (crude odds ratio=2.05). The adjusted odds ratio, however, was only 1.59 after adjustment for coexisting diseases associated with abdominal aortic aneurysm ( P = .13). The mean annual expansion was 2.74 mm per year among patients with COPD, 2.72 among patients without COPD, and 4.7 mm among patients who used oral steroids compared with 2.6 among patients who did not use steroids ( P 1 -antitrypsin complexes correlated negatively with forced expiratory volume in the first second (FEV 1 ) among patients with COPD. However, multivariate regression analysis showed that concentration of serum elastin peptide, therapy with β-agonists, and FEV 1 correlated positively with degree of expansion but that concentration of plasma elastase–α 1 -antitrypsin complexes and serum α 1 -antitrypsin did not influence expansion, suggesting that elastase plays an important role in the pathogenesis of COPD but not of abdominal aortic aneurysm. Conclusion: The high prevalence of abdominal aortic aneurysm among patients with COPD is more likely to be caused by medication and coexisting diseases rather than a common pathway of pathogenesis. (J Vasc Surg 1998;28:226-33.)