Systemic levels of cotinine and elastase, but not pulmonary function, are associated with the progression of small abdominal aortic aneurysms.

Abstract

to study whether smoking and impaired pulmonary function are associated with the expansion of abdominal aortic aneurysms (AAA). seventy-nine men with small (3-5 cm), screen-detected AAA underwent a simple 5-step smoking history, measurement of the forced first second expiratory volume (FEV1), venepuncture and annual ultrasound scan for mean follow-up period of 3.5 years. all but one patient had a significantly reduced FEV1 (p<0.05, Mann-Whitney). The FEV1/expected FEV1 ratio (rFEV1) was not related to AAA expansion but was negatively correlated with P-elastase-alpha1-antitrypsin-complexes (P-Elastase). P-Elastase was positively correlated with smoking and S-cotinine. Smoking, S-cotinine, and P-elastase were positively correlated with the mean annual AAA expansion rate but not rFEV1. in general, patients with AAA have impaired pulmonary function. A simple five step smoking classification is as predictive of AAA-expansion as S-cotinine. Smoking may cause elastase secretion leading to pulmonary and aortic elastin degradation but the lack of association between AAA-expansion and rFEV1 suggest that other mechanisms are important.