OBJECTIVE: to study whether smoking and impaired pulmonary function are associated with the expansion of abdominal aortic aneurysms (AAA). METHODS AND MATERIAL: 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. RESULTS: 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. CONCLUSION: 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.
OBJECTIVE: to study whether smoking and impaired pulmonary function are associated with the expansion of abdominal aortic aneurysms (AAA). METHODS AND MATERIAL: 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. RESULTS: 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. CONCLUSION: 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.
Authors: Femke A M V I Hellenthal; Willem A Buurman; Will K W H Wodzig; Geert Willem H Schurink Journal: Nat Rev Cardiol Date: 2009-05-26 Impact factor: 32.419
Authors: Femke A M V I Hellenthal; Willem A Buurman; Will K W H Wodzig; Geert Willem H Schurink Journal: Nat Rev Cardiol Date: 2009-06-23 Impact factor: 32.419
Authors: Cong-Lin Liu; Holger Wemmelund; Yi Wang; Mengyang Liao; Jes S Lindholt; Søren P Johnsen; Henrik Vestergaard; Cleverson Fernandes; Galina K Sukhova; Xiang Cheng; Jin-Ying Zhang; Chongzhe Yang; Xiaozhu Huang; Alan Daugherty; Bruce D Levy; Peter Libby; Guo-Ping Shi Journal: Arterioscler Thromb Vasc Biol Date: 2016-02-11 Impact factor: 8.311