Cong-Lin Liu1, Holger Wemmelund1, Yi Wang1, Mengyang Liao1, Jes S Lindholt1, Søren P Johnsen1, Henrik Vestergaard1, Cleverson Fernandes1, Galina K Sukhova1, Xiang Cheng1, Jin-Ying Zhang1, Chongzhe Yang1, Xiaozhu Huang1, Alan Daugherty1, Bruce D Levy1, Peter Libby1, Guo-Ping Shi2. 1. From the Department of Cardiology, Institute of Clinical Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China (C.L.L., J.Y.Z., G.P.S.); Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (C.L.L., Y.W., M.L., C.F., G.K.S., C.Y., B.D.L., P.L., G.P.S.); Department of Vascular Surgery, Viborg Regional Hospital, Viborg, Denmark (H.W.); Department of Cardiology, Shanghai First People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China (Y.W.); Department of Cardiology, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China (M.L., X.C.); Department of Cardiothoracic and Vascular Surgery, Elitary Research Centre of Individualized Medicine of Arterial Disease, Odense University Hospital, Odense, Denmark (J.S.L.); Department of Clinical Epidemiology, Institute of Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark (H.W., S.P.J.); Section for Metabolic Genetics, The Novo Nordisk Foundation Center for Basic Metabolic Research, Section of Metabolic Genetics, University of Copenhagen, Copenhagen, Denmark (H.V.); Department of Medicine, University of California, San Francisco (X.H.); and Departments of Physiology and Medicine, Saha Cardiovascular Research Center, University of Kentucky, Lexington (A.D.). 2. From the Department of Cardiology, Institute of Clinical Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China (C.L.L., J.Y.Z., G.P.S.); Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (C.L.L., Y.W., M.L., C.F., G.K.S., C.Y., B.D.L., P.L., G.P.S.); Department of Vascular Surgery, Viborg Regional Hospital, Viborg, Denmark (H.W.); Department of Cardiology, Shanghai First People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China (Y.W.); Department of Cardiology, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China (M.L., X.C.); Department of Cardiothoracic and Vascular Surgery, Elitary Research Centre of Individualized Medicine of Arterial Disease, Odense University Hospital, Odense, Denmark (J.S.L.); Department of Clinical Epidemiology, Institute of Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark (H.W., S.P.J.); Section for Metabolic Genetics, The Novo Nordisk Foundation Center for Basic Metabolic Research, Section of Metabolic Genetics, University of Copenhagen, Copenhagen, Denmark (H.V.); Department of Medicine, University of California, San Francisco (X.H.); and Departments of Physiology and Medicine, Saha Cardiovascular Research Center, University of Kentucky, Lexington (A.D.). gshi@bwh.harvard.edu.
Abstract
OBJECTIVE: Both asthma and abdominal aortic aneurysms (AAA) involve inflammation. It remains unknown whether these diseases interact. APPROACH AND RESULTS:Databases analyzed included Danish National Registry of Patients, a population-based nationwide case-control study included all patients with ruptured AAA and age- and sex-matched AAA controls without rupture in Denmark from 1996 to 2012; Viborg vascular trial, subgroup study of participants from the population-based randomized Viborg vascular screening trial. Patients with asthma were categorized by hospital diagnosis, bronchodilator use, and the recorded use of other anti-asthma prescription medications. Logistic regression models were fitted to determine whether asthma associated with the risk of ruptured AAA in Danish National Registry of Patients and an independent risk of having an AAA at screening in the Viborg vascular trial. From the Danish National Registry of Patients study, asthma diagnosed <1 year or 6 months before the index date increased the risk of AAA rupture before (odds ratio [OR]=1.60-2.12) and after (OR=1.51-2.06) adjusting for AAA comorbidities. Use of bronchodilators elevated the risk of AAA rupture from ever use to within 90 days from the index date, before (OR=1.10-1.37) and after (OR=1.10-1.31) adjustment. Patients prescribed anti-asthma drugs also showed an increased risk of rupture before (OR=1.12-1.79) and after (OR=1.09-1.48) the same adjustment. In Viborg vascular trial, anti-asthmatic medication use associated with increased risk of AAA before (OR=1.45) or after adjustment for smoking (OR=1.45) or other risk factors (OR=1.46). CONCLUSIONS: Recent active asthma increased risk of AAA and ruptured AAA. These findings document and furnish novel links between airway disease and AAA, 2 common diseases that share inflammatory aspects.
RCT Entities:
OBJECTIVE: Both asthma and abdominal aortic aneurysms (AAA) involve inflammation. It remains unknown whether these diseases interact. APPROACH AND RESULTS: Databases analyzed included Danish National Registry of Patients, a population-based nationwide case-control study included all patients with ruptured AAA and age- and sex-matched AAA controls without rupture in Denmark from 1996 to 2012; Viborg vascular trial, subgroup study of participants from the population-based randomized Viborg vascular screening trial. Patients with asthma were categorized by hospital diagnosis, bronchodilator use, and the recorded use of other anti-asthma prescription medications. Logistic regression models were fitted to determine whether asthma associated with the risk of ruptured AAA in Danish National Registry of Patients and an independent risk of having an AAA at screening in the Viborg vascular trial. From the Danish National Registry of Patients study, asthma diagnosed <1 year or 6 months before the index date increased the risk of AAArupture before (odds ratio [OR]=1.60-2.12) and after (OR=1.51-2.06) adjusting for AAA comorbidities. Use of bronchodilators elevated the risk of AAArupture from ever use to within 90 days from the index date, before (OR=1.10-1.37) and after (OR=1.10-1.31) adjustment. Patients prescribed anti-asthma drugs also showed an increased risk of rupture before (OR=1.12-1.79) and after (OR=1.09-1.48) the same adjustment. In Viborg vascular trial, anti-asthmatic medication use associated with increased risk of AAA before (OR=1.45) or after adjustment for smoking (OR=1.45) or other risk factors (OR=1.46). CONCLUSIONS: Recent active asthma increased risk of AAA and ruptured AAA. These findings document and furnish novel links between airway disease and AAA, 2 common diseases that share inflammatory aspects.
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