Kevin Chang1, Chio Yokose1, Craig Tenner2, Cheongeun Oh3, Robert Donnino4, Alana Choy-Shan5, Virginia C Pike1, Binita D Shah5, Jeffrey D Lorin5, Svetlana Krasnokutsky1, Steven P Sedlis5, Michael H Pillinger6. 1. Section of Rheumatology, Department of Medicine, Veterans Affairs New York Harbor Healthcare System; Division of Rheumatology, Department of Medicine, New York University School of Medicine; TRIAD (Translational Research in Inflammation and Atherosclerotic Disease), New York University School of Medicine. 2. TRIAD (Translational Research in Inflammation and Atherosclerotic Disease), New York University School of Medicine; Section of Primary Care, Department of Medicine, Veterans Affairs New York Harbor Healthcare System; Division of Primary Care, Department of Medicine, New York University School of Medicine. 3. TRIAD (Translational Research in Inflammation and Atherosclerotic Disease), New York University School of Medicine; Department of Biostatistics, New York University. 4. TRIAD (Translational Research in Inflammation and Atherosclerotic Disease), New York University School of Medicine; Section of Cardiology, Department of Medicine, Veterans Affairs New York Harbor Healthcare System; Division of Cardiology, Department of Medicine, New York University School of Medicine; Department of Radiology, New York University School of Medicine. 5. TRIAD (Translational Research in Inflammation and Atherosclerotic Disease), New York University School of Medicine; Section of Cardiology, Department of Medicine, Veterans Affairs New York Harbor Healthcare System; Division of Cardiology, Department of Medicine, New York University School of Medicine. 6. Section of Rheumatology, Department of Medicine, Veterans Affairs New York Harbor Healthcare System; Division of Rheumatology, Department of Medicine, New York University School of Medicine; TRIAD (Translational Research in Inflammation and Atherosclerotic Disease), New York University School of Medicine. Electronic address: Michael.Pillinger@nyumc.org.
Abstract
BACKGROUND: An independent association between gout and coronary artery disease is well established. The relationship between gout and valvular heart disease, however, is unclear. The aim of this study was to assess the association between gout and aortic stenosis. METHODS: We performed a retrospective case-control study. Aortic stenosis cases were identified through a review of outpatient transthoracic echocardiography (TTE) reports. Age-matched controls were randomly selected from patients who had undergone TTE and did not have aortic stenosis. Charts were reviewed to identify diagnoses of gout and the earliest dates of gout and aortic stenosis diagnosis. RESULTS: Among 1085 patients who underwent TTE, 112 aortic stenosis cases were identified. Cases and nonaortic stenosis controls (n = 224) were similar in age and cardiovascular comorbidities. A history of gout was present in 21.4% (n = 24) of aortic stenosis subjects compared with 12.5% (n = 28) of controls (unadjusted odds ratio 1.90, 95% confidence interval 1.05-3.48, P = .038). Multivariate analysis retained significance only for gout (adjusted odds ratio 2.08, 95% confidence interval 1.00-4.32, P = .049). Among subjects with aortic stenosis and gout, gout diagnosis preceded aortic stenosis diagnosis by 5.8 ± 1.6 years. The age at onset of aortic stenosis was similar among patients with and without gout (78.7 ± 1.8 vs 75.8 ± 1.0 years old, P = .16). CONCLUSIONS: Aortic stenosis patients had a markedly higher prevalence of precedent gout than age-matched controls. Whether gout is a marker of, or a risk factor for, the development of aortic stenosis remains uncertain. Studies investigating the potential role of gout in the pathophysiology of aortic stenosis are warranted and could have therapeutic implications. Published by Elsevier Inc.
BACKGROUND: An independent association between gout and coronary artery disease is well established. The relationship between gout and valvular heart disease, however, is unclear. The aim of this study was to assess the association between gout and aortic stenosis. METHODS: We performed a retrospective case-control study. Aortic stenosis cases were identified through a review of outpatient transthoracic echocardiography (TTE) reports. Age-matched controls were randomly selected from patients who had undergone TTE and did not have aortic stenosis. Charts were reviewed to identify diagnoses of gout and the earliest dates of gout and aortic stenosis diagnosis. RESULTS: Among 1085 patients who underwent TTE, 112 aortic stenosis cases were identified. Cases and nonaortic stenosis controls (n = 224) were similar in age and cardiovascular comorbidities. A history of gout was present in 21.4% (n = 24) of aortic stenosis subjects compared with 12.5% (n = 28) of controls (unadjusted odds ratio 1.90, 95% confidence interval 1.05-3.48, P = .038). Multivariate analysis retained significance only for gout (adjusted odds ratio 2.08, 95% confidence interval 1.00-4.32, P = .049). Among subjects with aortic stenosis and gout, gout diagnosis preceded aortic stenosis diagnosis by 5.8 ± 1.6 years. The age at onset of aortic stenosis was similar among patients with and without gout (78.7 ± 1.8 vs 75.8 ± 1.0 years old, P = .16). CONCLUSIONS:Aortic stenosispatients had a markedly higher prevalence of precedent gout than age-matched controls. Whether gout is a marker of, or a risk factor for, the development of aortic stenosis remains uncertain. Studies investigating the potential role of gout in the pathophysiology of aortic stenosis are warranted and could have therapeutic implications. Published by Elsevier Inc.
Authors: Rennie G Howard; Jonathan Samuels; Soterios Gyftopoulos; Svetlana Krasnokutsky; Joseph Leung; Christopher J Swearingen; Michael H Pillinger Journal: J Clin Rheumatol Date: 2015-03 Impact factor: 3.517