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Increased risk of atrial fibrillation in patients with coeliac disease: a nationwide cohort study
Arvika Hospital, Värmland County, Arvika, Sweden.
Department of Cardiology, Lund University, Lund, Sweden; Broad Institute of Harvard and MIT, Cambridge MA, USA; Department of Clinical Sciences, Lund University, Malmö, Sweden.
Division of Epidemiology and Public Health, Nottingham City Hospital, University of Nottingham, Nottingham, UK; NIHR Biomedical Research Unit, Nottingham Digestive Diseases Centre, Nottingham, UK.
Department of Clinical Sciences, Lund University, Malmö, Sweden.
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2011 (English)In: European Heart Journal, ISSN 0195-668X, E-ISSN 1522-9645, Vol. 32, no 19, p. 2430-7Article in journal (Refereed) Published
Abstract [en]

Aims: Inflammatory markers are established risk factors for atrial fibrillation (AF), but the role of autoimmune diseases is unknown. The aim of the study was to examine the association between coeliac disease (CD) and AF in a large cohort of patients with biopsy-verified CD.

Metods and results: We identified 28,637 patients with CD through biopsy reports (defined as Marsh 3: villous atrophy) from all pathology departments (n = 28) in Sweden. Biopsies had been performed between 1969 and 2008. Age- and sex-matched reference individuals (n = 141,731) were identified from the Swedish Total Population Register. Data on AF were obtained from the Swedish Hospital Discharge Register, the Hospital Outpatient Register, and the Cause of Death Register. Hazard ratios (HRs) for AF were estimated using Cox regression. In the CD cohort, 941 individuals developed AF (vs. 2918 reference individuals) during a median follow-up of 9 years. The corresponding adjusted HR for AF was 1.34 (95% CI = 1.24-1.44). The absolute risk of AF in CD was 321 of 100,000 person-years, with an excess risk of 81 of 100,000. A prior AF diagnosis was also associated with an increased risk of subsequent CD (odds ratio = 1.45, 95% CI = 1.31-1.62).

Conclusions Atrial fibrillation is more common both before and after CD diagnosis in patients with CD though the excess risk is small. Potential explanations for the increased risk of AF in CD include chronic inflammation and shared risk factors, but ascertainment bias may also have contributed.

CLINICAL IMPLICATIONS: Coeliac disease affects 1-2% of the Western population. Our results indicate that patients with coeliac disease, verified by intestinal biopsy, are at increased risk of atrial fibrillation. This observation is consistent with previous findings that elevation of inflammatory markers predicts atrial fibrillation. Additional studies are needed to clarify the mechanistic link between atrial fibrillation and autoimmune diseases such as coeliac disease.

Place, publisher, year, edition, pages
Oxford, United Kingdom: Oxford University Press, 2011. Vol. 32, no 19, p. 2430-7
Keywords [en]
Autoimmunity, Coeliac, Inflammation, Atrial fibrillation
National Category
Medical and Health Sciences
Research subject
Medicine
Identifiers
URN: urn:nbn:se:oru:diva-32520DOI: 10.1093/eurheartj/ehr167ISI: 000295684300023PubMedID: 21653560Scopus ID: 2-s2.0-80054052563OAI: oai:DiVA.org:oru-32520DiVA, id: diva2:666914
Available from: 2013-11-25 Created: 2013-11-25 Last updated: 2018-05-05Bibliographically approved
In thesis
1. Cardiac complications in celiac disease
Open this publication in new window or tab >>Cardiac complications in celiac disease
2013 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Background: Celiac disease (CD) is an immune-mediated enteropathy induced by dietary gluten that affects about 1% of western populations. CD has been associated to an increased risk of cardiovascular mortality in some studies; however associations to cardiovascular diseases have not been broadly researched.

Aim: The aim of this thesis was to examine the associations between CD and some cardiovascular diseases, namely; atrial fibrialltion, dilated cardiomyopathy and risk factors of ischemic heart disease.Methods: We used computerized data on all Swedish patients with biopsy-verified CD equal to villous atrophy from 1969 to 31st of December 2008. All CD patients were matched on age, sex, county and calendar year with up to five reference individuals. Altogether we had data on 29,096 CD patients and 144,522 reference individuals. Data were linked to different Swedish national registries and the Swedish quality and cardiac care registry SWEDEHEART. Main outcomes in the studies were: I: atrial fibrillation registered in the national patient registry or the cause of death registry, II: chart validated idiopathic dilated cardiomyopathy, III: different risk factors, clinical presentation and parameters in patients with first myocardial infarction (MI) registered in SWEDEHEART and IV: follow-up parameters, 6-10 weeks and one year after MI, registered in SWEDEHEART.

Result: We showed a 34% increased risk of atrial fibrillation in CD and a 73% increased risk of dilated cardiomyopathy, the latter only of borderline significance, p=0.052. In the third study we showed that CD patients with MI had a more beneficial cardiovascular risk factor profile, better left ventricular ejection fraction and fewer stenoses on coronary angiography compared to reference individuals with MI. The fourth study showed that follow-up after MI does not differ from follow-up in reference individuals.

Conclusion: This thesis supports an association of cardiovascular diseases in CD. Potential mechanisms include shared risk factors and chronic in-flammation.

Place, publisher, year, edition, pages
Örebro: Örebro universitet, 2013. p. 82
Series
Örebro Studies in Medicine, ISSN 1652-4063 ; 92
Keywords
atrial fibrillation, autoimmune, celiac disease, cohort, dilated cardiomyopathy, inflammation, myocardial infarction, registry
National Category
Cardiac and Cardiovascular Systems
Research subject
Cardiology
Identifiers
urn:nbn:se:oru:diva-28977 (URN)978-91-7668-955-4 (ISBN)
Public defence
2013-10-11, Wilandersalen, Universitetssjukhuset, Södra Grev Rosengatan, Örebro, 09:00 (English)
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Available from: 2013-05-06 Created: 2013-05-06 Last updated: 2017-10-17Bibliographically approved

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Emilsson, LouiseLudvigsson, Jonas F.

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