Venous thromboembolism increases the risk of atrial fibrillation: The Tromsø Study
Hald, Erin M., Enga, Kristin F., Løchen, Maja-Lisa, Mathiesen, Ellisiv B., Njølstad, Inger, Wilsgaard, Tom, Braekkan, Sigrid K. and Hansen, John-Bjarne. (2014). Venous thromboembolism increases the risk of atrial fibrillation: The Tromsø Study. Journal of the American Heart Association. 3(1), pp. 1 - 7. https://doi.org/10.1161/JAHA.113.000483
|Authors||Hald, Erin M., Enga, Kristin F., Løchen, Maja-Lisa, Mathiesen, Ellisiv B., Njølstad, Inger, Wilsgaard, Tom, Braekkan, Sigrid K. and Hansen, John-Bjarne|
Background: Pulmonary embolism (PE) may trigger atrial fibrillation through increased right atrial pressure and subsequent atrial strain, but the degree of evidence is low. In this study, we wanted to investigate the impact of incident venous thromboembolism (VTE) on future risk of atrial fibrillation in a prospective population-based study. Methods and Results: The study included 29 974 subjects recruited from the Tromsø study (1994–1995, 2001–2002, 2007–2008). Incident VTE and atrial fibrillation events were registered from date of enrolment to end of follow-up, December 31, 2010. Cox proportional hazard regression models using age as time-scale and VTE as a time-dependent variable were used to estimate crude and multivariable hazard ratios (HRs) for atrial fibrillation with 95% confidence intervals (CIs). During 16 years of follow up, 540 (1.8%) subjects had an incident VTE event, and 1662 (5.54%) were diagnosed with atrial fibrillation. Among those with VTE, 50 (9.3%) developed subsequent atrial fibrillation. Patients with VTE had 63% higher risk of atrial fibrillation compared to subjects without VTE (multivariable-adjusted HR: 1.63, 95% CI: 1.22 to 2.17). The risk of atrial fibrillation was particularly high during the first 6 months after the VTE event (HR 4.00, 95% CI: 2.21 to 7.25) and among those with PE (HR 1.78, 95% CI: 1.13 to 2.80). Conclusions: We found that incident VTE was associated with future risk of atrial fibrillation. Our findings support the hypothesis that PE may lead to cardiac dysfunctions that, in turn, could trigger atrial fibrillation.
|Keywords||epidemiology; fibrillation; pulmonary heart disease; thrombosis|
|Journal||Journal of the American Heart Association|
|Journal citation||3 (1), pp. 1 - 7|
|Publisher||Wiley-Blackwell Publishing, Inc.|
|Digital Object Identifier (DOI)||https://doi.org/10.1161/JAHA.113.000483|
|Open access||Open access|
|Page range||1 - 7|
|Research Group||Mary MacKillop Institute for Health Research|
© 2013 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
|Place of publication||United States of America|
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