Objective Traumatic intracranial haemorrhage (ICH) leads to systemic inflammatory response and arrhythmia. Atrial fibrillation (AF), the most common arrhythmia, is associated with systemic inflammation. However, limited evidence is available regarding the association between traumatic ICH and AF.
Methods This study used the National Health Insurance Research Database, a nationwide population-based cohort, in Taiwan and total 130 171 individuals with traumatic ICH from 2000 to 2011 were identified. Furthermore, individuals without traumatic ICH were selected as a comparison cohort by the propensity score method. Individuals with prior history of AF were excluded from this study. The endpoint of interest was the occurrence of AF and the follow-up was terminated by the occurrence of AF, loss of follow-up or the passing of 31 December 2011.
Results During the follow-up period, the incidence of AF was higher in patients with traumatic ICH than in those without traumatic ICH (4.24 vs 4.12 per 1000 person-years). After adjustment for age, sex and all AF-associated comorbidities, the individuals with traumatic ICH had a 1.25-fold increased risk of AF (HR=1.25, 95% CI=1.18 to 1.32; p<0.001). Stratified by sex and age, the incidence of AF was consistently higher in the traumatic ICH group. Relative to the individuals without traumatic ICH and without comorbidities, the risk of AF was the highest in the individuals with both traumatic ICH and comorbidities; this risk was higher than that of the individuals with only traumatic ICH; it was also higher than the risk for those only with comorbidities.
Conclusion In this large-scale cohort study, the future risks of AF are higher in patients with traumatic ICH compared with the comparison cohort. Carefully monitoring the occurrence of AF and proper anticoagulation therapy might be important in patients with traumatic ICH.
- Traumatic intracranial hemorrhage
- Traumatic brain injury
- Taiwan National Health Insurance Research Database
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Contributors All authors have contributed substantially to and are in agreement with the content of the manuscript. Conception and design: W-SL, C-HK; provision of study materials: C-HK; collection and/or assembly of data: W-SL, C-LL, C-HK; data analysis and interpretation, manuscript preparation, final approval of manuscript: all authors.
Funding This study was supported in part by grants from Taiwan’s Ministry of National Defense (MAB-105-014); Taiwan Ministry of Health and Welfare Clinical Trial and Research Center of Excellence (MOHW105-TDU-B-212-133019); China Medical University Hospital, Academia Sinica Taiwan Biobank Stroke Biosignature Project (BM10501010037); NRPB Stroke Clinical Trial Consortium (MOST105-2325-B-039-003); Tseng-Lien Lin Foundation, Taichung, Taiwan; Taiwan Brain Disease Foundation, Taipei, Taiwan; Katsuzo and Kiyo Aoshima Memorial Funds, Japan. No additional external funding received for this study.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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