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- Published on: 14 September 2017
- Published on: 3 August 2017
- Published on: 14 September 2017Is traumatic intracranial hemorrhage a specific risk factor of atrial fibrillation: Reply
To the Editor:
We thank Dr. Launey Y et al for their constructive comments regarding our recent report.[1] We also greatly appreciate their shared interests in traumatic intra-cranial hemorrhage (ICH) and the subsequent incidence of atrial fibrillation (AF).
Dr Launey and colleagues concerned about the acute effects of inflammation on the onset of AF.[2] In our study, the mean follow-up period was 4.36 (standard deviation, SD=3.41) and 5.35 (SD=3.19) years in traumatic ICH group and control group, respectively. Interestingly, the mean follow-up period of the onset of AF was 2.94 years (SD=2.64) in traumatic ICH group, which is significantly less than 3.57 (SD=2.67) years in control group (Table 1) (p<0.001). Although acute inflammation plays a role on the onset of AF,[3, 4] our study along with previous evidence indicate the chronic persistent inflammation, which occurs after traumatic brain injury (TBI), contributes the development of AF.[1, 5] This partly explains the results of AF occurrence on TBI patients in our study.
We agree that sepsis may contribute to the development of AF. In this study, after adjustment for age, sex, and comorbidities including sepsis and ventilator associated pneumonia, the adjusted HR (aHR) for developing AF was 1.24-fold higher (95% CI = 1.18-1.31) for patients with traumatic ICH compared with the control cohorts in multivariable cox regression models (Table 2). These results further support the association betwee...
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None declared. - Published on: 3 August 2017Is traumatic intracranial hemorrhage a specific risk factor of atrial fibrillation ?
We read the study of Wei-Shiang Lin et al.[1] with a great interest. In their large-scale cohort retrospective study, they found that traumatic intracranial hemorrhage was associated with an increased risk of atrial fibrillation (AF) and hypothesized that inflammation and/or secondary cardiac insult due to the traumatic brain injury (TBI) may cause AF. Nevertheless, several points should be discussed. First, acute inflammation is well-known to be related to AF in trauma patients. The risk of new-onset AF is reasonably expected to occur at the acute phase following the trauma. This point has already been previously demonstrated to occur during the days following cardiac surgery or septic shock onset.[2] In the same way, cardiac insult occurs at the very early phase of TBI and the consecutive cardiac systolic dysfunction was reported to be reversible within the first week after the trauma. [3] In this perspective, how to explain that the risk of AF persists one year after the trauma? It would be very helpful if the authors could provide data on the delay between the day of trauma and the day of new-onset AF. Furthermore, inflammation and cardiac dysfunction are related to the TBI severity and it would be valuable to know whether the more severe TBI patients are more prone to develop AF than mild or moderate TBI. Finally, in their statistical model, the authors have taken into account comorbidities which are also known to favor AF. But others factors, such as sepsis and relat...
Show MoreConflict of Interest:
None declared.