Risk of out-of-hospital cardiac arrest in patients with epilepsy and users of antiepileptic drugs

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Aims: A few studies suggested that epilepsy and antiepileptic drugs with sodium channel-blocking properties were independently associated with out-of-hospital cardiac arrest (OHCA). However, these findings have not yet been replicated. Methods: Using Danish registries, we conducted a nested case–control study in a cohort of individuals between 1 June 2001 and 31 December 2015. Cases were defined as OHCA from presumed cardiac causes, and were matched with non-OHCA-controls based on sex, and age on the date of OHCA. Exposure of interest was epilepsy or antiepileptic drug use. To study the association between individual antiepileptic drug use and the rate of OHCA, we compared each antiepileptic drug with valproic acid. Cox regression with time-dependent covariates was conducted to calculate hazard ratio (HR) and 95% confidence interval (CI). Results: We identified 35 195 OHCA-cases and 351 950 matched non-OHCA controls. Epilepsy (cases: 3.58%, controls: 1.60%) was associated with increased rate of OHCA compared with the general population (HR: 1.76, 95%CI: 1.64–1.88) when common OHCA risk factors were taken into account. When we studied antiepileptic drug use, we found that 2 antiepileptic drugs without sodium channel blockage, clonazepam (HR: 1.88, 95%CI: 1.45–2.44) and pregabalin (HR: 1.33, 95%CI: 1.05–1.69), were associated with OHCA, whereas none of the antiepileptic drugs with sodium channel blockage were associated with OHCA. Conclusion: Epilepsy is associated with increased rate of OHCA. Our findings do not support a possible association between antiepileptic drugs with sodium channel-blocking properties and OHCA.

TidsskriftBritish Journal of Clinical Pharmacology
Udgave nummer8
Sider (fra-til)3709-3715
Antal sider7
StatusUdgivet - 2022

Bibliografisk note

Funding Information:
The authors greatly appreciate the contributions of all participating regional ambulance services and fire brigades in the study region for their contribution and support. T.E.E. and H.L.T were supported by the European Union's Horizon 2020 research and innovation programme under the acronym ESCAPE‐NET, registered under grant agreement No 733381. H.L.T. was further supported by the COST Action PARQ (grant agreement No CA19137) supported by COST (European Cooperation in Science and Technology). The funders were not involved in designing the study, collecting and analysing the data, preparing the manuscript, or decision to publish.

Publisher Copyright:
© 2022 The Authors. British Journal of Clinical Pharmacology published by John Wiley & Sons Ltd on behalf of British Pharmacological Society.

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