Key result
Among patients with nonvalvular atrial fibrillation and no prior liver disease, initiation of rivaroxaban was associated with an increased risk of serious acute liver injury compared to vitamin K antagonists (HR 1.41), whereas dabigatran and apixaban showed no significant increase.
Why the study?
Does NOAC therapy compared to VKA therapy increase the risk of acute liver injury in patients with nonvalvular atrial fibrillation?
Cohort (n=434,015)
Does NOAC therapy compared to VKA therapy increase the risk of acute liver injury in patients with nonvalvular atrial fibrillation?
Hazard Ratio: 1.41 (95% CI 1.05–1.91)
Absolute Event Rate: 0.072% vs 0.051%
In a large nationwide cohort of NVAF patients, NOACs generally did not increase the 1-year risk of acute liver injury compared to VKAs, though specific signals were noted for rivaroxaban in patients without prior liver disease and dabigatran in those with chronic alcoholism.
Rivaroxaban may increase liver injury risk in AF; leaves open differential NOAC hepatotoxicity pending randomized confirmation.
Insufficient real-world data on acute liver injury (ALI) risk associated with oral anticoagulants (OACs) exist in patients with nonvalvular atrial fibrillation (NVAF). Using the French national healthcare databases, a propensity-weighted nationwide cohort study was performed in NVAF patients initiating OACs from 2011 to 2016, considering separately those (1) with no prior liver disease (PLD) as main population, (2) with PLD, (3) with a history of chronic alcoholism. A Cox proportional hazards model was used to estimate the hazard ratio with 95% confidence interval (HR [95% CI]) of serious ALI (hospitalised ALI or liver transplantation) during the first year of treatment, for each non-vitamin K antagonist (VKA) oral anticoagulant (NOAC: dabigatran, rivaroxaban, apixaban) versus VKA. In patients with no PLD (N = 434,015), only rivaroxaban new users were at increased risk of serious ALI compared to VKA initiation (adjusted HR: 1.41 [1.05-1.91]). In patients with chronic alcoholism history (N = 13,173), only those initiating dabigatran were at increased risk of serious ALI compared to VKA (2.88 [1.74-4.76]) but an ancillary outcome suggested that differential clinical follow-up between groups might partly explain this association. In conclusion, this study does not suggest an increase of the 1-year risk of ALI in NOAC versus VKA patients with AF.
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Maura et al. (2020) conducted a cohort in Nonvalvular atrial fibrillation (n=434,015). Non-vitamin K antagonist oral anticoagulants (NOACs) vs. Vitamin K antagonists (VKAs) was evaluated on Serious acute liver injury (hospitalised ALI or liver transplantation) (HR 1.41, 95% CI 1.05-1.91). Among patients with nonvalvular atrial fibrillation and no prior liver disease, initiation of rivaroxaban was associated with an increased risk of serious acute liver injury compared to vitamin K antagonists (HR 1.41), whereas dabigatran and apixaban showed no significant increase.
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