Key result
DOACs linked to ~21% less hepatic decompensation and reduced mortality versus warfarin in cirrhotic AF.
Why the study?
Anticoagulation in patients with AF and liver cirrhosis is challenging due to competing thrombosis and bleeding risks, and the comparative safety and effectiveness of DOACs versus warfarin remain incompletely defined.
Does DOAC use reduce hepatic decompensation and ischemic stroke in adult patients with atrial fibrillation and liver cirrhosis compared to warfarin?
Cohort (n=5,044)
Yes
Does DOAC use reduce hepatic decompensation and ischemic stroke in adult patients with atrial fibrillation and liver cirrhosis compared to warfarin?
In patients with atrial fibrillation and liver cirrhosis, DOACs are associated with a lower risk of hepatic decompensation and all-cause mortality compared to warfarin, without increasing the risk of ischemic stroke or major bleeding.
Answers are grounded in this paper and cite their sources.
Supports the safety of DOACs over warfarin in cirrhotic patients with AF; leaves.
Anticoagulation in patients with atrial fibrillation (AF) and liver cirrhosis is challenging due to competing risks of thrombosis and bleeding. While direct oral anticoagulants (DOACs) have emerged as alternatives to warfarin, their comparative safety and effectiveness in cirrhosis remain incompletely defined. We conducted a retrospective cohort study using the TriNetX Global Collaborative Network. Adult patients (≥ 18 years) with AF and cirrhosis receiving DOACs or warfarin were identified. Propensity score matching (1:1) was performed to balance baseline characteristics. The primary outcomes were hepatic decompensation and ischemic stroke within 1 year. Secondary outcomes included all-cause mortality, major bleeding, intracranial hemorrhage, gastrointestinal bleeding, and all-cause hospitalization. Survival (Kaplan-Meier) analysis and hazard ratios were estimated. After propensity score matching, 2,522 matched pairs (5,044 patients) were included. Over 1-year follow-up, hepatic decompensation occurred in 8.8% of DOAC patients and 11.1% of warfarin patients, with a significantly lower risk observed in the DOAC group (HR 0.79, 95% CI 0.67-0.95; p = 0.010). Ischemic stroke occurred in 2.9% of DOAC patients and 2.4% of warfarin patients, with no statistically significant difference between groups (HR 1.22, 95% CI 0.85-1.75; p = 0.289). All-cause mortality was lower in the DOAC group (17.7% vs. 20.3%; HR 0.87, 95% CI 0.77-0.99; p = 0.035). No significant differences were observed in major bleeding (HR 0.84, 95% CI 0.70-1.02), intracranial hemorrhage (HR 0.98, 95% CI 0.59-1.62), gastrointestinal bleeding (HR 0.97, 95% CI 0.77-1.23), or all-cause hospitalization (HR 1.04, 95% CI 0.97-1.12). In patients with atrial fibrillation and cirrhosis, DOAC use was associated with lower risks of hepatic decompensation and all-cause mortality compared with warfarin, while no significant difference was observed in ischemic stroke or other safety outcomes. Given the observational design and modest absolute differences, these findings should be interpreted as associative and hypothesis-generating rather than causal or definitive.
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Ahmed et al. (2026) conducted a cohort in Atrial fibrillation and liver cirrhosis (n=5,044). Direct oral anticoagulants (DOACs) vs. Warfarin was evaluated on Hepatic decompensation within 1 year (HR 0.79, 95% CI 0.67-0.95, p=0.010). Direct oral anticoagulants were associated with a lower risk of hepatic decompensation and all-cause mortality compared to warfarin in patients with atrial fibrillation and liver cirrhosis.
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