Key result
Direct oral anticoagulants were not significantly associated with lower all-cause mortality in the overall cohort (adjusted HR 0.71) compared to vitamin K antagonists, but were associated with lower mortality in patients with eGFR < 45 mL/min/1.73 m2.
Why the study?
In elderly patients with HF and AF at high thromboembolic risk, VKAs often yield inadequate INR control, prompting evaluation of DOACs versus VKAs.
Does DOAC therapy reduce all-cause mortality in elderly heart failure patients with non-valvular atrial fibrillation compared to VKAs?
Cohort (n=329)
Yes
Does DOAC therapy reduce all-cause mortality in elderly heart failure patients with non-valvular atrial fibrillation compared to VKAs?
Hazard Ratio: 0.71 (95% CI 0.45–1.13)
Absolute Event Rate: 20.1% vs 35%
p-value: p=0.146
In elderly patients with heart failure, non-valvular atrial fibrillation, and renal dysfunction (eGFR < 45), DOACs are associated with significantly lower all-cause mortality compared to VKAs.
Although high thromboembolic risk was assumed in elderly patients with heart failure (HF) and atrial fibrillation (AF), inadequate control of prothrombin time/international normalized ratio was often observed in patients using vitamin K antagonists (VKAs). We hypothesized that patients treated with direct oral anticoagulants (DOAC) would have a better outcome than those treated with VKAs. The aim of this study was to compare the efficacies of DOACs and VKAs in elderly patients with HF and AF. We retrospectively analyzed data from a multicenter, prospective observational cohort study. A total of 1036 patients who were hospitalized for acute decompensated HF were enrolled. We assessed 329 patients aged > 65 years who had non-valvular AF and divided them into 2 groups according to the anticoagulant therapy they received. A subgroup analysis was performed using renal dysfunction based on estimated glomerular filtration rate (eGFR; mL/min/1.73 m 2 ). The primary outcome was all-cause mortality, and the secondary outcomes were non-cardiovascular death or stroke. The median follow-up period was 730 days (range 334–1194 days). The primary outcome was observed in 84 patients; non-cardiovascular death, in 25 patients; and stroke, in 14 patients. The Kaplan–Meier analysis revealed that all-cause mortality was significantly lower in the DOAC group than in the VKA group (log-rank p = 0.033), whereas the incidence rates of non-cardiovascular death (log-rank p = 0.171) and stroke (log-rank p = 0.703) were not significantly different in the crude population. DOAC therapy was not associated with lower mortality in the crude population (log-rank p = 0.146) and in the eGFR ≥ 45 mL/min/1.73 m 2 subgroup (log-rank p = 0.580). However, DOAC therapy was independently associated with lower mortality after adjustments for age, diabetes mellitus, and albumin level (hazard ratio, 0.55; 95% confidence interval, 0.30–0.99; p = 0.045) in the eGFR < 45 mL/min/1.73 m 2 subgroup. Compared with VKA therapy, DOAC therapy was associated with lower risk of all-cause mortality in the elderly HF patients with AF and renal dysfunction.
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Sakai et al. (2022) conducted a cohort in Heart failure with non-valvular atrial fibrillation (n=329). Direct oral anticoagulants vs. Vitamin K antagonists was evaluated on All-cause mortality (HR 0.71, 95% CI 0.45-1.13, p=0.146). Direct oral anticoagulants were not significantly associated with lower all-cause mortality in the overall cohort (adjusted HR 0.71) compared to vitamin K antagonists, but were associated with lower mortality in patients with eGFR < 45 mL/min/1.73 m2.
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