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1 s with earlier initiation times for use of a direct oral anticoagulant.
2 149 were using warfarin, and 60 were using a direct oral anticoagulant.
3 reversal agent for anticoagulants including direct oral anticoagulants.
4 ssociated with higher risk of fractures than direct oral anticoagulants.
5 therapeutic doses of anticoagulation such as direct oral anticoagulants.
6 t data, appear superior to the more targeted direct oral anticoagulants.
7 injury, a defect that was phenocopied using direct oral anticoagulants.
8 independent effects of warfarin compared to direct oral anticoagulants.
9 h vitamin K antagonists (e.g., warfarin) and direct oral anticoagulants.
10 These findings support the continued use of direct oral anticoagulants.
11 ns, antihypertensives, P2Y12 inhibitors, and direct oral anticoagulants.
12 ular weight heparin or newer options such as direct oral anticoagulants.
13 7 to 0.54) low molecular weight heparin, and direct oral anticoagulants (0.17, 0.07 to 0.41) reduced
14 lecular-weight heparin (0.66, 0.46 to 0.93), direct oral anticoagulants (0.68, 0.33 to 1.34), and int
16 ractionated heparin (2.63, 1.00 to 6.21) and direct oral anticoagulants (2.31, 0.82 to 6.47) were mos
18 aspirin, 73 full-dose antiplatelet drugs, 51 direct oral anticoagulants, 36 warfarin, 32 daily nonste
19 years of age who newly initiated warfarin or direct oral anticoagulants after diagnosis with AF betwe
22 Sex-specific comparative effectiveness of direct oral anticoagulants among patients with nonvalvul
23 ht of decreased intracranial hemorrhage with direct oral anticoagulants and concerns about their safe
24 The dashboard includes information about direct oral anticoagulants and dose prescribed, renal fu
25 t of PVT in cirrhosis, including the role of direct oral anticoagulants and endovascular intervention
28 Special attention is given to the place of direct oral anticoagulants and to the management of pati
29 clopidogrel, a vitamin K antagonist (VKA), a direct oral anticoagulant, and combined antithrombotic d
30 possible PFO associated stroke, the role of direct oral anticoagulants, and very long term outcomes
31 illation treated with vitamin K antagonists, direct oral anticoagulants, antiplatelets, and combinati
32 e of similar efficacy and safety between the direct oral anticoagulants apixaban and rivaroxaban, and
35 tagonists, low-molecular-weight heparin, and direct oral anticoagulants are all reasonable anticoagul
46 al antiplatelet therapy, the availability of direct oral anticoagulants as a potential alternative op
47 laminated) thrombus, imaging of LV thrombus, direct oral anticoagulants as an alternative to warfarin
48 ), and higher total costs than patients with direct oral anticoagulant-associated major bleeding.
49 al mortality were seen between warfarin- and direct oral anticoagulant-associated major bleeding.
52 %; adjusted OR, 1.87 [95% CI, 1.57-2.24]), a direct oral anticoagulant (cases: 1.0%, controls: 0.6%;
53 k of gastrointestinal bleeding with use of a direct oral anticoagulant compared with warfarin or low-
54 e adjusted odds ratio for major bleeding for direct oral anticoagulants compared with placebo or no t
55 risk of major gastrointestinal bleeding with direct oral anticoagulants compared with warfarin or low
56 risk of major gastrointestinal bleeding with direct oral anticoagulants compared with warfarin or low
57 rt period of 72 h, followed by a switch to a direct oral anticoagulant (dabigatran), is effective and
59 risk of major gastrointestinal bleeding with direct oral anticoagulants did not differ from that with
61 0%) or dual antiplatelet therapy (16.2%), or direct oral anticoagulant (DOAC) (10.8%), with a median
64 trategies were warfarin and aspirin (36.9%), direct oral anticoagulant (DOAC) and aspirin (20.8%), wa
65 is unclear how many patients treated with a direct oral anticoagulant (DOAC) are using concomitant a
67 ial fibrillation, the frequency of off-label direct oral anticoagulant (DOAC) dosing, associated fact
68 aimed to estimate the effects of starting a direct oral anticoagulant (DOAC) early (<=4 days) versus
69 onvalvular atrial fibrillation (NVAF) in the direct oral anticoagulant (DOAC) era was rarely investig
70 anticoagulation treatment with warfarin or a direct oral anticoagulant (DOAC) in atrial fibrillation
71 efore and after switching from warfarin to a direct oral anticoagulant (DOAC) in patients grouped by
72 difies the treatment effect of early vs late direct oral anticoagulant (DOAC) initiation in people wi
74 ommon antithrombotic discharge regimens were direct oral anticoagulant (DOAC) plus aspirin (48.3%), D
75 stroke despite vitamin K-antagonist (VKA) or direct oral anticoagulant (DOAC) treatment across 11 str
76 tracerebral hemorrhage (ICH) associated with direct oral anticoagulant (DOAC) use carries extremely h
77 nsity-matched analysis, patients receiving a direct oral anticoagulant (DOAC) were matched with those
78 with venous thromboembolism (VTE) compared a direct oral anticoagulant (DOAC) with vitamin K antagoni
79 ching from a vitamin K antagonist (VKA) to a direct oral anticoagulant (DOAC), and vice versa, and 30
83 ompare causes of death in patients receiving direct oral anticoagulants (DOAC) or warfarin for preven
84 , provided validation for the development of direct oral anticoagulants (DOAC), and currently such in
85 he safety and effectiveness of dual therapy (direct oral anticoagulant [DOAC] plus P2Y12 inhibitor) v
87 cular-weight heparins (LMWHs) to include the direct oral anticoagulants (DOACs) apixaban, edoxaban an
90 tion, which may be related to a concern that direct oral anticoagulants (DOACs) are associated with a
92 bedside assays to measure the effect of the direct oral anticoagulants (DOACs) are not available.
94 ated macular degeneration (AMD) initiated on direct oral anticoagulants (DOACs) compared with matched
96 oward guests, which we demonstrate using the direct oral anticoagulants (DOACs) dabigatran, betrixaba
98 losure (LAAC) was noninferior to nonwarfarin direct oral anticoagulants (DOACs) for preventing major
99 e studies on the safety and effectiveness of direct oral anticoagulants (DOACs) for the treatment of
110 ortant atrial fibrillation subgroup in which direct oral anticoagulants (DOACs) have not been adequat
114 of early compared with delayed initiation of direct oral anticoagulants (DOACs) in patients with acut
115 There is uncertainty surrounding the use of direct oral anticoagulants (DOACs) in patients with kidn
116 has demonstrated advantages over alternative direct oral anticoagulants (DOACs) in some settings, its
118 atements have recommended against the use of direct oral anticoagulants (DOACs) in venous thromboembo
119 in patients with T2DM, assess the impact of direct oral anticoagulants (DOACs) introduction on oral
120 uence of race and ethnicity on initiation of direct oral anticoagulants (DOACs) is relatively underst
121 early stage CKD, the risk-benefit profile of direct oral anticoagulants (DOACs) is superior to that o
125 investigated effects of AC with warfarin and direct oral anticoagulants (DOACs) on all-cause mortalit
126 Patients were randomized (1:1) to receive direct oral anticoagulants (DOACs) or dual antiplatelet
127 eeding and thrombotic events associated with direct oral anticoagulants (DOACs) or VKAs in a prospect
132 justifies further attempts to reduce it with direct oral anticoagulants (DOACs) remains unclear.
138 outcomes in a trial analogous population of direct oral anticoagulants (DOACs) users and in patients
140 ulation with vitamin K antagonists (VKAs) or direct oral anticoagulants (DOACs) with stroke severity,
141 ata from 3 large randomized trials comparing direct oral anticoagulants (DOACs) with warfarin (ARISTO
142 It has been posited that the availability of direct oral anticoagulants (DOACs) would improve oral an
143 cording to the anticoagulant prescribed: (1) direct oral anticoagulants (DOACs), (2) low-molecular-we
144 ave evolved to include patients treated with direct oral anticoagulants (DOACs), but it is unknown wh
146 zed patients, especially older patients, use direct oral anticoagulants (DOACs), mainly to prevent st
155 ntrolled trials have subsequently shown that direct oral anticoagulants (DOACs; ie, apixaban, dabigat
157 These include the class of drugs called direct oral anticoagulants, (DOACs) which do not require
158 e evidence suggests that initiating use of a direct oral anticoagulant earlier is better than at late
160 3 was day 10; and group 4 was day 14) with a direct oral anticoagulant for secondary stroke preventio
161 A clearly superior day to initiate use of a direct oral anticoagulant for secondary stroke preventio
162 testinal absorption impairment; (3) LMWHs or direct oral anticoagulants for a minimum of 6 months to
163 rivaroxaban are the most commonly prescribed direct oral anticoagulants for adults with atrial fibril
166 eatment of cancer-associated thrombosis; (2) direct oral anticoagulants for the initial treatment and
169 fied 1159 and 3477 patients in the pLAAO and direct oral anticoagulant groups with a mean age of 78.1
170 ified 953 and 2859 patients in the pLAAO and direct oral anticoagulant groups with a mean age of 78.1
172 that specific inhibition of coagulation via direct oral anticoagulants had differential effects on g
173 in, in particular the intermediate dose, and direct oral anticoagulants had the least favourable prof
176 assessing primary thromboprophylaxis using a direct oral anticoagulant in paediatric patients with ac
177 rial appendage occlusion device [pLAAO]) and direct oral anticoagulants in 2 matched cohorts based on
178 The benefits of switching from warfarin to direct oral anticoagulants in atrial fibrillation remain
179 scribe recently completed clinical trials of direct oral anticoagulants in children and adolescents a
181 end point studies on thromboprophylaxis with direct oral anticoagulants in patients undergoing bariat
184 ELAN trial (Early Versus Late Initiation of Direct Oral Anticoagulants in Post-Ischaemic Stroke Pati
185 use low-molecular-weight heparins (LMWHs) or direct oral anticoagulants in the treatment of most pati
186 mainstay of therapy because the efficacy of direct oral anticoagulants is less well established.
190 r future investigation on whether the use of direct oral anticoagulants might be of therapeutic value
191 e improvements linked to the introduction of direct oral anticoagulants, more than one third of atria
192 rin (prophylactic (low) or higher dose) with direct oral anticoagulants or with no active treatment.
194 or intermediate dose unfractionated heparin, direct oral anticoagulants, pentasaccharides, placebo, o
195 t, and treatment with vitamin K antagonists, direct oral anticoagulants, platelet inhibitors, and com
196 aid expansion was not associated with higher direct oral anticoagulants prescription rates (DID estim
199 creased major bleeding (1.87, 1.06 to 3.31); direct oral anticoagulants reduced symptomatic venous th
200 ticoagulation with a vitamin K antagonist or direct oral anticoagulant reduces stroke risk by 60% to
201 some indications, lowering the dose of some direct oral anticoagulants reduces the risk of bleeding
202 dication (warfarin, standard-, or lower-dose direct oral anticoagulant regimen) during trial follow-u
203 gents for venous thromboembolism (VTE), with direct oral anticoagulants replacing warfarin as the dru
204 ional study assesses the availability of the direct oral anticoagulant reversal agents idarucizumab a
205 pirin combined with the vascular dose of the direct oral anticoagulant rivaroxaban) for patients with
206 e sex-specific, comparative effectiveness of direct oral anticoagulants (rivaroxaban and dabigatran),
207 axis of venous thromboembolism with LMWHs or direct oral anticoagulants (rivaroxaban or apixaban) in
209 e of therapeutic-dose rivaroxaban, and other direct oral anticoagulants, should be avoided in these p
211 such as warfarin followed by warfarin alone, direct oral anticoagulants such as apixaban, edoxaban, r
213 data on the relative efficacy and safety of direct oral anticoagulants, such as edoxaban, compared w
215 lure has focused on vitamin K antagonists or direct oral anticoagulants that inhibit thrombin or fact
216 ls assessing the optimal timing to introduce direct oral anticoagulant therapy after a stroke show th
219 -gp should be avoided in all patients taking direct oral anticoagulant unless previously proven to be
220 gnificant difference in CSH observed between direct oral anticoagulant use compared with continued wa
222 elative risk of CSH in patients treated with direct oral anticoagulant versus continued warfarin.
226 ding occurs in 1.1% of patients treated with direct oral anticoagulants vs 1.8% treated with warfarin
227 d the risk of gastrointestinal bleeding with direct oral anticoagulants, warfarin, and low-molecular-
229 al fibrillation who initiated treatment with direct oral anticoagulants were identified from Danish n
230 g, 1.28 (95% CI, 1.13-1.44) for therapy of a direct oral anticoagulant with an antiplatelet drug, 3.7
231 m head-to-head clinical trials that compared direct oral anticoagulant with low-molecular-weight hepa
234 th atrial fibrillation and were prescribed a direct oral anticoagulant within 2 weeks from stroke ons