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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
15  when comparing continued versus interrupted direct oral anticoagulant (2.1% in both groups).
16 ractionated heparin (2.63, 1.00 to 6.21) and direct oral anticoagulants (2.31, 0.82 to 6.47) were mos
17 ts (48.4%), parenteral heparins (27.7%), and direct oral anticoagulants (22.6%).
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
20                   The role of treatment with direct oral anticoagulant agents is unclear.
21 ng but are typically excluded from trials of direct oral anticoagulant agents.
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
26                                              Direct oral anticoagulants and low molecular weight hepa
27                                              Direct oral anticoagulants and low molecular weight hepa
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
33                                     Although direct oral anticoagulants are a welcome addition, clini
34                                              Direct oral anticoagulants are administered in fixed dos
35 tagonists, low-molecular-weight heparin, and direct oral anticoagulants are all reasonable anticoagul
36                                  Postpartum, direct oral anticoagulants are an option if a woman does
37                                              Direct oral anticoagulants are first-line therapy for co
38                                              Direct oral anticoagulants are increasingly used for a w
39                                              Direct oral anticoagulants are mainly affected by medica
40                                     Although direct oral anticoagulants are more convenient and safer
41                                              Direct oral anticoagulants are non-inferior to conventio
42                                              Direct oral anticoagulants are noninferior to warfarin w
43                                   Studies of direct oral anticoagulants are now emerging that show th
44                            Both warfarin and direct oral anticoagulants are susceptible to drug-drug
45                                              Direct oral anticoagulants are the primary stroke preven
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.
50                        The introduction of 4 direct oral anticoagulants beginning in 2010 has signifi
51                                              Direct oral anticoagulant care models were first indirec
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
58                     With the introduction of direct oral anticoagulants (dabigatran, rivaroxaban, api
59 risk of major gastrointestinal bleeding with direct oral anticoagulants did not differ from that with
60                                     Although direct oral anticoagulants do not need laboratory testin
61 0%) or dual antiplatelet therapy (16.2%), or direct oral anticoagulant (DOAC) (10.8%), with a median
62                           BACKGROUND & AIMS: Direct oral anticoagulant (DOAC) agents increase the ris
63                                              Direct oral anticoagulant (DOAC) agents increase the ris
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
66                       The effectiveness of a direct oral anticoagulant (DOAC) compared with LMWH for
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
73         Moreover, evidence of CRC risk under direct oral anticoagulant (DOAC) is limited.
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
80                                              Direct oral anticoagulant (DOAC)-associated intracranial
81 on involves the choice between warfarin or a direct oral anticoagulant (DOAC).
82 pidogrel, a vitamin K antagonist (VKA), or a direct oral anticoagulant (DOAC).
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
86                  The optimal timing to start direct oral anticoagulants (DOACs) after an acute ischae
87 cular-weight heparins (LMWHs) to include the direct oral anticoagulants (DOACs) apixaban, edoxaban an
88                                              Direct oral anticoagulants (DOACs) are an emerging treat
89                    Although reduced doses of direct oral anticoagulants (DOACs) are approved for pati
90 tion, which may be related to a concern that direct oral anticoagulants (DOACs) are associated with a
91                                              Direct oral anticoagulants (DOACs) are attractive option
92  bedside assays to measure the effect of the direct oral anticoagulants (DOACs) are not available.
93                           For most patients, direct oral anticoagulants (DOACs) are preferred over vi
94 ated macular degeneration (AMD) initiated on direct oral anticoagulants (DOACs) compared with matched
95                  The benefit-risk profile of direct oral anticoagulants (DOACs) compared with warfari
96 oward guests, which we demonstrate using the direct oral anticoagulants (DOACs) dabigatran, betrixaba
97                   The efficacy and safety of direct oral anticoagulants (DOACs) for patients with thr
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
100                                  Two RCTs of direct oral anticoagulants (DOACs) for the treatment of
101                          Introduction of the direct oral anticoagulants (DOACs) has long been conside
102                          The introduction of direct oral anticoagulants (DOACs) has transformed the t
103                                     However, direct oral anticoagulants (DOACs) have an improved safe
104                                              Direct oral anticoagulants (DOACs) have become first-lin
105                               More recently, direct oral anticoagulants (DOACs) have been demonstrate
106                                              Direct Oral Anticoagulants (DOACs) have been shown to be
107                                              Direct oral anticoagulants (DOACs) have comparable effic
108                                              Direct oral anticoagulants (DOACs) have emerged as prima
109                                              Direct oral anticoagulants (DOACs) have largely replaced
110 ortant atrial fibrillation subgroup in which direct oral anticoagulants (DOACs) have not been adequat
111                                              Direct oral anticoagulants (DOACs) have shown a positive
112                          Over the past 10 y, direct oral anticoagulants (DOACs) have shown similar ef
113                        Stroke reduction with direct oral anticoagulants (DOACs) in atrial fibrillatio
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
117                Evidence regarding the use of direct oral anticoagulants (DOACs) in the elderly, parti
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
122                                              Direct oral anticoagulants (DOACs) may be good alternati
123                     Dose-reduced regimens of direct oral anticoagulants (DOACs) may be used for 2 mai
124                          The availability of direct oral anticoagulants (DOACs) may improve overall 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
128  whether clinical outcomes differ when using direct oral anticoagulants (DOACs) or warfarin.
129           Current guidelines recommend using direct oral anticoagulants (DOACs) over warfarin in pati
130                          Concurrent use with direct oral anticoagulants (DOACs) poses the threat of a
131                                              Direct oral anticoagulants (DOACs) reduce the rate of th
132 justifies further attempts to reduce it with direct oral anticoagulants (DOACs) remains unclear.
133                                          The direct oral anticoagulants (DOACs) represent a major adv
134                                          The direct oral anticoagulants (DOACs) rivaroxaban and dabig
135                                              Direct oral anticoagulants (DOACs) targeting activated f
136                                              Direct oral anticoagulants (DOACs) that inhibit the coag
137                                              Direct oral anticoagulants (DOACs) used in fixed doses w
138  outcomes in a trial analogous population of direct oral anticoagulants (DOACs) users and in patients
139                           Beginning in 2012, direct oral anticoagulants (DOACs) were approved for tre
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
145                                              Direct oral anticoagulants (DOACs), comprising apixaban,
146 zed patients, especially older patients, use direct oral anticoagulants (DOACs), mainly to prevent st
147                    The recently FDA-approved direct oral anticoagulants (DOACs), such as dabigatran,
148                  Despite the introduction of direct oral anticoagulants (DOACs), the search for more
149                                              Direct oral anticoagulants (DOACs), vitamin K antagonist
150 arcity of data is present on the efficacy of direct oral anticoagulants (DOACs).
151 ulation with vitamin K antagonists (VKAs) or direct oral anticoagulants (DOACs).
152 ablation procedures in patients treated with direct oral anticoagulants (DOACs).
153 characteristics that are similar to those of direct oral anticoagulants (DOACs).
154 with atrial fibrillation treated with VKA or direct oral anticoagulants (DOACs).
155 ntrolled trials have subsequently shown that direct oral anticoagulants (DOACs; ie, apixaban, dabigat
156                                              Direct oral anticoagulants (DOACs; namely, rivaroxaban a
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
159       We investigated whether rivaroxaban, a direct oral anticoagulant factor Xa inhibitor, would red
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
164                 The rapid global adoption of direct oral anticoagulants for management of VTE in pati
165                                              Direct oral anticoagulants for stroke prevention in pati
166 eatment of cancer-associated thrombosis; (2) direct oral anticoagulants for the initial treatment and
167                   The efficacy and safety of direct oral anticoagulants for this indication are unexp
168                          The availability of direct oral anticoagulants further complicates decision
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
171 g with a 1:3 ratio for patients in pLAAO and direct oral anticoagulant groups.
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
174                                              Direct oral anticoagulants have been recently compared w
175                       The intervention was a direct oral anticoagulant in 209 (99%) of 212 participan
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
180     Limited data exists for alternate use of direct oral anticoagulants in children.
181 end point studies on thromboprophylaxis with direct oral anticoagulants in patients undergoing bariat
182                           Because studies of direct oral anticoagulants in patients with venous throm
183                Randomized clinical trials of direct oral anticoagulants in pediatric VTE are ongoing,
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.
187                                   Use of the direct oral anticoagulants is now supported for many pat
188                                              Direct oral anticoagulants may be considered in patients
189 al interacting medications, and the need for direct oral anticoagulant medication refills.
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.
193                               As compared to direct oral anticoagulants, patients with warfarin-assoc
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
197                                              Direct oral anticoagulants probably prevent symptomatic
198 would derive a greater safety benefit with a direct oral anticoagulant rather than warfarin.
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
208                              The efficacy of direct oral anticoagulants-rivaroxaban, apixaban, dabiga
209 e of therapeutic-dose rivaroxaban, and other direct oral anticoagulants, should be avoided in these p
210               First-line therapy consists of direct oral anticoagulants such as apixaban, edoxaban, r
211 such as warfarin followed by warfarin alone, direct oral anticoagulants such as apixaban, edoxaban, r
212                          In most patients, a direct oral anticoagulant, such as apixaban, rivaroxaban
213  data on the relative efficacy and safety of direct oral anticoagulants, such as edoxaban, compared w
214               This is now best achieved with direct oral anticoagulants that decrease the risk of int
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
217 mendations, including preference for type of direct oral anticoagulant treatment.
218 le therapy, and 2.28 (95% CI, 1.67-3.12) for direct oral anticoagulant triple therapy.
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
221                   This cohort study assesses direct oral anticoagulant use in patients with surgical
222 elative risk of CSH in patients treated with direct oral anticoagulant versus continued warfarin.
223       No difference in CSH was found between direct oral anticoagulant versus continued warfarin.
224                                              Direct oral anticoagulant versus low-molecular-weight he
225 files in patients discharged while receiving direct oral anticoagulant vs 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-
228                               Treatment with direct oral anticoagulants was also associated with lowe
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
232                    Dabigatran etexilate is a direct oral anticoagulant with potential to overcome the
233              1208 adult users of warfarin or direct oral anticoagulants with a general practice or ho
234 th atrial fibrillation and were prescribed a direct oral anticoagulant within 2 weeks from stroke ons
235             We hypothesised that apixaban, a direct oral anticoagulant, would safely reduce venous th

 
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