ライフサイエンスコーパス: vitamin K antagonist

1 py (low-molecular-weight heparin followed by vitamin K antagonists).

2 nsitioned from blinded therapy to open-label vitamin K antagonist.

3 Tecarfarin (ATI-5923) is a novel oral vitamin K antagonist.

4 re can predict the patient's suitability for vitamin K antagonists.

5 n confined to long-term anticoagulation with vitamin K antagonists.

6 and more particularly its susceptibility to vitamin K antagonists.

7 th an overall clinical benefit compared with vitamin K antagonists.

8 bolic events in patients receiving long-term vitamin K antagonists.

9 n inhibitors may represent an alternative to vitamin K antagonists.

10 nts requiring long-term anticoagulation with vitamin K antagonists.

11 All patients received vitamin K antagonists.

12 coagulated with a combination of aspirin and vitamin K antagonists.

13 nts to have greater benefits than risks over vitamin K antagonists.

14 (NOACs) that are attractive alternatives to vitamin K antagonists.

15 need to reverse the anticoagulant effect of vitamin K antagonists.

16 ng that has hindered usage and acceptance of vitamin K antagonists.

17 including 907 patients with AF treated with vitamin K antagonists (3,865 patient-years), to assess C

18 2) describe the advantages of the DOACs over vitamin K antagonists, (3) summarize the experience with

19 (RFA) in comparison with uninterrupted oral vitamin K antagonist administration.

20 ompared with treatment with enoxaparin and a vitamin K antagonist, although there was no difference b

21 (1) ablation was performed under therapeutic vitamin K antagonist and heparin to maintain activated c

22 vidence for adding aspirin to the regimen of vitamin K antagonists and clopidogrel seems to be weaken

23 t anticoagulation with specific guidance for vitamin K antagonists and direct-acting oral anticoagula

24 These drugs, which could replace vitamin K antagonists and heparins in many patients, are

25 aban, provide potential advantages over oral vitamin K antagonists and subcutaneous low-molecular-wei

26 ecular-weight heparin (LMWH) along with with vitamin K antagonists and the benefits and proven safety

27 sceptibility of some extrahepatic tissues to vitamin K antagonists and the lack of effects of vitamin

28 d to intravenous unfractionated heparin plus vitamin K antagonist, and reviparin once daily produced

29 x concentrate in the nonemergent reversal of vitamin K antagonists, and limiting routine computed tom

30 well-controlled vitamin K antagonists or non-vitamin K antagonist anticoagulants.

31 Vitamin K antagonists are also inhibitors of VKORC1L1, b

32 Vitamin K antagonists are commonly used by clinicians to

33 ed and low-molecular-weight heparins and the vitamin K antagonists are effective for the prevention a

34 Vitamin K antagonists are highly effective in preventing

35 For example, vitamin K antagonists are the most efficacious for preve

36 Vitamin K antagonists are widely used as treatment of ve

37 anticoagulant therapy and have replaced the vitamin K antagonists as the preferred treatment for man

38 lines recommended the use of triple therapy (vitamin K antagonists, aspirin, and clopidogrel) for the

39 may at least not be worse than that of major vitamin K antagonist bleeding, and probably better.

40 vidually, NOACs were at least noninferior to vitamin K antagonists, but a clear superiority in overal

41 ACs were pooled to perform a comparison with vitamin K antagonists, calculating pooled relative risks

42 amiliarity with the dosing and monitoring of vitamin K antagonists, clinicians are accustomed to usin

43 ere 1.84% (95% CrI, 1.33%-2.51%) for the UFH-vitamin K antagonist combination and 1.30% (95% CrI, 1.0

44 However, findings suggest that the UFH-vitamin K antagonist combination is associated with the

45 bination, a treatment strategy using the UFH-vitamin K antagonist combination was associated with an

46 Compared with the LMWH-vitamin K antagonist combination, a treatment strategy u

47 h a lower risk of bleeding than was the LMWH-vitamin K antagonist combination, with a lower proportio

48 nd 0.89% (95% CrI, 0.66%-1.16%) for the LMWH-vitamin K antagonist combination.

49 nd 1.30% (95% CrI, 1.02%-1.62%) for the LMWH-vitamin K antagonist combination.

50 enous thromboembolism compared with the LMWH-vitamin K antagonist combination.

51 icoagulants, such as edoxaban, compared with vitamin K antagonists during extended therapy for venous

52 Vitamin K antagonist (eg, warfarin) use is nowadays chal

53 Recent data suggest that BPVT responds to vitamin K antagonists, emphasizing the need for reliable

54 tcome measure was the use of anticoagulants (vitamin K antagonists, factor Xa inhibitors, and direct

55 with enoxaparin followed by an adjusted-dose vitamin K antagonist for 3, 6, or 12 months.

56 ving heparin bridging during interruption of vitamin K antagonists for elective procedures.

57 ew oral anticoagulants are poised to replace vitamin K antagonists for many patients with atrial fibr

58 NOACs) have been proposed as alternatives to vitamin K antagonists for the prevention of stroke and s

59 , usually overlapping with and followed by a vitamin K antagonist) for at least 3 months.

60 Although the use of oral anticoagulants (vitamin K antagonists) has been abandoned in primary car

61 But vitamin K antagonists have limitations, including causin

62 Many patients treated with vitamin K antagonists have unstable International Normal

63 of 301 patients allocated to enoxaparin and vitamin K antagonist (hazard ratio [HR] 0.67, 95% CI 0.3

64 nd clinical outcomes between NOAC-ICH versus vitamin K antagonists-ICH (VKA-ICH).

65 us durations of anticoagulant therapy with a vitamin K antagonist (ie, warfarin) for an initial episo

66 or glucose regulation (high protein-induced vitamin K antagonist-II).

67 ized, controlled trials comparing NOACs with vitamin K antagonists in patients with atrial fibrillati

68 Since the discovery of vitamin K antagonists in the early 1940s, there has been

69 roxaban compared with enoxaparin followed by vitamin K antagonists, in the subgroup of patients with

70 Reviparin administered twice daily plus vitamin K antagonist is more effective in inhibiting in

71 If transition from rivaroxaban to vitamin K antagonist is needed, timely monitoring and ca

72 risk in atrial fibrillation (AF) using oral vitamin K antagonists is closely related to bleeding ris

73 n vitro prediction of the in vivo potency of vitamin K antagonists is complicated by the complex mult

74 ndent proteins in patients not maintained on vitamin K antagonists is most commonly associated with p

75 agulant followed by long-term therapy with a vitamin K antagonist, many clinical questions remain una

76 vascular and renovascular calcification, and vitamin K antagonists may be associated with a decreased

77 tion of an OAC with warfarin sodium or a non-vitamin K antagonist OAC.

78 44 (59.8%) were treated with warfarin or non-vitamin K antagonist OACs.

79 09 (61.8%) were treated with warfarin or non-vitamin K antagonist OACs.

80 min K antagonists and the lack of effects of vitamin K antagonists on the functionality of the vitami

81 2), or standard therapy with a dose-adjusted vitamin K antagonist (once daily) plus DAPT for 1, 6, or

82 predictive ability for bleeding, whether on vitamin K antagonist or not (c-statistic approximately 0

83 ncreased risk of stroke with well-controlled vitamin K antagonists or non-vitamin K antagonist antico

84 OAC use, whether as well controlled vitamin K antagonists or nonvitamin K antagonists oral a

85 scade either by an indirect mechanism (e.g., vitamin K antagonists) or by a direct one (e.g., the nov

86 anticoagulants, with options including LMWH, vitamin K antagonists, or direct factor Xa or direct fac

87 ence regarding ICH related to the use of non-vitamin K antagonist oral anticoagulant (NOAC) agents.

88 to determine if they are candidates for non-vitamin K antagonist oral anticoagulant (NOAC) therapy.

89 ticoagulation, either with warfarin or a non-vitamin K antagonist oral anticoagulant (NOAC), is indic

90 of rt-PA in patients who are receiving a non-vitamin K antagonist oral anticoagulant (NOAC).

91 It is unclear whether the non-vitamin K antagonist oral anticoagulant agents rivaroxab

92 In comparing the 2 non-vitamin K antagonist oral anticoagulant agents with each

93 Non-vitamin K antagonist oral anticoagulant drugs have recen

94 icular thrombus plus the availability of non-vitamin K antagonist oral anticoagulant drugs may lead t

95 Non-vitamin K antagonist oral anticoagulant-associated ICH h

96 The non-vitamin K antagonist oral anticoagulants (NOACs) apixaba

97 Current guidelines recommend non-vitamin K antagonist oral anticoagulants (NOACs) as the

98 Although non-vitamin K antagonist oral anticoagulants (NOACs) do not

99 farin) use is nowadays challenged by the non-vitamin K antagonist oral anticoagulants (NOACs) for str

100 These novel non-vitamin K antagonist oral anticoagulants (NOACs) have be

101 The use of non-vitamin K antagonist oral anticoagulants (NOACs) instead

102 Dose reduction of non-vitamin K antagonist oral anticoagulants (NOACs) is indi

103 NR] >/=2) and 8290 (8.8%) were receiving non-vitamin K antagonist oral anticoagulants (NOACs) precedi

104 There are now 4 new non-vitamin K antagonist oral anticoagulants (NOACs) that ar

105 Phase III trials comparing non-vitamin K antagonist oral anticoagulants (NOACs) with wa

106 Of patients given OAC, 17.2% received non-vitamin K antagonist oral anticoagulants (NOACs).

107 Non-vitamin K antagonist oral anticoagulants are expensive a

108 Specific reversal agents for non-vitamin K antagonist oral anticoagulants are lacking.

109 Whether the use of non-vitamin K antagonist oral anticoagulants could lower the

110 s enrolled in phase 3 clinical trials of non-vitamin K antagonist oral anticoagulants in prevention o

111 acteristics and natural history of acute non-vitamin K antagonists oral anticoagulants (NOAC)-associa

112 Low-thromboembolic-risk and/or non-vitamin K antagonist patient groups were used for compar

113 umber of patients managed with uninterrupted vitamin K antagonist phenprocoumon (international normal

114 nt bleeding than was standard therapy with a vitamin K antagonist plus DAPT for 1, 6, or 12 months.

115 t of stents, standard anticoagulation with a vitamin K antagonist plus dual antiplatelet therapy (DAP

116 Anticoagulation with vitamin K antagonists reduces major thromboembolic compl

117 rial fibrillation, oral anticoagulation with vitamin K antagonists reduces the risk of stroke by more

118 nts experiencing major bleeding while taking vitamin K antagonists require rapid vitamin K antagonist

119 concentrate (4F-PCC) with plasma for urgent vitamin K antagonist reversal.

120 e taking vitamin K antagonists require rapid vitamin K antagonist reversal.

121 ment with low-molecular-weight heparin and a vitamin K antagonist (RR, 0.67; 95% CI, 0.37-1.20; I2 =

122 difference was identified between NOACs and vitamin K antagonists (RR, 0.84; 95% CI, 0.59-1.19; I2 =

123 Vitamin K antagonists such as warfarin inhibit the vitam

124 ncy, it may be excessive for patients taking vitamin K antagonists, such as warfarin, and jeopardize

125 Vitamin K antagonists, such as warfarin, are underused a

126 Vitamin K antagonists, such as warfarin, have been the m

127 togenic consequences of exposure in utero to vitamin K antagonists, such as warfarin-based anticoagul

128 zyme appears to be 50-fold more resistant to vitamin K antagonists than VKORC1.

129 able propeptide and sensitive to warfarin, a vitamin K antagonist that is widely used as an antithrom

130 eparin ameliorates Trousseau syndrome, while vitamin K antagonists that merely depress thrombin produ

131 The vitamin K antagonists, the only approved oral anticoagul

132 Vitamin K antagonists, the only available oral anticoagu

133 OAC in AF patients, but with low quality of vitamin K antagonist therapy and insufficient adherence

134 Long-term vitamin K antagonist therapy can be complicated by unsta

135 alternative to plasma for urgent reversal of vitamin K antagonist therapy in major bleeding events, a

136 d-dose idraparinux with adjustable-dose oral vitamin K antagonist therapy in patients with AF.

137 tion in rivaroxaban participants switched to vitamin K antagonist therapy.

138 d to reverse the effect of warfarin or other vitamin K-antagonist therapy following vitamin K adminis

139 Vitamin K antagonist-treated patients receiving periproc

140 Results from this trial suggest that during vitamin K antagonist treatment INR monitoring could be r

141 tients Who Have Failed or Are Unsuitable for Vitamin-K Antagonist Treatment (AVERROES) trial and othe

142 Vitamin K antagonist use in the first trimester compared

143 nd it was amplified by diabetes and previous vitamin K antagonist use.

144 r stroke, relative risk of stroke, and prior vitamin-K antagonist use in the life-time model.

145 Warfarin, a vitamin K "antagonist" used clinically for the preventio

146 ies suggest a protective association between vitamin K antagonist (VKA) anticoagulants and the incide

147 and safety of adding antiplatelet therapy to vitamin K antagonist (VKA) in atrial fibrillation patent

148 Compared with vitamin K antagonist (VKA) in prevalent AF, VKA plus ant

149 ine, 37,539 patients (52%) were treated with vitamin K antagonist (VKA) monotherapy, 25,458 (35%) wit

150 The safety and effectiveness of non-vitamin K antagonist (VKA) oral anticoagulants, dabigatr

151 ry stenting traditionally are treated with a vitamin K antagonist (VKA) plus dual antiplatelet therap

152 Managing vitamin K antagonist (VKA) therapy is challenging in chi

153 omen treated with any of the following: 1) a vitamin K antagonist (VKA) throughout pregnancy; 2) low-

154 e increased risk of bleeding associated with vitamin K antagonist (VKA) treatment was particularly ev

155 s quality of anticoagulation control amongst vitamin K antagonist (VKA) users.

156 treatment regimen: triple therapy (TT) with vitamin K antagonist (VKA)+aspirin+clopidogrel, VKA+anti

157 Use of low-dose aspirin, clopidogrel, a vitamin K antagonist (VKA), a direct oral anticoagulant,

158 Rapid reversal of vitamin K antagonist (VKA)-induced anticoagulation is of

159 tran and warfarin might be most equitable in vitamin K antagonist (VKA)-naive patients.

160 l anticoagulant (NOAC) who transitioned to a vitamin K antagonist (VKA).

161 Overall, 43,299 AF patients initiating vitamin K antagonists (VKA) (42%), dabigatran (29%), riv

162 Vitamin K antagonists (VKA) have long been the default d

163 acy and bleeding outcomes in comparison with vitamin K antagonists (VKA) in elderly participants (age

164 rivaroxaban or apixaban or dabigatran versus vitamin K antagonists (VKA) in patients with venous thro

165 Vitamin K antagonists (VKA) use is challenging because o

166 Thromboprophylaxis can be obtained with vitamin K antagonists (VKA, eg, warfarin) or a non-VKA o

167 ality in intracranial haemorrhage related to vitamin K antagonists (VKA-ICH).

168 t strategies for intracerebral hemorrhage on vitamin K antagonists (VKA-ICH).

169 aban) are effective and safe alternatives to vitamin K antagonists (VKAs) and low-molecular-weight he

170 erm (>/=3 months) vs short-term therapy with vitamin K antagonists (VKAs) associated with differences

171 the efficacy and safety of the NOACs versus vitamin K antagonists (VKAs) for atrial fibrillation and

172 Vitamin K antagonists (VKAs) have been the standard of c

173 onist oral anticoagulants (NOACs) instead of vitamin K antagonists (VKAs) in patients with atrial fib

174 Bleeding risk with vitamin K antagonists (VKAs) is closely related to the q

175 Women receiving vitamin K antagonists (VKAs) require adequate contracept

176 e these drugs have several benefits over the vitamin K antagonists (VKAs).

177 ared a direct oral anticoagulant (DOAC) with vitamin K antagonists (VKAs).

178 tment is the narrow therapeutic index of the vitamin K antagonists ([VKAs]: warfarin and related coum

179 Oral anticoagulants (both vitamin K antagonists [VKAs] and non-VKA oral anticoagul

180 better efficacy and safety compared with the vitamin K antagonist warfarin for preventing strokes or

181 Treatment with the vitamin K antagonist warfarin led to the accumulation of

182 iency to the administration of 1 mg/d of the vitamin K antagonist warfarin was studied in two groups

183 Furthermore, the vitamin K antagonists warfarin and dicoumarol and the di

184 Treatment with the vitamin K-antagonist warfarin prevents the increase in s

185 charide (fondaparinux); oral anticoagulants: vitamin K antagonists (warfarin), new oral Xa inhibitors

186 At the EOS visit, open-label vitamin K antagonist was recommended, and the internatio

187 initially for 6 uninterrupted months with a vitamin K antagonist were randomized and followed up bet

188 Until recently, vitamin K antagonists were the only available oral antic

189 For these reasons, we anticipate that the vitamin K antagonists will continue to be important anti

190 udies with LMWH, unfractionated heparin, and vitamin K antagonists, with overall encouraging but nonc