ライフサイエンスコーパス: vitamin K antagonist

1 ndard anticoagulants (heparin or switched to vitamin K antagonist).

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

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

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

5 necessitates lifelong anticoagulation with a vitamin K antagonist.

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

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

8 P2Y12 inhibitors compared with regimens with vitamin K antagonists.

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

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

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

12 and more particularly its susceptibility to vitamin K antagonists.

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

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

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

16 All patients received vitamin K antagonists.

17 f catheter-based LAAC, largely compared with vitamin K antagonists.

18 risk of intracranial bleeding compared with vitamin K antagonists.

19 antithrombotic therapy including the use of vitamin K antagonists.

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

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

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

23 SELECT2 trial (NCT03876457), 29 of 180 (16%; vitamin K antagonists 15, direct OACs 14) EVT, and 18 of

24 15, direct OACs 14) EVT, and 18 of 172 (10%; vitamin K antagonists 3, direct OACs 15) medical managem

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

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

27 7) and 30 on OAC (direct anticoagulants: 26, vitamin K antagonists: 4), with no differences in baseli

28 Patients were treated with vitamin K antagonists (48.4%), parenteral heparins (27.7

29 Thus, vitamin K antagonists act through mimicking the key inte

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

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

32 1.82 (95% CI, 1.76-1.89) for therapy with a vitamin K antagonist and an antiplatelet drug, 1.28 (95%

33 al to Evaluate the Safety of Apixaban Versus Vitamin K Antagonist and Aspirin Versus Aspirin Placebo

34 nt and randomized treatment (apixaban versus vitamin K antagonist and aspirin versus placebo) on 30-d

35 Trial to Evaluate the Safety of Apixaban vs Vitamin K Antagonist and Aspirin vs Aspirin Placebo in P

36 Trial to Evaluate the Safety of Apixaban vs Vitamin K Antagonist and Aspirin vs Aspirin Placebo in P

37 Trial to Evaluate the Safety of Apixaban vs. Vitamin K Antagonist and Aspirin vs. Aspirin Placebo in

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

39 a P2Y(12) inhibitor to receive apixaban or a vitamin K antagonist and to receive aspirin or matching

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

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

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

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

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

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

46 arge, 3027 patients (63.5%) were receiving a vitamin K antagonist, and 879 (18.5%) were receiving a n

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

48 ess bleeding and fewer hospitalizations than vitamin K antagonists, and aspirin caused more bleeding

49 Therapy with low-molecular-weight heparin, vitamin K antagonists, and direct-acting anticoagulants

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

51 potential alternative option to traditional vitamin K antagonists, and the use of diagnostic modalit

52 safety profile equal or superior to that of vitamin K antagonist anticoagulants (VKAs) in the genera

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

54 Vitamin K antagonists are also inhibitors of VKORC1L1, b

55 Vitamin K antagonists are commonly used by clinicians to

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

57 Vitamin K antagonists are highly effective in preventing

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

59 Vitamin K antagonists are widely used anticoagulants tha

60 Vitamin K antagonists are widely used as treatment of ve

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

62 schemic events than regimens that included a vitamin K antagonist, aspirin, or both.

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

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

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

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

67 Despite this, DOACs, like vitamin K antagonists, can still cause major and clinica

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

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

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

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

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

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

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

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

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

77 anticoagulant treatment, and treatment with vitamin K antagonists, direct oral anticoagulants, plate

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

79 This holds for both vitamin K antagonists (e.g., warfarin) and direct oral a

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

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

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

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

84 molecular weight heparin, fondaparinux, or a vitamin K antagonist for at least 2 months or, in childr

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

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

87 al anticoagulants (DOACs) are preferred over vitamin K antagonists for stroke prevention in atrial fi

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

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

90 latelet drugs, dual antiplatelet therapy, or vitamin K antagonists further reduces the risk of major

91 f death or hospitalization than those in the vitamin K antagonist group (23.5% vs. 27.4%; hazard rati

92 ccurred in the rivaroxaban group than in the vitamin K antagonist group (restricted mean survival tim

93 ents in the rivaroxaban group and 446 in the vitamin K antagonist group had a primary-outcome event.

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

95 But vitamin K antagonists have limitations, including causin

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

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

98 as compared with 14.7% of those receiving a vitamin K antagonist (hazard ratio, 0.69; 95% confidence

99 e for the different types of anticoagulants: vitamin K antagonists, heparins, fondaparinux, thrombin

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

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

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

103 anticoagulants (DOACs) have largely replaced vitamin K antagonists in many indications for anticoagul

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

105 y 2022, AXADIA-AFNET 8 (Compare Apixaban and Vitamin K Antagonists in Patients With Atrial Fibrillati

106 ATCHMAN has emerged as viable alternative to vitamin K antagonists in randomized controlled trials.

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

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

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

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

111 anticoagulation with warfarin or alternative vitamin K antagonist is the standard anticoagulant treat

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

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

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

115 BEST PRACTICE ADVICE 9: Vitamin K antagonists, low-molecular-weight heparin, and

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

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

118 In comparison with vitamin K antagonist monotherapy, adjusted hazard ratios

119 ischemic stroke-related hospitalizations in vitamin K antagonist naive patients and patients with CH

120 reater reductions with edoxaban were seen in vitamin K antagonist naive patients, patients with CHADS

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

122 09 (61.8%) were treated with warfarin or non-vitamin K antagonist OACs.

123 44 (59.8%) were treated with warfarin or non-vitamin K antagonist OACs.

124 ooled persistence was higher with DOACs than vitamin K antagonists (odds ratio, 1.44 [95% CI, 1.12-.8

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

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

127 e in the relative benefit of apixaban versus vitamin K antagonist or aspirin versus placebo when pati

128 or greater per year, anticoagulation with a vitamin K antagonist or direct oral anticoagulant reduce

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

130 lar-weight heparins, unfractionated heparin, vitamin K antagonists or fondaparinux) was compared with

131 Vitamin K antagonists or low molecular weight heparins a

132 Current standard of care (SOC), vitamin K antagonists or low-molecular-weight heparin, h

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

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

135 ifty-one patients with PVT were treated with Vitamin-K antagonists or Low-Molecular-Weight Heparin.

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

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

138 gonist, and 879 (18.5%) were receiving a non-vitamin K antagonist oral anticoagulant (direct OAC), wi

139 rably clopidogrel, in combination with a non-vitamin K antagonist oral anticoagulant (ie, double ther

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

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

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

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

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

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

146 Non-vitamin K antagonist oral anticoagulant drugs have recen

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

148 ials are assessing the optimal timing of non-vitamin K antagonist oral anticoagulant initiation after

149 mic stroke and the benefit:harm ratio of non-vitamin K antagonist oral anticoagulant treatment in pat

150 tiple Institutions to Better Investigate Non-Vitamin K Antagonist Oral Anticoagulant Use in Atrial Fi

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

152 rfarin and 2856 of 4069 (70.2%) taking a non-vitamin K antagonist oral anticoagulant.

153 function were excluded from the pivotal non-vitamin K antagonist oral anticoagulants (NOAC) trials,

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

155 er the clinical benefits associated with non-vitamin K antagonist oral anticoagulants (NOACs) are sim

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

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

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

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

160 Non-vitamin K antagonist oral anticoagulants (NOACs) have pr

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

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

163 The comparative effectiveness of non-vitamin K antagonist oral anticoagulants (NOACs) is unce

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

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

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

167 nclear whether the two once-daily dosing non-vitamin K antagonist oral anticoagulants (NOACs), edoxab

168 min K antagonists, such as warfarin, and non-vitamin K antagonist oral anticoagulants (NOACs).

169 roke in patients previously treated with non-vitamin K antagonist oral anticoagulants (NOACs).

170 ith acute ischemic stroke who are taking non-vitamin K antagonist oral anticoagulants (NOACs).

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

172 Non-vitamin K antagonist oral anticoagulants are being inves

173 Non-vitamin K antagonist oral anticoagulants are expensive a

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

175 Warfarin and non-vitamin K antagonist oral anticoagulants are underused a

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

177 Non-vitamin K antagonist oral anticoagulants have been prove

178 ant clinical outcome data: NOAH-AFNET 6 (Non-Vitamin K Antagonist Oral Anticoagulants in Patients Wit

179 Guidelines caution against the use of non-vitamin K antagonist oral anticoagulants in patients wit

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

181 The advent of non-vitamin K antagonist oral anticoagulants, which attenuat

182 to derive a benefit from treatment with non-vitamin K antagonist oral anticoagulants.

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

184 pixaban and 40 (24.8%) patients treated with vitamin K antagonist (P=0.675).

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

186 Compared with vitamin K antagonists, patients assigned apixaban had lo

187 ssion ratio >=80%), persistence, DOAC versus vitamin K antagonists persistence, and clinical outcomes

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

189 plus P2Y12 inhibitor) versus triple therapy (vitamin K antagonist plus aspirin and P2Y12 inhibitor) i

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

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

192 Anticoagulation with vitamin K antagonists reduces major thromboembolic compl

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

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

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

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

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

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

199 pite of DOAC therapy, anticoagulation with a Vitamin K antagonist should be considered in patients wi

200 igher, compared with heparin combined with a vitamin K antagonist such as warfarin followed by warfar

201 Vitamin K antagonists such as warfarin inhibit the vitam

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

203 ical heart valves, treatment options include vitamin K antagonists, such as warfarin, and non-vitamin

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

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

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

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

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

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

210 The vitamin K antagonists, the only approved oral anticoagul

211 Vitamin K antagonists, the only available oral anticoagu

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

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

214 favorable risk-benefit profile compared with vitamin K antagonist therapy for venous thromboembolism

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

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

217 eart disease-associated atrial fibrillation, vitamin K antagonist therapy led to a lower rate of a co

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

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

220 ation (parenteral anticoagulants followed by vitamin K antagonists), these agents showed improved saf

221 Vitamin K antagonist-treated patients receiving periproc

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

223 gies of Rivaroxaban and a Dose-Adjusted Oral Vitamin K Antagonist Treatment Strategy in Subjects With

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

225 iplatelet drug, 3.73 (95% CI, 3.23-4.31) for vitamin K antagonist triple therapy, and 2.28 (95% CI, 1

226 Vitamin K antagonist use in the first trimester compared

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

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

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

230 sign randomized trial compared apixaban with vitamin K antagonist (VKA) and aspirin with placebo in p

231 vention had less bleeding with apixaban than vitamin K antagonist (VKA) and with placebo than aspirin

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

233 ovascular rehospitalizations compared with a vitamin K antagonist (VKA) based triple therapy regimen.

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

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

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

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

238 lysis to either apixaban (2.5 mg BID) or the vitamin K antagonist (VKA) phenprocoumon (international

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

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

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

242 ing the association between switching from a vitamin K antagonist (VKA) to a direct oral anticoagulan

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

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

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

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

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

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

249 zed ratio (INR) among subjects administrated Vitamin K antagonist (VKA)-triple therapy.

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

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

252 rmine the efficacy and safety of apixaban or vitamin K antagonists (VKA) and aspirin or placebo accor

253 es to low molecular weight heparin (LMWH) or vitamin K antagonists (VKA) for treatment of cancer asso

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

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

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

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

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

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

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

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

262 Elderly patients in long-term treatment with vitamin K antagonists (VKAs) are at high risk of osteopo

263 analogy with surgical mitral bioprosthesis, vitamin K antagonists (VKAs) are predominantly used.

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

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

266 or Xa (FXa) have replaced warfarin and other vitamin K antagonists (VKAs) for most indications requir

267 l appendage closure (LAAC) is noninferior to vitamin K antagonists (VKAs) for preventing atrial fibri

268 a favorable risk-benefit profile compared to vitamin K antagonists (VKAs) for preventing stroke and s

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

270 Vitamin K antagonists (VKAs) have been used in 1% of the

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

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

273 he association of prior anticoagulation with vitamin K antagonists (VKAs) or direct oral anticoagulan

274 inuous therapeutic oral anticoagulation with vitamin K antagonists (VKAs) or direct oral anticoagulan

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

276 (4-PCC) is recommended for rapid reversal of vitamin K antagonists (VKAs) such as warfarin, yet optim

277 ation treated with heparins, heparinoids, or vitamin K antagonists (VKAs) to prevent recurrent ischae

278 Vitamin K antagonists (VKAs), although commonly used to

279 Direct oral anticoagulants (DOACs), vitamin K antagonists (VKAs), single antiplatelet therap

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

281 nticoagulants (DOACs) is superior to that of vitamin K antagonists (VKAs).

282 Millions of people take vitamin K antagonists (VKAs).

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

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

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

286 itant use of SSRIs and OACs (direct OACs and vitamin K antagonists [VKAs]) compared with OAC use alon

287 ring pregnancy, and anticoagulation (LMWH or vitamin K antagonists [VKAs]) should be continued until

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

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

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

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

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

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

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

295 mitant treatment with warfarin or equivalent vitamin K antagonists was prohibited.

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

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

298 For decades, vitamin K antagonists were the only oral option availabl

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

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