ライフサイエンスコーパス: anticoagulant

1 se of its negative charge, and is a powerful anticoagulant.

2 tes require long-term treatment with an oral anticoagulant.

3 ng warfarin, and 60 were using a direct oral anticoagulant.

4 with the antithrombin III domain and act as anticoagulant.

5 arin while 79.8% received direct acting oral anticoagulant.

6 efect that was phenocopied using direct oral anticoagulants.

7 a blood-fluid level, 15 (83.3%) were taking anticoagulants.

8 arameters and platelets and is aggravated by anticoagulants.

9 effects of warfarin compared to direct oral anticoagulants.

10 treatment with non-vitamin K antagonist oral anticoagulants.

11 antagonists (e.g., warfarin) and direct oral anticoagulants.

12 uced risk of bleeding compared with standard anticoagulants.

13 tion, atrial fibrillation, or treatment with anticoagulants.

14 it from more convenient, and possibly safer, anticoagulants.

15 lems preventing clinical use of nucleic acid anticoagulants.

16 so the target of several clinically approved anticoagulants.

17 rtensives, P2Y12 inhibitors, and direct oral anticoagulants.

18 antiviral therapies, immune modulators, and anticoagulants.

19 n part due to an increase in the use of oral anticoagulants.

20 ncreased bleeding, as compared with standard anticoagulants.

21 acokinetics, and pharmacodynamics of various anticoagulants.

22 tients on warfarin versus direct acting oral anticoagulant (16.7% versus10.0%).

23 ing continued versus interrupted direct oral anticoagulant (2.1% in both groups).

24 parenteral heparins (27.7%), and direct oral anticoagulants (22.6%).

25 (dual: 31, single: 17) and 30 on OAC (direct anticoagulants: 26, vitamin K antagonists: 4), with no d

26 The study aimed to compare oral anticoagulants across the range of kidney function in pa

27 Protein C is a natural anticoagulant activated by thrombin in a reaction accele

28 ously shown that thrombin's procoagulant and anticoagulant activities can be effectively disassociate

29 er venom induced haemorrhagic, coagulant and anticoagulant activities were effectively neutralized bo

30 that an oligosaccharide that possesses both anticoagulant activity and binding affinity to HMGB1, th

31 Its potent anticoagulant activity and safety makes it the drug of c

32 MAA868 also caused robust and sustained anticoagulant activity in cynomolgus monkeys as assessed

33 MAA868 exhibited favorable anticoagulant activity in mice with a dose-dependent pro

34 aptamers and showing significantly improved anticoagulant activity is described.

35 The RNA origami constructs show anticoagulant activity sevenfold greater than free aptam

36 f HS3ST1, a key enzyme involved in imparting anticoagulant activity to heparin, and HS3ST3A1, another

37 b binding to an exosite on APC (required for anticoagulant activity) as shown by X-ray crystallograph

38 toprotective properties, but greatly reduced anticoagulant activity, provided similar results.

39 ce and presence of activated protein C (APC) anticoagulant activity.

40 harides that only bind to HMGB1 or only have anticoagulant activity.

41 inding have been previously shown to possess anticoagulant activity; however, problems with rapid ren

42 We calculated the effect of parenteral anticoagulant administration on all-cause mortality, ven

43 erosclerosis and endothelial injury, whereas anticoagulant agents are favored for cardiogenic embolis

44 ombotic drugs because all currently approved anticoagulant agents interfere with hemostasis, leading

45 evere injury]) who had a contraindication to anticoagulant agents to have a vena cava filter placed w

46 f 73 +/- 8 years (28% women, 90% taking oral anticoagulant agents).

47 ypically excluded from trials of direct oral anticoagulant agents.

48 ation are partially mediated by lower use of anticoagulants among black, Hispanic, and Asian patients

49 choice of therapy, and appropriate dosing of anticoagulant and antiplatelet agents, in secondary prev

50 ed protein C is a trypsin-like protease with anticoagulant and cytoprotective properties that is gene

51 in order to select the most appropriate oral anticoagulant and monitoring plan for PWH.

52 Inhibition of the anticoagulant and signaling properties of aPC abolished

53 Despite the development of numerous anticoagulants and antiplatelet agents, the mortality ra

54 of double therapy with full-dose novel oral anticoagulants and P2Y12 inhibitors compared with regime

55 to expand the available therapeutics beyond anticoagulants and to target both thrombocytopathy and e

56 Non-vitamin K oral anticoagulants and warfarin have also entered clinical i

57 , including 60.7% >75 years of age, 34.1% on anticoagulants, and 14.7% with renal failure.

58 ndothelial cells), a decrease of the natural anticoagulants, and complex changes, including changes i

59 , as well as coagulation factors, endogenous anticoagulants, and fibrinolytic enzymes.

60 ated paths for antivirals, immunomodulators, anticoagulants, and other agents have been developed and

61 nt generation of activated protein C's (APC) anticoagulant, anti-inflammatory, and antiapoptotic func

62 associated with triple positivity (for lupus anticoagulant, anticardiolipin, and anti-beta2GPI antibo

63 Combined inhibition of the natural anticoagulants antithrombin (Serpinc1) and protein C (Pr

64 e in the endothelial cofactors that generate anticoagulant APC can contribute to bleeding in CCMs, an

65 efficacy and safety between the direct oral anticoagulants apixaban and rivaroxaban, and warfarin in

66 ticularly informative because, despite using anticoagulant approaches with different pharmacological

67 Antiplatelet agents and anticoagulants are a mainstay for the prevention and tre

68 Although direct oral anticoagulants are a welcome addition, clinicians need t

69 Postpartum, direct oral anticoagulants are an option if a woman does not breastf

70 Non-vitamin K antagonist oral anticoagulants are being investigated for the treatment

71 Although direct oral anticoagulants are more convenient and safer than warfar

72 strategies, this article explains why safer anticoagulants are needed, provides the rationale for fa

73 Direct oral anticoagulants are noninferior to warfarin with regard t

74 Studies of direct oral anticoagulants are now emerging that show the favorable

75 Warfarin and non-vitamin K antagonist oral anticoagulants are underused and often underdosed in the

76 ban and rivaroxaban, both direct-acting oral anticoagulants, are being increasingly used in routine c

77 CT), has been suggested as a marker for oral anticoagulant-associated ICH (OAC-ICH), but the diagnost

78 r total costs than patients with direct oral anticoagulant-associated major bleeding.

79 were seen between warfarin- and direct oral anticoagulant-associated major bleeding.

80 hensive Cancer Network guidelines; reversing anticoagulants; auditing returns to intensive care, time

81 The introduction of 4 direct oral anticoagulants beginning in 2010 has significantly affec

82 hypothesis that specific inhibition of APC's anticoagulant but not its cytoprotective activity can be

83 gement considerations, whether pertaining to anticoagulant choice, as in antiphospholipid antibody sy

84 trial fibrillation, were similar between the anticoagulant cohorts.

85 vitamin K antagonist (VKA) to a direct oral anticoagulant (DOAC), and vice versa, and 30-day risks o

86 d effectiveness of dual therapy (direct oral anticoagulant [DOAC] plus P2Y12 inhibitor) versus triple

87 Direct oral anticoagulants (DOACs) are an emerging treatment option

88 Two RCTs of direct oral anticoagulants (DOACs) for the treatment of VTE in patie

89 Introduction of the direct oral anticoagulants (DOACs) has long been considered a major

90 However, direct oral anticoagulants (DOACs) have an improved safety profile o

91 Direct oral anticoagulants (DOACs) have become first-line treatment

92 Direct oral anticoagulants (DOACs) have largely replaced vitamin K a

93 Over the past 10 y, direct oral anticoagulants (DOACs) have shown similar efficacy with

94 Stroke reduction with direct oral anticoagulants (DOACs) in atrial fibrillation (AF) is de

95 with T2DM, assess the impact of direct oral anticoagulants (DOACs) introduction on oral anticoagulan

96 Direct oral anticoagulants (DOACs) may be good alternatives to low m

97 effects of AC with warfarin and direct oral anticoagulants (DOACs) on all-cause mortality and hepati

98 Direct oral anticoagulants (DOACs) used in fixed doses without labor

99 Beginning in 2012, direct oral anticoagulants (DOACs) were approved for treatment and p

100 lar aspirin, warfarin, or direct-acting oral anticoagulants (DOACs) were defined as users.

101 vitamin K antagonists (VKAs) or direct oral anticoagulants (DOACs) with stroke severity, utilization

102 fibrillation treated with VKA or direct oral anticoagulants (DOACs).

103 cedures in patients treated with direct oral anticoagulants (DOACs).

104 als have subsequently shown that direct oral anticoagulants (DOACs; ie, apixaban, dabigatran, edoxaba

105 ugh VTE in surgical patients, and identifies anticoagulant dose adequacy as a novel target for proces

106 romycin, and low-molecular-weight heparin at anticoagulant dose.

107 VKOR is also the target of the widely used anticoagulant drug, warfarin.

108 s that combine an antiplatelet agent with an anticoagulant drug.

109 etics associated with efficacy and safety of anticoagulant drugs and justify studies with larger samp

110 ombophlebitis, who were not treated with any anticoagulant during follow-up; neither of these recurre

111 pharmacy benefits, and those who used other anticoagulants during the baseline period were excluded.

112 ning or massive hemorrhages, reversal of the anticoagulant effect is also crucial.

113 Complete reversal of the dabigatran anticoagulant effect occurred within minutes in almost a

114 stop their cellular internalization, but the anticoagulant effect of these agents has been limiting t

115 he RE-VERSE AD study (Reversal of Dabigatran Anticoagulant Effect With Idarucizumab), a prospective,

116 (Reversal of Dabigatran Anticoagulant Effect With Idarucizumab; NCT02104947).

117 ecific cellular responses unrelated to their anticoagulant effect.

118 e of melting temperature and a 2-fold higher anticoagulant effect.

119 Replication cohorts included ACE-IPF (Anticoagulant Effectiveness in Idiopathic Pulmonary Fibr

120 ns regarding the ability to neutralize their anticoagulant effects after intracranial hemorrhage (ICH

121 ression and inflammation, despite comparable anticoagulant effects and infarct sizes.

122 itor (fXai) at doses that induced comparable anticoagulant effects ex vivo and in vivo (tail-bleeding

123 tasis genes to help Komodo dragons evade the anticoagulant effects of their own saliva.

124 es of fIIai and fXai that induced comparable anticoagulant effects resulted in a comparable reduction

125 ated with locally elevated expression of the anticoagulant endothelial receptors thrombomodulin (TM)

126 n complex concentrate contains both pro- and anticoagulant factors that offer an attractive low-volum

127 ith conventional anticoagulation (parenteral anticoagulants followed by vitamin K antagonists), these

128 In 429 patients prescribed an anticoagulant for atrial fibrillation, incidence of stro

129 In 366 patients prescribed an anticoagulant for venous thromboembolism, the incidence

130 are the most commonly prescribed direct oral anticoagulants for adults with atrial fibrillation, but

131 h better benefit-risk profiles and for safer anticoagulants for existing and new indications.

132 2010 has significantly affected selection of anticoagulants for patients with VTE.

133 ociated with fXai, while inhibiting only the anticoagulant function of aPC had no effect.

134 tory antibodies that blocked all or only the anticoagulant function of aPC were used to determine the

135 e type II mAb can specifically inhibit APC's anticoagulant function without compromising its cytoprot

136 Rare mutations in the anticoagulant genes PROC, PROS1 and SERPINC1 result in p

137 ic inhibition of coagulation via direct oral anticoagulants had differential effects on gene expressi

138 l anti-inflammatory drugs (NSAIDs) with oral anticoagulants has been associated with an increased ris

139 ry prevention, the development of novel oral anticoagulants has renewed interest in the use of antico

140 Non-vitamin K antagonist oral anticoagulants have been proven to be safer and equally

141 Direct oral anticoagulants have been recently compared with low-mole

142 aban and five (3%) of 165 receiving standard anticoagulants (hazard ratio [HR] 0.40, 95% CI 0.11-1.41

143 er advance the possibility of bioengineering anticoagulant heparin in cultured cells.

144 Unfractionated heparin, non-anticoagulant heparin, heparin lyases, and lung heparan

145 sion) in a 20-mg equivalent dose or standard anticoagulants (heparin or switched to vitamin K antagon

146 due to systemic inflammation, liver failure, anticoagulants (heparins, phenprocoumon, apixaban), and

147 5%) or were not (0.82%) treated with an oral anticoagulant (HR, 0.93; 95% CI, 0.47-1.83).

148 major and one non-major) receiving standard anticoagulants (HR 1.58, 95% CI 0.51-6.27).

149 d sulfation patterns and show that synthetic anticoagulant HS oligosaccharides limit liver ischemia r

150 in, vitamin K antagonists, and direct-acting anticoagulants improve portal vein repermeation vs obser

151 idence for the net clinical benefit (NCB) of anticoagulant in older adults is sparse.

152 This agent is protein S, which is both an anticoagulant in the blood coagulation cascade and an ac

153 The potential role of new oral anticoagulants in antiphospholipid antibody syndrome (AP

154 cy and safety of rivaroxaban versus standard anticoagulants in children with venous thromboembolism.

155 in peritonitis, and suggest caution against anticoagulants in individuals susceptible to peritoneal

156 DOACs appear to be effective and safe anticoagulants in KTRs with stable renal function.

157 nst the use of non-vitamin K antagonist oral anticoagulants in patients with extremely high (>120 kg)

158 Because studies of direct oral anticoagulants in patients with venous thromboembolism a

159 Randomized clinical trials of direct oral anticoagulants in pediatric VTE are ongoing, with result

160 ry data can be of some help, but not for all anticoagulants in the emergency setting.

161 t is unclear how the use of aspirin and oral anticoagulants in the screening population affects the d

162 ding the use of nonvitamin K antagonist oral anticoagulants in this population.

163 imal timing of non-vitamin K antagonist oral anticoagulant initiation after a recent ischemic stroke

164 ack (82%) and male (82%), with a mean age at anticoagulant initiation of 56 years.

165 ew of randomized controlled trials comparing anticoagulant interventions for SPAF.

166 Use of the direct oral anticoagulants is now supported for many patients with c

167 5 we identified individuals tested for lupus anticoagulant(LA), anti-cardiolipin (aCL), and anti-beta

168 lationships and the identification of potent anticoagulant leads, but also revealed subtleties in the

169 of collagen I and the commonly administered anticoagulant, low-molecular-weight (LMW) heparin, in th

170 Antiplatelet and anticoagulant medications are the cornerstone of therapy

171 estigation on whether the use of direct oral anticoagulants might be of therapeutic value in AD.

172 om the pivotal non-vitamin K antagonist oral anticoagulants (NOAC) trials, thereby raising questions

173 atients with atrial fibrillation, novel oral anticoagulants (NOACs) have been shown to confer equival

174 Nonvitamin K antagonist oral anticoagulants (NOACs) have emerged as the preferred cho

175 Non-vitamin K antagonist oral anticoagulants (NOACs) have proven a favorable risk-bene

176 fectiveness of non-vitamin K antagonist oral anticoagulants (NOACs) is uncertain, as they have not be

177 e-daily dosing non-vitamin K antagonist oral anticoagulants (NOACs), edoxaban and rivaroxaban, have s

178 warfarin, and non-vitamin K antagonist oral anticoagulants (NOACs).

179 The optimal time to start oral anticoagulant (OAC) in patients with ischaemic stroke du

180 anticoagulants (DOACs) introduction on oral anticoagulant (OACs) prescribing rates, and factors asso

181 rial fibrillation who are unsuitable to oral anticoagulants (OACs) require other stroke prevention st

182 nce of pharmacological concentrations of the anticoagulant on the growth, invasion and vascularisatio

183 the efficacy and safety of approaches using anticoagulants on top of antiplatelet therapy.

184 In this study the influence of a set of anticoagulants on tumour formation, invasion and vascula

185 serious comorbidities, 772 (18%) were taking anticoagulant or antiplatelet medication, and alcohol wa

186 mbolism and were randomly assigned to either anticoagulant or antiplatelet therapy versus placebo or

187 Antithrombotic (anticoagulant or antiplatelet) therapy is withheld from

188 thrombotic burden as compared with standard anticoagulants (p=0.012).

189 ntifies an endogenous, vascular bed-specific anticoagulant pathway in microvasculature exposed to low

190 As compared to direct oral anticoagulants, patients with warfarin-associated major

191 ment with vitamin K antagonists, direct oral anticoagulants, platelet inhibitors, and combinations of

192 brillation, double therapy with a novel oral anticoagulant plus single antiplatelet therapy (SAPT) re

193 January 2011 to March 2017, to describe oral anticoagulant prescribing among PWH >= 18 years old and

194 DOAC use increased from 3% of total anticoagulant prescribing in 2011 to 43% in 2016, accoun

195 We identified the first filled oral anticoagulant prescription within 30 days of discharge o

196 n was not associated with higher direct oral anticoagulants prescription rates (DID estimate [95% CI]

197 Among 8315 PWH, there were 236 anticoagulant prescriptions (96 DOAC, 140 warfarin) for

198 16, accounting for 64% of all newly recorded anticoagulant prescriptions by 2016.

199 raphic and clinical characteristics, ARV and anticoagulant prescriptions, and International Classific

200 Anticoagulants, primarily low-molecular-weight heparin a

201 process, revealing a particularly attractive anticoagulant profile of the antibody.

202 by-products varied, each displaying distinct anticoagulant profiles in different assays, and all exhi

203 d 1,2,4-triazol-5-amines were proved to have anticoagulant properties and the ability to affect throm

204 h cerebral cavernous malformations (CCMs) to anticoagulant properties of lesion endothelial cells, su

205 rinogen is an isoform of fibrinogen that has anticoagulant properties.

206 Whether anticoagulant prophylaxis for these patients should be w

207 termine any potential benefit of intensified anticoagulant prophylaxis in COVID-19 patients.

208 In contrast, activated protein C (APC), an anticoagulant protease, activates PAR1 through a distinc

209 ulation factors and extrahepatic endothelial anticoagulant protein S, required for thrombosis prevent

210 ent, but imply the neutralization of natural anticoagulant proteins, have recently emerged.

211 Anticoagulant-refractory thrombotic antiphospholipid syn

212 he factors (genetic and cellular) that cause anticoagulant-refractory thrombotic antiphospholipid syn

213 otal LVT regression, obtained with different anticoagulant regimens, was associated with reduced mort

214 The importance of ZPI-PZ complex anticoagulant regulation of FXa both before and after in

215 Appropriate selection and monitoring of anticoagulants remains a critical element of high-qualit

216 ed with the vascular dose of the direct oral anticoagulant rivaroxaban) for patients with chronic isc

217 The efficacy of direct oral anticoagulants-rivaroxaban, apixaban, dabigatran, and ed

218 ight the public health impact of long-acting anticoagulant rodenticides (LAARs).

219 together, these results suggest an important anticoagulant role for the ZPI-PZ complex in regulating

220 events occurred among subjects on novel oral anticoagulant+SAPT compared with 87 (29.6%) among subjec

221 wenty subjects (3.3%) assigned to novel oral anticoagulant+SAPT, and 15 (5.1%) subjects assigned to V

222 gement of these complications in patients on anticoagulants should follow the same routines as for no

223 Adjunctive treatment regimens, including anticoagulants, statins, and neurohormonal inhibition, w

224 -defined blood-fluid level (rated blinded to anticoagulant status) for identifying concomitant antico

225 BEST PRACTICE ADVICE 12: Direct-acting anticoagulants, such as the factor Xa and thrombin inhib

226 AF with 1) a case-defining outcome and 2) an anticoagulant switch during the 180 days preceding the o

227 ma separator tubes containing five different anticoagulant systems [K2EDTA, Li-Hep, Li-Hep (gel), Na-

228 ng the structure-function relationship of an anticoagulant targeting a zymogen serving as a scaffold

229 Ixolaris is a potent tick salivary anticoagulant that binds coagulation factor Xa (FXa) and

230 This is now best achieved with direct oral anticoagulants that decrease the risk of intracranial bl

231 nd factor XI have emerged as targets for new anticoagulants that may be safer.

232 Vitamin K antagonists are widely used anticoagulants that target vitamin K epoxide reductases

233 quate reversal requires information on which anticoagulant the patient has taken and when the last do

234 h a handful of studies have targeted certain anticoagulants, the full range of anticoagulation factor

235 in stroke pathogenesis, and antiplatelet and anticoagulant therapies are central to stroke prevention

236 However, anticoagulant therapies have been reported to have benef

237 ay inhibition is superior to antiplatelet or anticoagulant therapy alone, (3) compares the results wi

238 (0.57%) or were not (0.55) treated with oral anticoagulant therapy at hospital discharge (HR, 1.03; 9

239 s ulcer bleeding who require antiplatelet or anticoagulant therapy for cardiovascular prophylaxis.

240 s, laboratory and imaging studies, and early anticoagulant therapy for suspected pulmonary arterial t

241 To date, anticoagulant therapy for thrombosis at unusual sites is

242 evidence for combining antiplatelet and oral anticoagulant therapy in patients with coronary and peri

243 Poor adherence to anticoagulant therapy is also an issue for older patient

244 Anticoagulant therapy is often refrained from out of fea

245 Anticoagulant therapy is the most effective strategy to

246 Recent studies have suggested that anticoagulant therapy might dampen the protective role o

247 Anticoagulant therapy was initiated in 675 patients (97%

248 e who were already receiving antiplatelet or anticoagulant therapy were excluded.

249 onary embolism initially and did not receive anticoagulant therapy, 1 patient (0.05%; 95% CI, 0.01 to

250 s); all but one re-BPVT patient responded to anticoagulant therapy.

251 ion as a potential once-monthly subcutaneous anticoagulant therapy.

252 h risk of VTE recurrence and bleeding during anticoagulant therapy.

253 was not diagnosed, patients did not receive anticoagulant therapy.

254 xtracorporeal membrane oxygenation receiving anticoagulant therapy.

255 Ten of the 11 patients received prophylactic anticoagulant therapy; venous thromboembolism was not cl

256 We find that ERG drives transcription of the anticoagulant thrombomodulin (TM), as shown by reporter

257 athway; (4) a local, suppressive role of the anticoagulant thrombomodulin/protein C pathway under flo

258 ave demonstrated that WE thrombin acts as an anticoagulant through activated protein C (APC) generati

259 competing mortality risks when recommending anticoagulants to older adults with AF.

260 rnative vitamin K antagonist is the standard anticoagulant treatment for thrombotic antiphospholipid

261 :harm ratio of non-vitamin K antagonist oral anticoagulant treatment in patients with atrial fibrilla

262 venous thromboembolism (VTE) should receive anticoagulant treatment in the absence of absolute contr

263 Initial anticoagulant treatment is crucial for reducing mortalit

264 of bleeding complications, in whom long-term anticoagulant treatment is likely safe.

265 These included no anticoagulant treatment, and treatment with vitamin K an

266 asymptomatic CVC-related thrombosis require anticoagulant treatment, as the results demonstrate that

267 is an important cause of stroke, and without anticoagulant treatment, patients with AFib have approxi

268 enous thromboembolism is significant despite anticoagulant treatment.

269 and 2.28 (95% CI, 1.67-3.12) for direct oral anticoagulant triple therapy.

270 ta on the factor XII- and factor XI-directed anticoagulants under development, describes novel therap

271 5% CI:1.24-17.44, p = 0.02) and a history of anticoagulant use (OR:37.52, 95% CI:6.49-216.8, p < 0.00

272 factors including multiple polypectomies and anticoagulant use are no need to performing prophylactic

273 fference in CSH observed between direct oral anticoagulant use compared with continued warfarin (odds

274 l cases to illustrate common challenges with anticoagulant use in older patients and discuss our appr

275 Herein, we present 4 cases of anticoagulant use in the obese to illustrate the common

276 oagulant status) for identifying concomitant anticoagulant use.

277 Therefore, the anticoagulant used in plasma separator tubes, storage-ti

278 ossover population was identified among oral anticoagulant users during 2011-2018 (n = 123,217) as pa

279 of CSH in patients treated with direct oral anticoagulant versus continued warfarin.

280 Direct oral anticoagulant versus low-molecular-weight heparin for tr

281 pitalizations among subjects on a novel oral anticoagulant versus VKA based double therapy.

282 is reviewed here for the different types of anticoagulants: vitamin K antagonists, heparins, fondapa

283 or superior to that of vitamin K antagonist anticoagulants (VKAs) in the general population.

284 in 1.1% of patients treated with direct oral anticoagulants vs 1.8% treated with warfarin.

285 the Randomized Controlled Trial of New Oral Anticoagulants vs. Warfarin for post Cardiac Surgery Atr

286 tients on warfarin versus direct acting oral anticoagulant were equally likely to restart OAC (58.0%

287 Anticoagulants were a factor in 3 retrobulbar hemorrhage

288 PWH prescribed anticoagulants were predominantly Black (82%) and male (

289 Diuretics and anticoagulants were underutilized in women.

290 The advent of non-vitamin K antagonist oral anticoagulants, which attenuate fibrin formation by sele

291 or XIa (FXIa) inhibitors are promising novel anticoagulants, which show excellent efficacy in preclin

292 Warfarin is a widely used anticoagulant with a narrow therapeutic index and large

293 CI, 1.13-1.44) for therapy of a direct oral anticoagulant with an antiplatelet drug, 3.73 (95% CI, 3

294 Dabigatran etexilate is a direct oral anticoagulant with potential to overcome the limitations

295 Acenocoumarol is an oral anticoagulant with significant interindividual dose vari

296 ed laboratory data, 34 569 new users of oral anticoagulants with atrial fibrillation and estimated gl

297 New users of anticoagulants with nonvalvular atrial fibrillation were

298 mised controlled trials comparing parenteral anticoagulants with placebo or standard care in ambulato

299 usses the evidence for the use of novel oral anticoagulants, with an emphasis on patient selection, c

300 osclerosis) with incident AF who were not on anticoagulants within 1 year of AF diagnosis.