ライフサイエンスコーパス: anticoagulants

1 ts) or by a direct one (e.g., the novel oral anticoagulants).

2 or non-accelerated alteplase plus parenteral anticoagulants).

3 sk of gastrointestinal bleeding while taking anticoagulants.

4 agent to reverse the effects of several new anticoagulants.

5 in K antagonists or non-vitamin K antagonist anticoagulants.

6 tting test is used in the diagnosis of lupus anticoagulants.

7 after exposure to various concentrations of anticoagulants.

8 recurrence of VTE and bleeding while taking anticoagulants.

9 er cardiac medication, and switching between anticoagulants.

10 nists, hydralazine/isosorbide dinitrate, and anticoagulants.

11 but also ensure their perfusion by acting as anticoagulants.

12 the high-throughput screening for potential anticoagulants.

13 riod when SVT was not treated routinely with anticoagulants.

14 can be achieved may benefit from the use of anticoagulants.

15 She was not taking anticoagulants.

16 o support a novel role for acylcarnitines as anticoagulants.

17 ers received therapeutic doses of nonheparin anticoagulants.

18 patients who are currently not treated with anticoagulants.

19 brinogen-deficient mice and in WT mice given anticoagulants.

20 o inherent bleeding diatheses and prescribed anticoagulants.

21 when patients are transitioned between oral anticoagulants.

22 nized as a prime target for developing safer anticoagulants.

23 as an immediate precursor of these synthetic anticoagulants.

24 TE prevention using indirect or novel direct anticoagulants.

25 presence or absence of various perioperative anticoagulants.

26 rs promotes an ongoing effort to develop new anticoagulants.

27 cluding antiplatelet agents and the new oral anticoagulants.

28 HIT requires treatment with alternative anticoagulants.

29 el mode of action compared with conventional anticoagulants.

30 g, which may be prevented by the addition of anticoagulants.

31 both rivaroxaban and warfarin, or other oral anticoagulants.

32 ging guided the initiation and withdrawal of anticoagulants.

33 of use and when used concomitantly with oral anticoagulants.

34 ngs support the continued use of direct oral anticoagulants.

35 ts with nonvalvular AF not treated with oral anticoagulants.

36 the proportion of patients treated with oral anticoagulants.

37 g between groups that did vs did not receive anticoagulants (11% for both groups).

38 vitamin K antagonists and direct-acting oral anticoagulants; 4) evaluate whether to bridge with a par

39 nalization than patients who did not receive anticoagulants (71% vs 42%, respectively; P < .0001).

40 Parenteral anticoagulants administered in doses greater than those

41 New oral anticoagulants also significantly reduced all-cause mort

42 s the risk and benefit of non-vitamin K oral anticoagulants among patients at high risk for stroke wi

43 fic comparative effectiveness of direct oral anticoagulants among patients with nonvalvular atrial fi

44 general interest to the clinical community: anticoagulants, analgesics and buffers.

45 ed safely in high-risk patients, taking both anticoagulants and antiplatelet drugs when topical anest

46 e aware of the limitations of the novel oral anticoagulants and avoid the use of these agents because

47 ns of ED visits for adverse drug events from anticoagulants and diabetes agents have increased, where

48 curred in 3 of 187 patients assigned to oral anticoagulants and in 7 of 174 patients assigned to anti

49 Heart Association guidelines suggest holding anticoagulants and initiating antiplatelet therapy among

50 se in metastases while a number of different anticoagulants and platelet depletion attenuated this ef

51 when considering the use of antithrombotics, anticoagulants and statins.

52 The identification of novel natural anticoagulants and the understanding of their mechanism

53 treatment with aspirin, clopidogrel, or oral anticoagulants and their combinations, as well as ongoin

54 associated with previous treatment with oral anticoagulants and/or antiplatelet agents and with highe

55 completely suppressed by the application of anticoagulants and/or improvement of surface chemistry.

56 e last 25 years, despite the introduction of anticoagulants, and are projected to treble again by 205

57 Two patients were treated with oral anticoagulants, and both developed life-threatening intr

58 olysis), advances in antiplatelet agents and anticoagulants, and greater use of secondary prevention

59 Anticoagulants, antibiotics, and diabetes agents were im

60 The most common drug classes implicated were anticoagulants, antibiotics, diabetes agents, and opioid

61 r burden of comorbidity and increased use of anticoagulants, antiplatelets and aspirin to treat cardi

62 Mice deficient in the anticoagulants antithrombin (Serpinc1) or protein C (Pro

63 combination], eptifibatide, or abciximab) or anticoagulants (antithrombin dabigatran etexilate or ant

64 The target-specific oral anticoagulants are a class of agents that inhibit factor

65 New oral anticoagulants are effective for thromboprophylaxis afte

66 Non-vitamin K antagonist oral anticoagulants are expensive and contraindicated for sev

67 Direct oral anticoagulants are increasingly used for a wide range of

68 sal agents for non-vitamin K antagonist oral anticoagulants are lacking.

69 Because emboli consist mainly of thrombus, anticoagulants are likely to reduce recurrent brain isch

70 When oral anticoagulants are managed well, the risk of recurrence

71 Direct oral anticoagulants are non-inferior to conventional anticoag

72 Novel anticoagulants are now available for use in adults.

73 Novel oral anticoagulants are uniformly associated with an overall

74 ) is treated with the alternative nonheparin anticoagulants argatroban, lepirudin, or danaparoid.

75 a more comprehensive picture of the new oral anticoagulants as a therapeutic option to reduce the ris

76 Experience with new oral anticoagulants as acute, long-term, and extended therapy

77 irudin, or one of the new direct-acting oral anticoagulants as appropriate.

78 erated infusion of alteplase with parenteral anticoagulants as background therapy, streptokinase and

79 tenecteplase, and reteplase with parenteral anticoagulants as background therapy.

80 The decision to stop anticoagulants at 3 months or to treat indefinitely is d

81 The decision to stop anticoagulants at 3 months or to treat indefinitely is m

82 illation patients who started treatment with anticoagulants at the Leiden Anticoagulation Clinic in t

83 lenge to treat patients with cirrhosis using anticoagulants, because of the perception that the coexi

84 Oral anticoagulants block the coagulation cascade either by a

85 Oral anticoagulants (both vitamin K antagonists [VKAs] and no

86 n K antagonists were the only available oral anticoagulants, but with numerous limitations that promp

87 tudies are needed before the target-specific anticoagulants can be recommended for patients with canc

88 Four new oral anticoagulants compare favourably with warfarin for stro

89 r gastrointestinal bleeding with direct oral anticoagulants compared with warfarin or low-molecular-w

90 r gastrointestinal bleeding with direct oral anticoagulants compared with warfarin or low-molecular-w

91 risk of intraocular bleeding with novel oral anticoagulants compared with warfarin.

92 nts and associated risk ratio for novel oral anticoagulants compared with warfarin.

93 her the use of non-vitamin K antagonist oral anticoagulants could lower the threshold for treatment d

94 The new oral anticoagulants dabigatran and rivaroxaban have shorter e

95 With the introduction of direct oral anticoagulants (dabigatran, rivaroxaban, apixaban, and e

96 eness of non-vitamin K antagonist (VKA) oral anticoagulants, dabigatran or rivaroxaban, were compared

97 Oral anticoagulants decrease ischemic stroke rates in patient

98 Because these anticoagulants decrease thrombin generation, we hypothes

99 r adults (aged >/=65 years), 3 drug classes (anticoagulants, diabetes agents, and opioid analgesics)

100 r gastrointestinal bleeding with direct oral anticoagulants did not differ from that with warfarin or

101 risk of intraocular bleeding with novel oral anticoagulants differs compared with warfarin.

102 ocedures, ischaemic preconditioning, and new anticoagulants (direct thrombin or Xa inhibitors).

103 slational strategy to deliver locally active anticoagulants directly within grafts and decrease micro

104 Although direct oral anticoagulants do not need laboratory testing for dose a

105 s of death in patients receiving direct oral anticoagulants (DOAC) or warfarin for prevention of stro

106 alidation for the development of direct oral anticoagulants (DOAC), and currently such inhibitors of

107 Direct oral anticoagulants (DOACs) are attractive options for treatm

108 Evidence regarding the use of direct oral anticoagulants (DOACs) in the elderly, particularly blee

109 The availability of direct oral anticoagulants (DOACs) may improve overall OAC rates in

110 The direct oral anticoagulants (DOACs) represent a major advance in oral

111 The recently FDA-approved direct oral anticoagulants (DOACs), such as dabigatran, rivaroxaban,

112 Despite the introduction of direct oral anticoagulants (DOACs), the search for more effective an

113 complications, including discontinuation of anticoagulants, dose reduction, or low-molecular-weight

114 s was less frequent among patients receiving anticoagulants (eight [4%] of 224) than among those rece

115 considerable risk of bleeding and, with some anticoagulants, fetotoxicity.

116 Hospital utilization rates of parenteral anticoagulants for AF during sepsis varied (median, 33%;

117 The rapid global adoption of direct oral anticoagulants for management of VTE in patients with ca

118 f stroke risk reduction with the use of oral anticoagulants for patients who have atrial fibrillation

119 tion in arterial thrombosis and aspirin with anticoagulants for primary and secondary prevention of v

120 Randomised trials testing direct-acting oral anticoagulants for secondary prevention of embolic strok

121 New oral anticoagulants for stroke prevention in atrial fibrillat

122 ht to identify any differences in the use of anticoagulants for stroke prevention in women and men.

123 a significant difference favoring novel oral anticoagulants for systemic embolism (OR, 0.84; 95% CI,

124 latest evidence and development of new oral anticoagulants for the prevention of ischaemic stroke, a

125 pite the availability of multiple nonheparin anticoagulants for the treatment of heparin-induced thro

126 icoagulants are non-inferior to conventional anticoagulants for the treatment of venous thromboemboli

127 ate the safety and efficacy of the different anticoagulants for treating HIT.

128 K antagonists will continue to be important anticoagulants for years to come.

129 4-Hydroxycoumarin (4HC) type anticoagulants (for example, warfarin) are known to have

130 New oral anticoagulants, for example, offer cost-effective risk r

131 ng and inhibition by this family of salivary anticoagulants from anopheline mosquitoes.

132 the proportion of patients treated with oral anticoagulants from baseline assessment to evaluation at

133 0-24 days); 29 (64%) of the 45 not receiving anticoagulants fulfilled criteria for disseminated intra

134 The availability of direct oral anticoagulants further complicates decision making and g

135 Development of new oral anticoagulants further simplifies acute-phase treatment

136 New oral anticoagulants had a favourable risk-benefit profile, wi

137 lants vs 33% of patients who did not receive anticoagulants had complete PVT recanalization (P = .002

138 ucizumab administration in a patient in whom anticoagulants had not been reinitiated.

139 be useful, and restoration of physiological anticoagulants has been suggested, but has not been prov

140 Although oral anticoagulants have been found effective in reducing str

141 uces thromboembolic complications; the newer anticoagulants have eased management for both the patien

142 New oral anticoagulants have not been compared with warfarin, asp

143 Currently available anticoagulants have some drawbacks including their non-s

144 low identity to the well-characterized 3FTx anticoagulants-hemextin and naniproin.

145 210A defect, and deficiencies of the natural anticoagulants (ie, antithrombin, protein C, and protein

146 Aptamers can function as anticoagulants if they are directed against enzymes of t

147 e dinitrate in 8.6% (93.1% of eligible), and anticoagulants in 18.0% (58.0% of eligible).

148 Guideline recommendations for oral anticoagulants in AF are based on the CHA2DS2-VASc strok

149 point score threshold for recommending oral anticoagulants in AF.

150 d to assess the relative benefit of new oral anticoagulants in key subgroups, and the effects on impo

151 milar variation in therapeutic windows among anticoagulants in our assay.

152 e-coating technology could reduce the use of anticoagulants in patients and help to prevent thromboti

153 osis (RVT) to assess the optimal duration of anticoagulants in patients with cancer who have deep vei

154 eater absolute benefit of non-vitamin K oral anticoagulants in patients with type 2 diabetes.

155 Guidelines for the use of anticoagulants in pediatrics are largely extrapolated fr

156 ical trials of non-vitamin K antagonist oral anticoagulants in prevention of arterial thromboembolism

157 Xa, might be more suitable than conventional anticoagulants in the management of cancer-associated ve

158 disorders, and discuss strategies for using anticoagulants in this population using cases to illustr

159 tion of stroke risk could prevent overuse of anticoagulants in very low stroke risk patients with AF.

160 acerebral hemorrhage (ICH) related to direct anticoagulants including dabigatran (OAC-ICH).

161 nt of the effects of clotting-activators and anticoagulants (including non-pharmacological methods) a

162 s prasugrel and ticagrelor, and, in terms of anticoagulants, inhibitors that directly target factor I

163 7.7; 95% CI, 56.9-58.4) for those exposed to anticoagulants (IRR, 1.55; 95% CI, 1.52-1.59), and 110.7

164 ether or not to bridge with heparin or other anticoagulants is a common clinical dilemma.

165 nge in designing and administering effective anticoagulants is achieving the proper therapeutic windo

166 the acute setting, the decision to withhold anticoagulants is based on an individual patient's risk

167 uggest HMP graft pretreatment with cytotopic anticoagulants is feasible and ameliorates perfusion def

168 t that HMP graft pretreatment with cytotopic anticoagulants is feasible and ameliorates perfusion def

169 Use of novel oral anticoagulants is not currently recommended for patients

170 Use of novel oral anticoagulants is not currently recommended for patients

171 Novel oral anticoagulants is superior to warfarin for stroke preven

172 Despite rapid clinical adoption of novel anticoagulants, it is unknown whether outcomes differ am

173 ng and dose adjustment, target-specific oral anticoagulants like dabigatran do not.

174 ative period, in which the use of novel oral anticoagulants may be superior.

175 e raises the question of whether alternative anticoagulants may have a therapeutic role.

176 New anticoagulants may improve health outcomes in patients w

177 Concomitant use of anticoagulants may increase the risk substantially (RR,

178 nificant adverse events, such as hemorrhage (anticoagulants), moderate to severe allergic reactions (

179 ts linked to the introduction of direct oral anticoagulants, more than one third of atrial fibrillati

180 A new generation of oral anticoagulants (nOAC), which includes thrombin and facto

181 tory of acute non-vitamin K antagonists oral anticoagulants (NOAC)-associated intracerebral haemorrha

182 Novel oral anticoagulants (NOACs) (rivaroxaban, dabigatran, apixaba

183 The non-vitamin K antagonist oral anticoagulants (NOACs) apixaban, dabigatran, edoxaban, a

184 Non-vitamin K oral anticoagulants (NOACs) are commonly prescribed with othe

185 Non-vitamin K oral anticoagulants (NOACs) are now widely used as alternativ

186 ines recommend non-vitamin K antagonist oral anticoagulants (NOACs) as the first-choice therapy in pa

187 Although non-vitamin K antagonist oral anticoagulants (NOACs) do not require frequent laborator

188 Non-vitamin K oral anticoagulants (NOACs) do not require routine laboratory

189 llenged by the non-vitamin K antagonist oral anticoagulants (NOACs) for stroke prevention in atrial f

190 These novel non-vitamin K antagonist oral anticoagulants (NOACs) have been shown to be at least as

191 Novel oral anticoagulants (NOACs) have been shown to be at least as

192 ppendage closure (LAAC) and nonwarfarin oral anticoagulants (NOACs) have emerged as safe and effectiv

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

194 e reduction of non-vitamin K antagonist oral anticoagulants (NOACs) is indicated in patients with atr

195 r aortic valves and the effect of novel oral anticoagulants (NOACs) on the subclinical leaflet thromb

196 were receiving non-vitamin K antagonist oral anticoagulants (NOACs) preceding the stroke.

197 are now 4 new non-vitamin K antagonist oral anticoagulants (NOACs) that are attractive alternatives

198 rials comparing nonvitamin K antagonist oral anticoagulants (NOACs) vs warfarin largely focused on re

199 ials comparing non-vitamin K antagonist oral anticoagulants (NOACs) with warfarin excluded patients w

200 In noninferiority trials, novel oral anticoagulants (NOACs), also known as non-vitamin K oral

201 New oral anticoagulants (NOACs), including direct thrombin inhibi

202 The new oral anticoagulants (NOACs), which include dabigatran, rivaro

203 nial hemorrhage (ICH) with use of novel oral anticoagulants (NOACs).

204 17.2% received non-vitamin K antagonist oral anticoagulants (NOACs).

205 itamin K antagonists [VKAs] and non-VKA oral anticoagulants [NOACs]) have been demonstrated to be eff

206 .88; 2.17% [23/1061] vs 3.89% [41/1054] with anticoagulants; number needed to treat [NNT] = 59) and g

207 Overall, 1960 patients (73.6%) received oral anticoagulants (OAC) and 762 (28.6%) received antiplatel

208 Oral anticoagulants (OAC) reduce stroke risk but increase the

209 Although use of oral anticoagulants (OACs) is increasing, there is a substant

210 the CHA2DS2-VASc system for initiating oral anticoagulants (OACs) might be lower in Taiwanese AF pat

211 ow-up period among patients not treated with anticoagulants on the basis of a negative age-adjusted D

212 However, the influence of several anticoagulants on the prothrombin time limits its diagno

213 %) using antiplatelets only, 77 (6.6%) using anticoagulants only, and 17 (1.5%) using both.

214 She was not taking any anticoagulants or immunosuppressive medication.

215 Patients with contraindications to anticoagulants or to PFO closure were randomly assigned

216 caution when initiating either non-VKA oral anticoagulants or VKA in patients with nonvalvular atria

217 tion who were randomised to receive new oral anticoagulants or warfarin, and trials in which both eff

218 titious ingestion of warfarin, warfarin-like anticoagulants, or potent rodenticides ("superwarfarins"

219 ystemic embolism was favored with novel oral anticoagulants over warfarin (OR, 0.77; 95% CI, 0.68-0.8

220 ted in 20 (91%) of 22 patients not receiving anticoagulants (p<0.0001).

221 hospital-referred patients for antiplatelets/anticoagulants (p<0.05) and lipid-lowering agents (p<0.0

222 88 [1.24-2.86] for reteplase plus parenteral anticoagulants plus glycoprotein inhibitors).

223 1.10-1.98] for tenecteplase plus parenteral anticoagulants plus glycoprotein inhibitors; RR 1.88 [1.

224 The latter strategy could reduce the use of anticoagulants, potentially decreasing bleeding events.

225 As a result, although all the novel oral anticoagulants produce greater quality-adjusted life exp

226 corticosteroids, aldosterone antagonists, or anticoagulants produces significant excess risk of UGIB.

227 atelet therapy studies and investigations of anticoagulants provide important insights into the balan

228 These results suggest that novel oral anticoagulants reduce the risk of intraocular bleeding b

229 xposure to a PAR1 agonist in the presence of anticoagulants rescued the angiogenic potential.

230 ic, comparative effectiveness of direct oral anticoagulants (rivaroxaban and dabigatran), compared to

231 celerated infusion alteplase plus parenteral anticoagulants (RR 1.47 [95% CI 1.10-1.98] for tenectepl

232 1.05-1.24] for streptokinase plus parenteral anticoagulants; RR 1.26 [1.10-1.45] for non-accelerated

233 New oral anticoagulants significantly reduced stroke or systemic

234 t to rivaroxaban therapy and are taking both anticoagulants simultaneously.

235 New oral anticoagulants, statins and concomitant therapy with war

236 first to include data for all four new oral anticoagulants studied in the pivotal phase 3 clinical t

237 Binding was not affected by anticoagulants such as aspirin or heparin.

238 sm prophylaxis, more recently the novel oral anticoagulants such as dabigatran (initial dose of 110 m

239 New oral anticoagulants (such as dabigatran, rivaroxaban, apixaba

240 D20 monoclonal antibodies and new-generation anticoagulants (such as direct thrombin and anti-Xa inhi

241 relative efficacy and safety of direct oral anticoagulants, such as edoxaban, compared with vitamin

242 a distinct mechanism when compared to other anticoagulants targeting ETC, with its selective prefere

243 s that prompted the introduction of new oral anticoagulants targeting the single coagulation enzymes

244 ctor Xa (FXa) or thrombin are promising oral anticoagulants that are becoming widely adopted.

245 This concept may lead to a new class of anticoagulants that are completely devoid of bleeding.

246 Dabigatran and rivaroxaban are new oral anticoagulants that are eliminated through the kidneys.

247 and the recently developed orally available anticoagulants that directly target factor Xa or thrombi

248 factor XII (FXII) and FXI as targets for new anticoagulants that may be even safer than the DOACs.

249 and, second, whether antiplatelet agents and anticoagulants that perturb thrombus structure affect th

250 Therefore novel anticoagulants that target specific steps in the coagula

251 e small trial of heparin compared with other anticoagulants, the risk of major hemorrhage was signifi

252 In trials comparing heparin to other anticoagulants, the risk ratio for death was 1.30 (95% C

253 an event occurs and to improve management of anticoagulants thereby avoiding further recurrences.

254 17% normal respectively; further decline in anticoagulants; thrombocytopenia; neutrophilia and endot

255 to measure the Hill coefficient of available anticoagulants to gain insight into their therapeutic wi

256 oth and the potential for non-vitamin K oral anticoagulants to have greater benefits than risks over

257 ssionals, who are hesitant to prescribe oral anticoagulants to older adults with atrial fibrillation.

258 y that enables therapeutic agents, including anticoagulants, to bind to cell surfaces and protect the

259 Target-specific oral anticoagulants (TSOACs) have been developed and found to

260 Target-specific oral anticoagulants (TSOACs) that directly inhibit thrombin (

261 Target-specific oral anticoagulants (TSOAs) have recently emerged as alternat

262 y higher proportion of patients treated with anticoagulants underwent PVT recanalization than patient

263 lycoprotein IIb/IIIa receptor blockers), and anticoagulants (unfractionated and low-molecular-weight

264 of results justified the use of alternative anticoagulants until HIT could be excluded.

265 ime (PTT), and lower levels of both pro- and anticoagulants up to 24 hours.

266 dicated, and the relative role of novel oral anticoagulants versus the device which has not been test

267 Although the use of oral anticoagulants (vitamin K antagonists) has been abandone

268 The main outcome measure was the use of anticoagulants (vitamin K antagonists, factor Xa inhibit

269 217 patients), 53% of patients treated with anticoagulants vs 33% of patients who did not receive an

270 VT progressed in 9% of patients treated with anticoagulants vs 33% of patients who did not receive th

271 ly lower proportion of patients who received anticoagulants vs those who did not (P = .04).

272 .9%) of ED visits for adverse drug events; 4 anticoagulants (warfarin, rivaroxaban, dabigatran, and e

273 f gastrointestinal bleeding with direct oral anticoagulants, warfarin, and low-molecular-weight hepar

274 coagulants was 2.4, of COX-2 inhibitors with anticoagulants was 0.1, and of low-dose aspirin with ant

275 ulants was 0.1, and of low-dose aspirin with anticoagulants was 1.9.

276 person-years) for patients treated with oral anticoagulants was 13.6, in comparison with 27.3 for non

277 ess risk of concomitant use of nsNSAIDs with anticoagulants was 2.4, of COX-2 inhibitors with anticoa

278 100 person-years) patients treated with oral anticoagulants was 8.0, in comparison with 8.6 for nontr

279 se of low-molecular-weight-heparin and other anticoagulants was assessed.

280 Randomization to novel oral anticoagulants was associated with a 22% relative reduct

281 The relative efficacy and safety of new oral anticoagulants was consistent across a wide range of pat

282 In contrast, the use of anticoagulants was not associated with a survival benefi

283 The groups were novel oral anticoagulants, Watchman left atrial appendage occlusion

284 me preclinical and clinical studies, inhaled anticoagulants were associated with a favorable effect o

285 tients presenting a contraindication to oral anticoagulants were excluded.

286 eatment with >/=1 dose of the aforementioned anticoagulants were included.

287 isks of intraocular bleeding with novel oral anticoagulants were seen in subgroup analyses, with no s

288 Bridging anticoagulants were used in 24% (n=665), predominantly l

289 Anticoagulants were used less often in patients with par

290 ts (NOACs), also known as non-vitamin K oral anticoagulants, were at least noninferior to standard ca

291 ve reduction in major bleeding with new oral anticoagulants when the centre-based time in therapeutic

292 warfarin 24 [67%]; NOACs 12 [33%]) receiving anticoagulants, whereas it persisted in 20 (91%) of 22 p

293 VIIa complex (TF-FVIIa) are promising novel anticoagulants which show excellent efficacy and minimal

294 f 13611 patients (35.3%) received parenteral anticoagulants, while 24971 (64.7%) did not.

295 Anticoagulants will probably always increase bleeding ri

296 ous thrombosis has prompted trials comparing anticoagulants with aspirin for secondary prevention in

297 to open up a major route to allosteric FXIa anticoagulants with clinical relevance.

298 s, compared with patients who do not receive anticoagulants, with no excess of major and minor bleedi

299 patients require 3 months of treatment with anticoagulants, with options including LMWH, vitamin K a

300 Ia (FXIa) is a novel paradigm for developing anticoagulants without major bleeding consequences.