ライフサイエンスコーパス: anticoagulant

1 or non-accelerated alteplase plus parenteral anticoagulants).

2 omized clinical trials, especially regarding anticoagulant.

3 ts with nonvalvular AF not treated with oral anticoagulants.

4 the proportion of patients treated with oral anticoagulants.

5 sk of gastrointestinal bleeding while taking anticoagulants.

6 agent to reverse the effects of several new anticoagulants.

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

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

9 after exposure to various concentrations of anticoagulants.

10 recurrence of VTE and bleeding while taking anticoagulants.

11 both rivaroxaban and warfarin, or other oral anticoagulants.

12 ging guided the initiation and withdrawal of anticoagulants.

13 of use and when used concomitantly with oral anticoagulants.

14 ngs support the continued use of direct oral anticoagulants.

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

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

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

18 ss the Xase complex is to inhibit endogenous anticoagulant activities.

19 ted protein C (APC) is a blood protease with anticoagulant activity and cell-signaling activities med

20 ping new therapeutics that safely neutralize anticoagulant activity and inhibit activators of the int

21 ound 16, had a FXIa Ki = 0.16 nM with potent anticoagulant activity in an in vitro clotting assay (aP

22 A), which is nontoxic and can neutralize the anticoagulant activity of heparins and the prothrombotic

23 analyses indicate that plasma drug levels or anticoagulant activity of the NOACs predict stroke and b

24 complexes; nor did antibodies that block APC anticoagulant activity suppress the prophylactic anti-in

25 es in mice reveal that UHRA reverses heparin anticoagulant activity without the lung injury seen with

26 and/or its other mutants with reduced (>90%) anticoagulant activity, engineered to reduce APC-associa

27 n, bovine intestinal heparin (BIH) has a low anticoagulant activity.

28 uch as the risk of bleeding due to heparin's anticoagulant activity.

29 Parenteral anticoagulants administered in doses greater than those

30 th nonvalvular AF who started taking an oral anticoagulant agent between October 1, 2010 and April 30

31 This study aimed to compare 4 oral anticoagulant agents (apixaban, dabigatran, rivaroxaban,

32 Nonvitamin K-dependent oral anticoagulant agents (NOACs) are currently recommended f

33 arboxamide derivatives) and 3 antithrombotic/anticoagulant agents (platelet aggregation inhibitors ex

34 New oral anticoagulant agents are effective and safe alternatives

35 linical research is required before new oral anticoagulant agents can be considered standard of care

36 ixaban, and edoxaban), and a number of other anticoagulant agents in common clinical use, as well.

37 The role of treatment with direct oral anticoagulant agents is unclear.

38 Development of anticoagulant agents that are homogeneous, efficacious,

39 The recent availability of oral anticoagulant agents that can be administered in fixed d

40 omparing the 2 non-vitamin K antagonist oral anticoagulant agents with each other, no differences wer

41 tegies with new drugs, both antiplatelet and anticoagulant agents, and new coronary stents will conti

42 mon among patients with AF treated with oral anticoagulant agents.

43 d in the weighted population to compare oral anticoagulant agents.

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

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

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

47 I, 112.8-121.8) for those exposed to both an anticoagulant and antiplatelet agent (IRR, 10.48; 95% CI

48 ut remained significant after adjustment for anticoagulant and antiplatelet use in patients >/=66 yea

49 The incremental cost, including cost of anticoagulant and monitoring, of achieving these benefit

50 ptive coagulopathy and preserved endothelial anticoagulant and vascular barrier functions.

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

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

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

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

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

56 Improving prescription of lipid-lowering, anticoagulant, and antihypertensive drugs is important t

57 endothelium results in an anti-inflammatory, anticoagulant, and antithrombotic effect that contribute

58 a vitamin K antagonist (VKA), a direct oral anticoagulant, and combined antithrombotic drug treatmen

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

60 ulation, activated protein C functions as an anticoagulant, anti-inflammatory and regenerative factor

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

62 rinogen, lipoprotein(a), homocysteine, lupus anticoagulant, anticardiolipin antibodies and genotyping

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

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

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

66 Direct oral anticoagulants are non-inferior to conventional anticoag

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

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

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

70 FXa(I16L) also reduces the anticoagulant-associated bleeding in vivo that is induce

71 Anticoagulant-associated heavy menstrual bleeding (HMB)

72 Non-vitamin K antagonist oral anticoagulant-associated ICH has a high mortality and an

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

74 antioxidant properties, but may also display anticoagulant attributes.

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

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

77 OR, 1.87 [95% CI, 1.57-2.24]), a direct oral anticoagulant (cases: 1.0%, controls: 0.6%; adjusted OR,

78 er, we think that the growing number of oral anticoagulant choices creates an urgent need for expandi

79 These results demonstrate a new anticoagulant (cofactor) function of FV that targets the

80 ntestinal bleeding with use of a direct oral anticoagulant compared with warfarin or low-molecular-we

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

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

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

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

85 C) is a multifunctional serine protease with anticoagulant, cytoprotective, and anti-inflammatory act

86 enous thromboembolism, compared a novel oral anticoagulant (dabigatran, rivaroxaban, apixaban, or edo

87 Oral anticoagulants decrease ischemic stroke rates in patient

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

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

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

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

92 BACKGROUND & AIMS: Direct oral anticoagulant (DOAC) agents increase the risk of gastroi

93 Direct oral anticoagulant (DOAC) agents increase the risk of gastroi

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

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

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

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

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

99 spitalization or surgery, with adjustment of anticoagulant dosing in patients with severe obesity.

100 contamination of the widely used lifesaving anticoagulant drug heparin in 2007 has drawn renewed att

101 Associations between use of antiplatelet or anticoagulant drugs and hemorrhage were evaluated among

102 Non-vitamin K antagonist oral anticoagulant drugs have recently expanded therapeutic o

103 vailability of non-vitamin K antagonist oral anticoagulant drugs may lead to better prevention of str

104 olic stroke of undetermined source, and oral anticoagulant drugs may prove to reduce stroke risk from

105 duronic acid being an essential component of anticoagulant drugs with diastereoselectivity superior t

106 drugs, 52% (1,647/3,194) were not prescribed anticoagulant drugs, and 25% (1,740/7,008) were not pres

107 28 had lipid-lowering drugs indicated, 3,194 anticoagulant drugs, and 7,008 antihypertensive drugs.

108 Obesity alters the pharmacokinetics of some anticoagulant drugs, and IBD patients present the added

109 08 participants (52.2%) used antiplatelet or anticoagulant drugs, including 514 participants (44.1%)

110 287 692 patients exposed to 230 090 years of anticoagulant drugs.

111 were interviewed for use of antiplatelet or anticoagulant drugs.

112 d in the development of new antiplatelet and anticoagulant drugs.

113 us idarucizumab would be able to reverse the anticoagulant effect of dabigatran in patients who had u

114 t was the maximum percentage reversal of the anticoagulant effect of dabigatran within 4 hours after

115 ibody fragment, was developed to reverse the anticoagulant effect of dabigatran.

116 ab rapidly, durably, and safely reversed the anticoagulant effect of dabigatran.

117 = 15) or solution with inactive-TLN (absent anticoagulant effect, n = 4).

118 The ability to reverse their anticoagulant effects is important when serious bleeding

119 The ability of FXa(I16L) to reverse the anticoagulant effects of FXa inhibitor depends, at least

120 carotid endarterectomy (CEA) to reverse the anticoagulant effects of heparin and to limit the risk f

121 y restores hemostasis in the presence of the anticoagulant effects of these inhibitors.

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

123 ubtilis, can shift the delicate procoagulant-anticoagulant equilibrium toward thrombosis.

124 soesophageal echocardiography [TEE] or not), anticoagulant experience, selected edoxaban dose, and re

125 atelet numbers and function, procoagulant or anticoagulant factors, fibrinolysis, and interactions be

126 hould help clinicians choose the appropriate anticoagulant for their patients.

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

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

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

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

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

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

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

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

135 0-24 days); 29 (64%) of the 45 not receiving anticoagulants fulfilled criteria for disseminated intra

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

137 gh ischemic stroke risk was similar in the 3 anticoagulant groups, rivaroxaban use significantly incr

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

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

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

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

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

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

144 point score threshold for recommending oral anticoagulants in AF.

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

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

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

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

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

150 The frequency of anticoagulant interruption in preparation for a procedur

151 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

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

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

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

155 s (VKA) have long been the default drugs for anticoagulant management in venous thrombosis.

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

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

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

159 ostasis by expressing and releasing pro- and anticoagulant mediators into the circulation.

160 his review examines the historical basis for anticoagulant monitoring, discusses methods to measure a

161 aban are administered in fixed doses without anticoagulant monitoring.

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

163 to the use of non-vitamin K antagonist oral anticoagulant (NOAC) agents.

164 candidates for non-vitamin K antagonist oral anticoagulant (NOAC) therapy.

165 warfarin or a non-vitamin K antagonist oral anticoagulant (NOAC), is indicated for stroke prevention

166 re receiving a non-vitamin K antagonist oral anticoagulant (NOAC).

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

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

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

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

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

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

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

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

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

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

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

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

179 17.2% received non-vitamin K antagonist oral anticoagulants (NOACs).

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

181 , higher CHADS2/CHA2DS2-VASc score, and oral anticoagulant (OAC) use.

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

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

184 tients who received at least one dose of the anticoagulant of interest) comprised 2619 patients in th

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

186 %) using antiplatelets only, 77 (6.6%) using anticoagulants only, and 17 (1.5%) using both.

187 opriate drug and dose from a growing list of anticoagulant options (including warfarin), (2) to help

188 Receipt of an oral anticoagulant or antiplatelet medication.

189 Anticoagulant or antiplatelet therapy is the preferred t

190 She was not taking any anticoagulants or immunosuppressive medication.

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

192 idered under-prescribed when lipid-lowering, anticoagulant, or antihypertensive drugs were clinically

193 half of people eligible for lipid-lowering, anticoagulant, or antihypertensive drugs were not prescr

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

195 Pretreating organs with novel cytotopic anticoagulant peptides that localize to endothelial cell

196 88 [1.24-2.86] for reteplase plus parenteral anticoagulants plus glycoprotein inhibitors).

197 1.10-1.98] for tenecteplase plus parenteral anticoagulants plus glycoprotein inhibitors; RR 1.88 [1.

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

199 gly, inhibiting PAR-1 signaling, but not the anticoagulant properties of aPC, abolished the ability o

200 trypsin-like protease thrombin activates the anticoagulant protein C in a reaction that requires the

201 entification and characterization of a novel anticoagulant protein from the venom of Hemachatus haema

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

203 dures were associated with increased risk of anticoagulant-related hemorrhage (HR: 5.6; p = 0.008) co

204 y the fact that although LAAC attenuates the anticoagulant-related lifetime risk of bleeding, implant

205 Observations: The predictable anticoagulant response of NOACs has provided the pharmac

206 The efficacy and safety of the anticoagulant rivaroxaban for the treatment and secondar

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

208 s study investigates the effects of the oral anticoagulant, rivaroxaban (RVXB), a direct antifactor X

209 itiation of coagulation, exerts an important anticoagulant role through the factor Xa (FXa)-dependent

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

211 1.05-1.24] for streptokinase plus parenteral anticoagulants; RR 1.26 [1.10-1.45] for non-accelerated

212 A strategy optimizing anticoagulant selection remains an unmet clinical need.

213 Protein C, a secretory vitamin K-dependent anticoagulant serine protease, inactivates factors Va/VI

214 Antithrombin (AT) is an anticoagulant serpin that irreversibly inactivates the c

215 These emerging anticoagulant strategies should address unmet needs and

216 Practice patterns in anticoagulant strategies used during percutaneous corona

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

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

219 These results demonstrate that the protein C anticoagulant system can be successfully targeted by eng

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

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

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

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

224 Therefore novel anticoagulants that target specific steps in the coagula

225 ng the basis for the use of antiplatelet and anticoagulant therapies to optimize procedural success a

226 reatment regimen, including antiplatelet and anticoagulant therapies, for these high-risk patients wi

227 g 353 patients, that assessed the effects of anticoagulant therapy (low-weight heparin or warfarin vs

228 ts (DOACs) represent a major advance in oral anticoagulant therapy and have replaced the vitamin K an

229 ese procedures between patients who received anticoagulant therapy and those who received no anticoag

230 safety and cost-effectiveness of continuing anticoagulant therapy beyond the acute treatment period

231 ovide reassuring data that women taking oral anticoagulant therapy for venous thromboembolism (VTE) m

232 Oral anticoagulant therapy for venous thromboembolism is very

233 e rivaroxaban group and 2149 in the standard anticoagulant therapy group.

234 patients with cirrhosis and PVT who receive anticoagulant therapy have increased recanalization and

235 , experience-informed approach for tailoring anticoagulant therapy in patients with cancer-associated

236 nd meta-analysis to determine the effects of anticoagulant therapy in patients with cirrhosis and PVT

237 ing or thrombosis and to monitor response to anticoagulant therapy in patients.

238 An extended duration of anticoagulant therapy is often recommended for obese or

239 should be advised of the potential effect of anticoagulant therapy on menstrual bleeding at the time

240 e published literature on real-world data on anticoagulant therapy use, the risks and risk factors of

241 017, for studies that assessed the effect of anticoagulant therapy vs no treatment in patients with c

242 The risk of thrombosis during anticoagulant therapy with these treatments is not well

243 LY trial (Randomized Evaluation of Long-Term Anticoagulant Therapy) compared dabigatran 150 and 110 m

244 in 418 patients with spontaneous ICH without anticoagulant therapy, and hematoma expansion was calcul

245 and observational studies of antiplatelet or anticoagulant therapy, published in any language and rep

246 The choice of anticoagulant therapy, the degree of monitoring, and the

247 Anticoagulant therapy-associated bleeding and pathologic

248 icoagulant therapy and those who received no anticoagulant therapy.

249 permanent AF, underlining the importance of anticoagulant therapy.

250 among patients receiving direct-acting oral anticoagulant therapy.

251 opulations, including the subgroup receiving anticoagulant therapy.

252 making regarding the discontinuation of oral anticoagulant therapy.

253 deep-vein thrombosis despite treatment with anticoagulant therapy.

254 due to casting in the POT-CAST trial) or no anticoagulant therapy.

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

256 quire exogenous thrombomodulin, unlike other anticoagulant thrombin derivatives engineered to date.

257 17% normal respectively; further decline in anticoagulants; thrombocytopenia; neutrophilia and endot

258 cal inflammation is present and that natural anticoagulant/thrombomodulin activity is important after

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

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

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

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

263 Contemporary guidelines suggest anticoagulant treatment decisions in atrial fibrillation

264 properties were evaluated after 3 months of anticoagulant treatment since the index event.

265 ed a meta-analysis to estimate the effect of anticoagulant treatment vs no therapy on recanalization

266 ts of such testing should prompt a change in anticoagulant treatment.

267 of cava filters in patients who can receive anticoagulant treatments.

268 pairment were excluded from the non-VKA oral anticoagulant trials, so limited data are available.

269 P for heterogeneity = .49) or the novel oral anticoagulant type (P for heterogeneity = .15).

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

271 open fracture (OR, 1.66; 95% CI, 1.55-1.77), anticoagulant use (OR, 1.58; 95% CI, 1.51-1.66), osteoar

272 ges were not associated with antiplatelet or anticoagulant use at baseline (P = 0.28) or during follo

273 sk of initiation or aggravation of bleeding; anticoagulant use at the time of injury can also contrib

274 nal intervention, versus usual care, on oral anticoagulant use in patients with atrial fibrillation.

275 Oral anticoagulant use increased in the intervention group fr

276 Whether oral anticoagulant use should be considered in patients under

277 with hypertension (n = 807), antiplatelet or anticoagulant use was associated with a higher rate of h

278 Among all CATT participants, antiplatelet or anticoagulant use was not associated significantly with

279 METHODS AND Trends in anticoagulant use were examined among 553 562 PCIs perfo

280 e type, dose, or duration of antiplatelet or anticoagulant use.

281 However, BAT protocols vary in blood anticoagulant used and temperature and time of storage b

282 the type of sample (serum or plasma) or the anticoagulant used but was reduced in a sample from a pa

283 hage was present in 64.5% of antiplatelet or anticoagulant users and in 59.6% of nonusers (P = 0.09;

284 217 patients), 53% of patients treated with anticoagulants vs 33% of patients who did not receive an

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

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

287 .9%) of ED visits for adverse drug events; 4 anticoagulants (warfarin, rivaroxaban, dabigatran, and e

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

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

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

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

292 Anticoagulants were used less often in patients with par

293 '' for a dose administration of the new oral anticoagulant, where the Deltaf/DeltaGamma ratio of the

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

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

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

297 itial treatment using a non-DOAC/non-heparin anticoagulant with transition to a DOAC during HIT-assoc

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

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

300 se or coprescription of an NSAID and an oral anticoagulant without gastroprotection).