ライフサイエンスコーパス: anticoagulants

1 or non-accelerated alteplase plus parenteral anticoagulants).

2 tion, atrial fibrillation, or treatment with anticoagulants.

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

4 lems preventing clinical use of nucleic acid anticoagulants.

5 so the target of several clinically approved anticoagulants.

6 ors of factor XI or XII as potentially safer anticoagulants.

7 both rivaroxaban and warfarin, or other oral anticoagulants.

8 ging guided the initiation and withdrawal of anticoagulants.

9 of use and when used concomitantly with oral anticoagulants.

10 ngs support the continued use of direct oral anticoagulants.

11 ts with nonvalvular AF not treated with oral anticoagulants.

12 antiviral therapies, immune modulators, and anticoagulants.

13 rtensives, P2Y12 inhibitors, and direct oral anticoagulants.

14 the proportion of patients treated with oral anticoagulants.

15 sk of gastrointestinal bleeding while taking anticoagulants.

16 agent to reverse the effects of several new anticoagulants.

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

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

19 after exposure to various concentrations of anticoagulants.

20 recurrence of VTE and bleeding while taking anticoagulants.

21 er cardiac medication, and switching between anticoagulants.

22 nists, hydralazine/isosorbide dinitrate, and anticoagulants.

23 but also ensure their perfusion by acting as anticoagulants.

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

25 ncreased bleeding, as compared with standard anticoagulants.

26 acokinetics, and pharmacodynamics of various anticoagulants.

27 efect that was phenocopied using direct oral anticoagulants.

28 arameters and platelets and is aggravated by anticoagulants.

29 effects of warfarin compared to direct oral anticoagulants.

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

31 treatment with non-vitamin K antagonist oral anticoagulants.

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

33 uced risk of bleeding compared with standard anticoagulants.

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

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

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

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

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

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

40 Parenteral anticoagulants administered in doses greater than those

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

59 Anticoagulants, antibiotics, and diabetes agents were im

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

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

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

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

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

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

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

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

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

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

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

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

72 Direct oral anticoagulants are non-inferior to conventional anticoag

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 Oral anticoagulants decrease ischemic stroke rates in patient

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

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

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

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

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

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

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

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

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

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

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

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

105 More recently, direct oral anticoagulants (DOACs) have been demonstrated to reduce

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 2010 has significantly affected selection of anticoagulants for patients with VTE.

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

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

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

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

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

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

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

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

140 0-24 days); 29 (64%) of the 45 not receiving anticoagulants fulfilled criteria for disseminated intra

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

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

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

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

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

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

147 Although oral anticoagulants have been found effective in reducing str

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

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

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

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

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

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

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

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

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

157 210A defect, and deficiencies of the natural anticoagulants (ie, antithrombin, protein C, and protein

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

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

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

161 point score threshold for recommending oral anticoagulants in AF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

178 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

212 17.2% received non-vitamin K antagonist oral anticoagulants (NOACs).

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

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

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

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

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

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

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

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

221 In addition, the influence of these anticoagulants on vascularisation was examined using the

222 %) using antiplatelets only, 77 (6.6%) using anticoagulants only, and 17 (1.5%) using both.

223 justified switch from heparin to alternative anticoagulants or delays in anticoagulation.

224 She was not taking any anticoagulants or immunosuppressive medication.

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

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

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

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

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

230 88 [1.24-2.86] for reteplase plus parenteral anticoagulants plus glycoprotein inhibitors).

231 1.10-1.98] for tenecteplase plus parenteral anticoagulants plus glycoprotein inhibitors; RR 1.88 [1.

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

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

234 Anticoagulants, primarily low-molecular-weight heparin a

235 lance of hemostasis by targeting the natural anticoagulants protein C, protein S, tissue factor pathw

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

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

238 tions, lowering the dose of some direct oral anticoagulants reduces the risk of bleeding without comp

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

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

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

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

243 1.05-1.24] for streptokinase plus parenteral anticoagulants; RR 1.26 [1.10-1.45] for non-accelerated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

258 Therefore novel anticoagulants that target specific steps in the coagula

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

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

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

262 17% normal respectively; further decline in anticoagulants; thrombocytopenia; neutrophilia and endot

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

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

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

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

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

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

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

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

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

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

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

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

275 217 patients), 53% of patients treated with anticoagulants vs 33% of patients who did not receive an

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

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

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

279 .9%) of ED visits for adverse drug events; 4 anticoagulants (warfarin, rivaroxaban, dabigatran, and e

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

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

282 Anticoagulants were a factor in 3 retrobulbar hemorrhage

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

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

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

286 Diuretics and anticoagulants were underutilized in women.

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

288 Anticoagulants were used less often in patients with par

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

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

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

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

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

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

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

296 New users of anticoagulants with nonvalvular atrial fibrillation were

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

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

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

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