ライフサイエンスコーパス: INR

1 INR had higher blood levels of the enterocyte damage mar

2 INR is inversely related to thrombotic events occurring

3 INR remained normal in Controls.

4 INR triggers varied depending on resection type, patient

5 INR values <2.0 increase the rate of thrombotic events o

6 INR variability was the most strongly associated predict

7 INR was inversely associated with thrombotic events (haz

8 INR-dependent activation by HMGA1 and Mediator requires

9 INRs<2.0 and >3.0 were associated with a >2-fold increas

10 (451 mumol/L versus 262 mumol/L, P = 0.02), INR (1.62 versus 1.33, P = 0.005), model for endstage li

11 ioned to VKA, 85% of patients had at least 1 INR >/= 2 by day 14 after the transition and 99% by day

12 from sigmoid colon and terminal ileum of 19 INR and 20 IR in addition to 20 HIV negative individuals

13 keletal system (207 days; 11%), costing 19% (INR 4.4 billion), 13% (3.03 billion), and 11% (2.5 billi

14 geries (53 023; 8%) alone accounted for 21% (INR 4.9 billion) of cost.

15 39 physicians, yielding a total of 2 683 674 INR results.

16 0.53 mg/dl p < 0.001 (95% CI 0.23 to 0.78), INR 0.91 p < 0.001 (95% CI 0.72 to 1.09), gammaGT 7.9 IU

17 ing Poisson models, we analyzed their 10 927 INRs to determine INR-specific rates of thrombotic (isch

18 3 showed similar decreased TFII-I and NELF-A INR binding and increased RNAPII SerP2 in the gene body

19 ide evidence for the existence of additional INR subtypes sharing ubiquitin immunoreactivity as a com

20 o examine the associations between admission INR level, early antithrombotic treatment and invasive t

21 reased bleeding risk regardless of admission INR level.

22 therapeutic, and supratherapeutic admission INR levels, respectively.

23 Among patients with admission INR >/=2, 45% were treated with early (within 24 hours)

24 atients with ALF or acute liver injury (ALI; INR >= 2.0 with no encephalopathy), over two decades.

25 significant increase in complications at all INRs (odds ratio=3.1; +/-95% confidence interval, 1.4-7.

26 ericardial tamponade (1%) was similar at all INRs.

27 accuracy and significantly outperformed ALT, INR, and plasma acetaminophen concentration for the pred

28 arning method) was set up to predict altered INR levels after novel prescriptions.

29 cations, with a further steep rise beyond an INR>3.5.

30 ed 1234 (8.4%) of 14 743 patients who had an INR of 1.5 or above and were included in this investigat

31 h FFP during the postoperative period had an INR of less than 1.7, indicating possible overutilizatio

32 and her average dose required to maintain an INR of 2.0 to 3.0 appears to have decreased.

33 The hypothesis was that an INR target of 1.8 would be noninferior to an INR target

34 INR target of 1.8 would be noninferior to an INR target of 2.5, using a noninferiority margin of 3% f

35 tween patients continued on warfarin with an INR > or =1.5 (n = 46) and patients who had warfarin wit

36 = 0.2 anti-X(a) U/mL and on warfarin with an INR >/= 2.0 were associated with significant reductions

37 less of the proportion of time spent with an INR >3 (hazard ratio ranges=0.59-0.67 and 0.42-0.69; P<0

38 in therapeutic range and time spent with an INR >3.

39 nted within 12 h after symptom onset with an INR of at least 2.0 were randomly assigned (1:1) by numb

40 Ambulatory adults on warfarin with an INR target of 2-3 managed by an anticoagulation dosing s

41 ived FFP in the postoperative period with an INR trigger less than 1.7.

42 g RFA was reduced by 50% in patients with an INR>2.0.

43 ouped according to INR <2.0 (G<2; n=129) and INR >/=2.0 (G>/=2; n=41).

44 h baseline activated clotting time (ACT) and INR values was performed.

45 Using only initial AST, ALT, and INR measurements, the model accurately predicted subsequ

46 evidence of coagulopathy (prolonged aPTT and INR, decreased platelet count), hepatic injury (high bil

47 th unconjugated and conjugated bilirubin and INR (p < 0.05), except HAZ or LAZ.

48 Secondary end points were bleeding and INR values of 4 or more.

49 umol/l, ALT >10x upper limit of normal, and INR >1.5 were included.

50 ransition strategies, clinical outcomes, and INR values.

51 coagulation (significantly increased PTT and INR, decreased haemoglobin and platelet count).

52 ce of both CSPH and SPH, whereas ICG-r15 and INR were related to EV.

53 ion of percent time in therapeutic range and INR variability (odds ratio of 4.34, comparing the lowes

54 ryonic stem cells tend to have both TATA and INR elements in a synergistic configuration.

55 and is required for the synergy of TATA and INR elements in mammalian cells.

56 ase deficit, product volumes transfused, and INR after resuscitation.

57 eiling effects that limit the use of TTR and INR variability as separate measures.

58 wer incidences of excessive anticoagulation (INR >/=4.0) in the genotype-guided group.

59 had subtherapeutic warfarin anticoagulation (INR <2) at the time of stroke, 37674 (39.9%) were receiv

60 The rates of the combined outcome of any INR of 4 or more, major bleeding, or thromboembolism did

61 ameters capable of detecting TIC (defined as INR > 1.2), hypofibrinogenemia (< 2.0 g/L), and thromboc

62 an at 0 h and continued to 'ALF', defined as INR >3.

63 icant coagulopathy (defined in this study as INR >1.8 and/or platelet count <50 x 10(9) /L) who will

64 icant coagulopathy (defined in this study as INR >1.8 and/or PLT count < 50 x 10(9) /L) and nonvarice

65 Baseline INR and ACT, in addition to weight, are the only predict

66 Baseline INR, ACT, and weight were predictors of the UFH dosage t

67 mproved INR only in patients with a baseline INR greater than 2.5.

68 For the initial 170 patients, the baseline INR (2.47+/-0.31 versus 1.53+/-0.31) and ACT (185+/-26 v

69 erences in gut microbial composition between INR and IR.

70 gnificant interactions were observed between INR level and use of each early treatment in its associa

71 Age, bilirubin, INR, and creatinine (ABIC) score was B or C in 83%.

72 In gut mucosal biopsies, INR had lower fractions of CD4 + T cells, higher fractio

73 d point was the composite of major bleeding, INR of 4 or greater, venous thromboembolism, or death.

74 reduced the combined risk of major bleeding, INR of 4 or greater, venous thromboembolism, or death.

75 ient-year) was in the INR range of <1.5, but INR values of 1.5 to 1.99 also had high rates (0.16 thro

76 ducts compared to SOC (transfusion guided by INR and platelet count), without an increase in bleeding

77 nts compared with SOC (transfusion guided by INR and PLT count), without an increase in failure to co

78 ed with venous plasma testing, point-of-care INR measuring devices allow greater testing frequency an

79 65 years old did not achieve well-controlled INR and had higher associated clinical events rates than

80 fixed-dose protocol provided well-controlled INR only in normal responders >/=65, whereas for normal

81 col was necessary to achieve well-controlled INR.

82 -guided protocols to achieve well-controlled INR.

83 ed individuals with >/=2 months of INR data, INR results of >1.2, and an ICD-9 diagnosis code of atri

84 etexilate], and heparins) causing decreasing INR.

85 , we analyzed their 10 927 INRs to determine INR-specific rates of thrombotic (ischemic stroke and su

86 r the first time that biochemically distinct INR subtypes can coexist within a single nucleus where t

87 ition element (BREd), and initiator element (INR)-in constrained positions.

88 ease in his transaminase levels and elevated INR and alkaline phosphatase.

89 ), serum bilirubin >34 mumol/L, and elevated INR.

90 nsfusion of preoperative plasma for elevated INR.

91 h respect to normalising the INR, and faster INR normalisation seemed to be associated with smaller h

92 (RR, 0.24; 95% CI, 0.05-1.15), 56 vs 77 for INR of 4 or greater (RR, 0.71; 95% CI, 0.51-0.99), 33 vs

93 en-label fashion, either daily warfarin (for INR 2.0-3.0) plus 81 mg of aspirin (n=28) or 325 mg of a

94 Coma grade, INR, levels of bilirubin and phosphorus, and log(10) M30

95 of 804) in the low-intensity-warfarin group (INR target, 1.8) vs 3.8% (30 of 793) in the standard-tre

96 3) in the standard-treatment-warfarin group (INR target, 2.5), for a difference of 1.3% (1-sided 95%

97 At 18 +/- 1 h, INR > 3 was associated with: hypocoagulable TEG profile

98 Her INR control was excellent; however, over the past few mo

99 enia was present in 7875 patients (9%), high INR levels in 1393 (2%), and prolonged APTT in 2604 (3%)

100 .41% (4.09-4.73), respectively, and, in high INR variability, were 3.04% (2.85-3.24) and 3.48% (3.27-

101 lso may have thromboembolic events at higher INR levels.

102 (2.1, 3.0); 78.5% of patients had a pre-ICH INR <3.0.

103 Plasma transfusion significantly improved INR only in patients with a baseline INR greater than 2.

104 day 2) model including additional changes in INR and lactate.

105 (adjusted OR, 1.10 per 0.1-unit increase in INR [95% CI, 1.00-1.20]; P = .06).

106 GB induced significantly greater increase in INR in the whole group and NASH patients than SG.

107 actions were rediscovered causing increasing INR (antiarrhythmics class III [amiodarone], other opioi

108 pulsives had an unknown signal of increasing INR.

109 mplications with risk factors and individual INR control, we evaluated the efficacy and safety of war

110 atterns of warfarin daily dosage and induced INRs were characterized during pregnancy.

111 containing both a TATA box and an Initiator (INR) element but not from "TATA-only" core promoters.

112 ion sites have the locally "best" initiator (INR) sequence and/or shape.

113 s in association with individual TTR (iTTR), INR variability, and aspirin use and identification of f

114 Adding 'labile INR' (TTR < 65%) to ORBIT, ATRIA and HEMORR2HAGES signif

115 Adding 'labile INR' to ATRIA, ORBIT and HEMORR2HAGES improved their pre

116 , bleeding history or predisposition, labile INR [international normalized ratio], elderly, drugs/alc

117 mination performance, but adding the 'labile INR' criteria (i.e. TTR <65%) to ATRIA, ORBIT and HEMORR

118 djustments, increased time in range and less INR variability than reported with standard PT monitorin

119 ariability) but was weak between TTR and log INR variability (kappa=0.13).

120 0%; moderate, 50% to 70%; low, <50%) and log INR variability into 2 categories (stable and unstable).

121 INR variability separately; (2) TTR and log INR variability together; and (3) both predictors togeth

122 t control quintile compared with TTR and log INR variability, but not for major bleeding.

123 e (kappa=0.56 for TTR and kappa=0.62 for log INR variability) but was weak between TTR and log INR va

124 with interaction terms showed that High log INR variability predicted a significantly higher risk fo

125 Higher log INR variability (ie, unstable control) predicted ischemi

126 oke and major bleeding compared with low log INR variability, at moderate TTR levels (HR= 1.27 and HR

127 regression models, including (1) TTR or log INR variability separately; (2) TTR and log INR variabil

128 based on their level of control for TTR, log INR variability, and WCM.

129 ever its effectiveness relies on maintaining INR in therapeutic range.

130 Mean INR and platelet triggers for FFP and platelet transfusi

131 raction was 56% vs. 74% (p < 0.001) and mean INR was 2.0 vs. 1.3 (p < 0.001), respectively.

132 mg (22%; 0.38 events per patient year; mean INR at event, 2.0), and in 38 patients on ASA 325 mg (54

133 ole (26%; 0.42 events per patient year; mean INR at event, 2.2), 4 patients on ASA 81 mg (22%; 0.38 e

134 5 mg (54%; 1.4 events per patient year; mean INR at event, 2.2); P = 0.004.

135 Median INR prior to ICH was 2.6 (2.1, 3.0); 78.5% of patients h

136 After plasma transfusion, the median INR and aPTT changes were -0.2 and -5, respectively.

137 ted with tPA were receiving warfarin (median INR, 1.20; interquartile range [IQR], 1.07-1.40).

138 At 12 months, INR and albumin returned to baseline.

139 No INR values were reported for approximately 5% of partici

140 41.9% 95% CI 30.5-53.9) vs those with normal INR (28.2%; 95% CI, 27.7%-28.75%).

141 The combination of INR reversal <1.3 within 4 hours and systolic BP of <160

142 ary households receive an annual coverage of INR 200 000 (US$3333) for admissions to any empanelled p

143 Frequency of INR testing and time in the therapeutic range were analy

144 ients with iTTR 70% or greater, the level of INR variability did not alter event rates.

145 aminophen use is contributing to her loss of INR control, and (2) does this interaction place her at

146 We selected individuals with >/=2 months of INR data, INR results of >1.2, and an ICD-9 diagnosis co

147 Variables predictive of INR change after 1 month included operation type, NAS >/

148 various measures, from simple (proportion of INR values in range) to complex (eg, area under the curv

149 om the quadratic model, the optimal range of INR was calculated as 2.1 to 2.5.

150 f 0.80% per year with warfarin regardless of INR control and at a rate of 0.33% per year with apixaba

151 atients with OAC-associated ICH, reversal of INR <1.3 within 4 hours and systolic BP <160 mm Hg at 4

152 enlargement were associated with reversal of INR levels <1.3 within 4 hours after admission (43/217 [

153 These findings support continued use of INR variability, time in therapeutic range, or both for

154 n sections, we identified a novel variant of INR that is immunoreactive for the 40 kDa huntingtin ass

155 The optimal INR based on weighted mortality of thrombotic and bleedi

156 The optimal INR range during uninterrupted periprocedural anticoagul

157 (18 IU/L [13,22] versus 16 IU/L [13,21]) or INR (1.2 versus 1.2) 20 hours after starting acetylcyste

158 In patients presenting with normal ALT or INR, miR-122, HMGB1, and necrosis K18 identified the dev

159 on significantly correlated with peak ALT or INR.

160 ssive RBC transfusion better than PT/aPTT or INR (P < 0.001).

161 are associated with increase in bilirubin or INR should prompt temporary or permanent cessation of in

162 Patient INR control was characterized using various measures, fr

163 avenous tPA among warfarin-treated patients (INR </=1.7) was not associated with increased sICH risk

164 l failure, concomitant aspirin use, and poor INR control.

165 rgoing non-cardiac surgery with preoperative INR greater than or equal to 1.5.

166 iation of a novel prescription in previously INR-stable warfarin-treated patients with nonvalvular at

167 l stay, postoperative serum bilirubin and PT-INR, as well as infectious and overall complications fol

168 mbin time-international normalized ratio (PT-INR) levels were also lower in the steroid group (p = 0.

169 in time [Fiix-PT]) compared with standard PT-INR monitoring that includes factor VII measurement as w

170 ients were assigned to Fiix-PT and 575 to PT-INR monitoring after exclusion of four patients from eac

171 cal outcome compared with monitoring with PT-INR.

172 correlation and high concordance between PT/INR measured using the two approaches.

173 To measure PT/INR, conventional coagulation testing (CCT) is performed

174 optical sensor that can rapidly quantify PT/INR within seconds by measuring alterations in the visco

175 of our optical sensing approach for rapid PT/INR testing in whole blood and highlight the potential f

176 In this study, PT/INR values were measured in 60 patients using the optica

177 A blinded research INR (R-INR) based on results of the respective test was reporte

178 Rapid INR reduction was achieved in 48 (55%) patients in the 4

179 on-inferior and superior to plasma for rapid INR reversal and effective haemostasis in patients needi

180 tasis, and the co-primary endpoint was rapid INR reduction (</=1.3 at 0.5 h after infusion end).

181 ing based on international normalised ratio (INR) and weight.

182 n change the international normalised ratio (INR) but contribute little to the antithrombotic effect.

183 ime (PT) and international normalised ratio (INR) characterise acute liver injury (ALI) and failure (

184 ation of the international normalised ratio (INR) is recommended, but optimum haemostatic management

185 ith elevated international normalised ratio (INR) undergoing non-cardiac surgery.

186 creatinine, international normalised ratio (INR), and cardiovascular failure were used to derive an

187 < 0.01), and International Normalized Ratio (INR) >1.2 (P < 0.01).

188 use with an international normalized ratio (INR) </= 1.7.

189 alization of International normalized ratio (INR) (80% of patients), creatinine (84% of patients), ne

190 1.35-3.21), international normalized ratio (INR) (P < 0.001, HR = 9.83, 95% CI = 4.51-21.45), serum

191 seconds, internationalized normalized ratio (INR) 1.3, fibrinogen 199 mg/dL, D-dimer greater than 1.0

192 how baseline international normalized ratio (INR) affects the dosing of unfractionated heparin (UFH).

193 range of the international normalized ratio (INR) among subjects administrated Vitamin K antagonist (

194 , the median international normalized ratio (INR) and activated partial thromboplastin time (aPTT) va

195 relation to international normalized ratio (INR) and BP.

196 Data on international normalized ratio (INR) and platelet counts that triggered the perioperativ

197 e associated international normalized ratio (INR) are routinely tested to assess the risk of bleeding

198 summarizing international normalized ratio (INR) control over time.

199 3.0 for the international normalized ratio (INR) during the first 12 weeks after warfarin initiation

200 150 x 109/L, international normalized ratio (INR) greater than 1.4, or activated partial thromboplast

201 At 1 month international normalized ratio (INR) increased after RYGB (0.98 +/- 0.05 vs 1.14 +/- 0.1

202 nts if their international normalized ratio (INR) is 1.7 or lower, there are few data on safety of in

203 lex, and the international normalized ratio (INR) is often outside the target range.

204 the optimal international normalized ratio (INR) levels during RFA have not been defined.

205 by admission international normalized ratio (INR) levels: subtherapeutic (INR <2), therapeutic (INR,

206 e (ALT), and international normalized ratio (INR) measurements on admission to estimate overdose amou

207 ith a target international normalized ratio (INR) of 2 to 3 from June 2006 to August 2009; (2) ASA 81

208 to a target international normalized ratio (INR) of either 1.8 or 2.5.

209 reach target international normalized ratio (INR) represented the main stem of such protocol.

210 f predefined international normalized ratio (INR) thresholds for each adjusted dose.

211 increase in international normalized ratio (INR) to >3.0 in patients with chronic kidney disease (CK

212 most recent international normalized ratio (INR) to ICH was 13 days (6, 21 days).

213 The optimal international normalized ratio (INR) to prevent venous thromboembolism (VTE) in warfarin

214 that target international normalized ratio (INR) values <2.5 (range, 2-3) may be used.

215 ge (TTR) and international normalized ratio (INR) variability both measure warfarin control and are a

216 ge (TTR) and international normalized ratio (INR) variability predict adverse events individually.

217 The international normalized ratio (INR) was absent in 3% of cases (97 of 2951 patients), th

218 ime that the international normalized ratio (INR) was in the therapeutic range from day 4 or 5 throug

219 in until the international normalized ratio (INR) was normal (n = 258; 14.3% vs. 4.3%; p < 0.001) and

220 ded, and the international normalized ratio (INR) was not to be measured until 3 days later to preser

221 IU/L), peak international normalized ratio (INR), and adverse drug reactions.

222 rubin, day-3 international normalized ratio (INR), and day-7 AST were independently associated with P

223 time (APTT), international normalized ratio (INR), and other measures of heparin and warfarin anticoa

224 ine (Creat), International Normalized Ratio (INR), and serum albumin (Alb) at the second transplantat

225 essed by the international normalized ratio (INR), is challenging.

226 time (aPTT), international normalized ratio (INR), platelet count and fibrinogen] for transfusion req

227 se (ALT) and International Normalized Ratio (INR).

228 expressed as International Normalized Ratio (INR).

229 coma grade; international normalized ratio (INR); serum pH; body mass index; levels of creatinine, b

230 atherapeutic international normalized ratio (INR; median, 6.5) at onset of limb ischemia, rising plat

231 ange for the international normalized ratio (INR; target range, 2.0 to 3.0) in the 12-week period aft

232 ic warfarin (international normalized ratio [INR] >/=2) and 8290 (8.8%) were receiving non-vitamin K

233 oagulopathy (international normalized ratio [INR] >= 1.5) and encephalopathy, may occur during pregna

234 utine tests (international normalized ratio [INR] and platelet [PLT] count), and its use may avoid un

235 utine tests (international normalized ratio [INR] and platelet count), and its use may avoid unnecess

236 (measured as international normalized ratio [INR]) after initiation of a novel prescription in previo

237 d bilirubin, international normalized ratio [INR], sodium, and GRAIL) versus MELD-Na.

238 therapeutic international normalized ratios (INRs), and evidence of persistent thrombin generation de

239 s at higher international normalized ratios (INRs).

240 A blinded research INR (R-INR) based on results of the respective test was

241 HIV-infected immunological non-responders (INR) fail to reconstitute their CD4 + T cell pool after

242 Intranuclear rodlets (INRs), also known as rodlets of Roncoroni, are poorly un

243 Quest Diagnostics offers standardized INR laboratory testing services to approximately half of

244 rmalized ratio (INR) levels: subtherapeutic (INR <2), therapeutic (INR, 2-3), and supratherapeutic (I

245 anifest as a characteristic supratherapeutic INR caused by parallel severe factor VII depletion.

246 Despite supratherapeutic INRs, patient plasma contained markedly elevated thrombi

247 herapeutic (INR, 2-3), and supratherapeutic (INR >3).

248 September 2009 to August 2011 with a target INR of 1.5 to 2; and (3) ASA 325 mg daily from September

249 gn, participants were randomized to a target INR of 1.8 (n = 823) or 2.5 (n = 827) and to either geno

250 eptember 2011 to November 2014 with a target INR of 2 to 3 (n = 70).

251 on low-dose anticoagulation therapy (target INR: 1.5 to 2.5) were allowed in a highly selected subse

252 Patients were randomized to VKAs with target INR 2-3, rivaroxaban 10 mg daily, or rivaroxaban 10 mg d

253 ponding leucine-rich repeat receptor, termed INR, specific to select legume species and sufficient to

254 The INR values of 4 or more occurred in 4.5% of patients in

255 ere was a quadratic relationship between the INR and bleeding and vascular complications (P<0.001).

256 All but the INR also reside at Pol III promoters, where TBP makes si

257 plasma samples showed that variations in the INR corresponded most closely with changes in factor VII

258 rombotic events per patient-year) was in the INR range of <1.5, but INR values of 1.5 to 1.99 also ha

259 erior to FFP with respect to normalising the INR, and faster INR normalisation seemed to be associate

260 lowering bleeding outcomes regardless of the INR stability.

261 Patients were grouped based on the INR on the day of RFA.

262 was absent in 1% (32 of 2986 patients), the INR was more than 1 week old in 8% (229 of 2888 patients

263 A prevailing hypothesis is that the INR phenotype is caused by a persistently disrupted muco

264 Mapping experiments suggest that the INR region of the GLI2 promoter is necessary for GLI2 re

265 eta reduced endogenous TFII-I binding to the INR and increased RNAPII SerP2 in the gene body.

266 patients who had warfarin withheld until the INR was normal (n = 258; 6.5% vs. 4.3%; p = 0.50).

267 t in the percentage of time during which the INR was within the target range (absolute difference bet

268 f the rivaroxaban group had >/=1 therapeutic INR value.

269 The median time to reach a therapeutic INR was 21 days in the genotype-guided group as compared

270 Median time to first therapeutic INR was 3 days in the warfarin group and 13 days in the

271 ve the percentage of time in the therapeutic INR range during the 12 weeks after the initiation of th

272 higher percentage of time in the therapeutic INR range than was standard dosing during the initiation

273 The percentage of time in the therapeutic INR range was 61.6% for patients receiving genotype-guid

274 evels: subtherapeutic (INR <2), therapeutic (INR, 2-3), and supratherapeutic (INR >3).

275 Therefore, INR levels should be carefully monitored in preparation

276 We describe a selective association of these INRs with melanin concentrating hormone (MCH) and tyrosi

277 hIP studies showed that TFII-I binds to this INR.

278 alopathy; median levels of prothrombin time, INR, and total bilirubin were, respectively, 33% (Q1-Q3,

279 Patients were grouped according to INR <2.0 (G<2; n=129) and INR >/=2.0 (G>/=2; n=41).

280 rivaroxaban and VKA strategies, according to INR stability of subjects administrated VKA.

281 -month mortality risk was higher compared to INR (p = 0.04).

282 In contrast to INR, it is independent of anticoagulation and other anal

283 dardized TTR to standardized log-transformed INR variability using 103 897 warfarin-experienced patie

284 TTR and log-transformed INR variability were calculated for each patient.

285 The post-transfusion INR was decreased in whole blood vs component cohort [me

286 resolution of shock, lower post-transfusion INR, and decreased component product transfusion.

287 t that during vitamin K antagonist treatment INR monitoring could be replaced by Fiix-PT and that thi

288 4 hours after admission (43/217 [19.8%]) vs INR of >/=1.3 (264/636 [41.5%]; P < .001) and systolic B

289 The strongest single predictor was INR variability, followed closely by time in therapeutic

290 Complications were less prevalent when INR was >/=2.0 and </=3.0 (5% [31/572]) than when INR wa

291 as >/=2.0 and </=3.0 (5% [31/572]) than when INR was <2.0 (10% [49/485]; P=0.004) and >3.0 (12% [9/76

292 s of CE fraction were in good agreement with INR (R(2) = 0.73; p < 0.001).

293 3,437 patients with ischemic stroke and with INR of 1.7 or lower, treated with intravenous tPA in 120

294 endpoint was the proportion of patients with INR 1.2 or lower within 3 h of treatment initiation.

295 occurred more frequently among patients with INR levels of 1.5 to 2.0 (36.8%; 95% CI, 33.3%-40.4%), 2

296 Warfarin treatment with INR </= 1.7 did not increase the risk for SICH or death,

297 atients had baseline warfarin treatment with INR </= 1.7.

298 When combining triFc_AGP with INR and AFP, the panel had the greatest benefit in detec

299 Patients on warfarin with INR </= 1.7 were older, had more comorbidities, and had

300 Among warfarin-treated patients with INRs of 1.7 or lower, the degree of anticoagulation was