ライフサイエンスコーパス: INR

1 INR is inversely related to thrombotic events occurring

2 INR remained normal in Controls.

3 INR triggers varied depending on resection type, patient

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

5 INR variability was the most strongly associated predict

6 INR was inversely associated with thrombotic events (haz

7 INR-dependent activation by HMGA1 and Mediator requires

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

9 (451 mumol/L versus 262 mumol/L, P = 0.02), INR (1.62 versus 1.33, P = 0.005), model for endstage li

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

11 After inclusion of week 1 INRs, CYP2C9 (P = .08) and VKORC1 (P = .30) were not ass

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

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

14 39 physicians, yielding a total of 2 683 674 INR results.

15 g for early (days 4-6) and week 1 (days 7-9) INR values.

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

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

18 Admission INR was inversely correlated with acute perfusion defect

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

20 reased bleeding risk regardless of admission INR level.

21 therapeutic, and supratherapeutic admission INR levels, respectively.

22 ts with preadmission warfarin use, admission INR was inversely correlated with lesion volume on diffu

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

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

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

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

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

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

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

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

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

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

33 = 0.2 anti-X(a) U/mL and on warfarin with an INR >/= 2.0 were associated with significant reductions

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

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

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

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

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

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

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

41 ransition strategies, clinical outcomes, and INR values.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 eria including identification of TATA boxes, INRs, and DPEs plus support from proteomic and gene expr

62 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

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

64 International Normalized Ratio calibration (INR), as well as the Watala, Golanski, and Kardas relati

65 o were competent in the use of point-of-care INR devices to either weekly self-testing at home or mon

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

67 65 years old did not achieve well-controlled INR and had higher associated clinical events rates than

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

69 col was necessary to achieve well-controlled INR.

70 -guided protocols to achieve well-controlled INR.

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

72 daily supplementation may lead to decreased INR variability.

73 etexilate], and heparins) causing decreasing INR.

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

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

76 warfarin initiation is captured by the early INR response.

77 it of therapeutic range, adding either early INRs or genotypes to a baseline model (clinical variable

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

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

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

81 nsfusion of preoperative plasma for elevated INR.

82 arfarin users who do not receive in-facility INR monitoring.

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

84 therapeutic range (P=0.02) and to the first INR of more than 4 (P=0.003).

85 gnificant predictor of the time to the first INR of more than 4 (P=0.03).

86 the therapeutic range, the time to the first INR of more than 4, the time above the therapeutic INR r

87 of VKORC1 had a decreased time to the first INR within the therapeutic range (P=0.02) and to the fir

88 gnificant predictor of the time to the first INR within the therapeutic range (P=0.57) but was a sign

89 he study outcomes were the time to the first INR within the therapeutic range, the time to the first

90 (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

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

92 Less frequent INR monitoring may be feasible in stable patients.

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

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

95 patients with stable INRs (defined as having INR values exclusively within the INR range) and compara

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

97 .41% (4.09-4.73), respectively, and, in high INR variability, were 3.04% (2.85-3.24) and 3.48% (3.27-

98 lso may have thromboembolic events at higher INR levels.

99 (2.1, 3.0); 78.5% of patients had a pre-ICH INR <3.0.

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

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

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

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

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

105 pulsives had an unknown signal of increasing INR.

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

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

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

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

110 An intact INR element was required for proficient ICP4 activation

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

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

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

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

115 , Bleeding History or Predisposition, Labile INR, Elderly, Drugs/Alcohol Concomitantly) score perform

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

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

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

119 0%; moderate, 50% to 70%; low, <50%) and log INR variability into 2 categories (stable and unstable).

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

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

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

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

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

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

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

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

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

129 Mean INR and platelet triggers for FFP and platelet transfusi

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

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

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

133 5 mg (54%; 1.4 events per patient year; mean INR at event, 2.2); P = 0.004.

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

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

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

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

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

139 Warfarin users who received no INR monitoring in the first 90 d of dialysis had the hig

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 comparator patients (defined as at least one INR outside the INR range) in a retrospective, longitudi

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

156 The optimal INR range during uninterrupted periprocedural anticoagul

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

158 on significantly correlated with peak ALT or INR.

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

160 Patient INR control was characterized using various measures, fr

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

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

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

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

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

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

167 cal outcome compared with monitoring with PT-INR.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

183 < 0.01), and International Normalized Ratio (INR) >1.2 (P < 0.01).

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

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

186 1.35-3.21), international normalized ratio (INR) (P < 0.001, HR = 9.83, 95% CI = 4.51-21.45), serum

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

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

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

190 en admission international normalized ratio (INR) and acute infarct volume in patients with ischemic

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

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

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

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

195 3.0 for the international normalized ratio (INR) during the first 12 weeks after warfarin initiation

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

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

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

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

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

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

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

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

204 therapy, an international normalized ratio (INR) recall interval not exceeding 4 weeks has tradition

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

206 alysis using international normalized ratio (INR) suggested a dose-response relationship between the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

223 expressed as International Normalized Ratio (INR).

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

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

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

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

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

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

230 mined by the international normalized ratio [INR]), and bleeding events.

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

232 s at higher international normalized ratios (INRs).

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

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

235 that vitamin K supplementation may stabilize INRs, although the success varies among patients.

236 size that many patients demonstrating stable INR control could be safely treated with INR recall inte

237 Independent predictors of stable INR control were age older than 70 years and the absence

238 to identify independent predictors of stable INR control.

239 We sought to identify patients with stable INRs (defined as having INR values exclusively within th

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

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

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

243 Despite supratherapeutic INRs, patient plasma contained markedly elevated thrombi

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

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

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

247 ere significantly less likely to have target INR of 3.0 or higher or chronic diseases.

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

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

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

251 he experimental calibration equation for the INR, combined with the experimental WGK relation, withou

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

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

254 Initial variability in the INR response to warfarin was more strongly associated wi

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

256 das relation (WGK) for the dependence of the INR on the concentrations of coagulation factors.

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

258 nts (defined as at least one INR outside the INR range) in a retrospective, longitudinal cohort study

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

260 he time above the therapeutic INR range, the INR response over time, and the warfarin dose requiremen

261 red to stabilize the binding of TFIID to the INR-mutated late promoter.

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

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

264 as having INR values exclusively within the INR range) and comparator patients (defined as at least

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

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

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

268 Patients who were on therapeutic INR (>or=2.0) had smaller infarcts compared with patient

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

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

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

272 more than 4, the time above the therapeutic INR range, the INR response over time, and the warfarin

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

274 Therefore, INR levels should be carefully monitored in preparation

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

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

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

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

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

280 ietary vitamin K intake are known to lead to INR variability.

281 /= lower limit of therapeutic range; time to INR > 4; and first stable warfarin dose) after adjusting

282 ly measures of warfarin sensitivity (time to INR >/= lower limit of therapeutic range; time to INR >

283 For time to INR more than or equal to the lower limit of therapeutic

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

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

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

287 aily) in patients with a history of unstable INRs indicate that vitamin K supplementation may stabili

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 ble INR control could be safely treated with INR recall intervals greater than the traditional 4 week

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

299 In 214 patients starting warfarin with INR-guided dose adjustments, we determined whether CYP2C

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