ライフサイエンスコーパス: UFH

1 UFH effects were lower in infants compared with older ch

2 UFH has been reported to bind and induce modest conforma

3 cations (28.4% pooled M118 arms versus 31.1% UFH).

4 tion profile was observed from digests of 20 UFH samples.

5 A total of 564 patients (274 in abciximab/UFH group vs. 290 in bivalirudin group) were enrolled in

6 persist in patients previously administered UFH is unknown.

7 Blood samples were drawn before and after UFH administration at 30, 60, and 90 minutes.

8 The rate of TIMI 3 flow among all UFH patients was 50% and was 51% among enoxaparin patien

9 We analyzed the outcome of all UFH-treated patients enrolled in 4 large, contemporary P

10 Under serum conditions, both UFH-PS-cis and UFH-PS-trans decreased cell viability, the reduction for

11 ) were 80.1% and 75.1% in the enoxaparin and UFH groups, respectively.

12 the comparison of the pooled enoxaparin and UFH groups.

13 s 0.8%, P=0.37) were similar in the LMWH and UFH groups.

14 The adverse event profiles of M118 and UFH were comparable.

15 ding was observed between the otamixaban and UFH groups.

16 With full-dose TNK and UFH, the rate of TIMI 3 flow at 60 minutes was 52% and w

17 zed in an open-label fashion to 1 of 4 arms: UFH 70 U/kg, M118 50 IU/kg IV, M118 75 IU/kg IV, or M118

18 Enoxaparin was at least as effective as UFH as an adjunct to thrombolysis, with a trend toward h

19 ve than placebo and at least as effective as UFH in reducing the hard end points of death and recurre

20 During CPB, Ir-CPI was as efficient as UFH in preventing clot formation within the extracorpore

21 associated with similar TIMI 3 flow rates as UFH at an early time point while exhibiting advantages o

22 the assays; and (4) the association between UFH effect and clinical outcome.

23 d ACT all showed good discrimination between UFH doses.

24 to investigate (1) the relationship between UFH dose and its anticoagulant effect as assessed by ant

25 Under serum conditions, both UFH-PS-cis and UFH-PS-trans decreased cell viability, th

26 At one month, both UFH and LMWH produced an emphysematous lung phenotype.

27 GST-HB3 showed a linear detection of both UFH (15kDa) and low-molecular-weight heparin (LMWH; 6kDa

28 ets exceeding approximately 30% (achieved by UFH, LMWH, 16-, 8-, 6-mer), (2) formation of multimolecu

29 bition of thrombin-induced clot formation by UFH.

30 , (2) formation of multimolecular complexes (UFH, 16-, 8-mer), and (3) energy (needed for a conformat

31 Under serum-free conditions, UFH-PS-trans with a high DS stimulated proliferation of

32 ed heparin (UFH), enoxaparin, 6-O-desulfated UFH, and 6-O-desulfated enoxaparin with 50% inhibitory c

33 nic molecules shown previously to dissociate UFH from antithrombin III and to inhibit polyphosphates.

34 ls evaluated 10 mug/kg rNAPc2 with half-dose UFH (n = 26) and no UFH (n = 26).

35 eated without UFH, but none in the half-dose UFH group (19% vs. 0%; p = 0.051).

36 ore pronounced at low-dose than at high-dose UFH.

37 infusion in randomized children) vs low-dose UFH (50 U/kg bolus) during cardiac catheterization in ch

38 GPI use was 50.5% during UFH PCIs and 12.0% during bivalirudin PCIs.

39 ed the following determinants of UFH effect: UFH dose, age, baseline antithrombin (for anti-Xa), and

40 , or half-dose TNK plus abciximab and either UFH (bolus 40 U/kg; infusion 7 U/kg per hour) or enoxapa

41 acute coronary syndrome who received either UFH (n=1008) or enoxaparin (n=151) before proceeding to

42 For UFH, the range examined was 78 to over 2000ng/ml (equiva

43 point was 15.7% enoxaparin versus 17.3% for UFH (odds ratio 0.89 [95% confidence interval CI = 0.66

44 rate was 1.5% for enoxaparin versus 1.3% for UFH (odds ratio 1.16 [95% CI 0.44 to 3.02]) and 1.8% ver

45 zation, the change being more pronounced for UFH-PS with a higher degree of substitution (DS), while

46 decreased cell viability, the reduction for UFH-PS-cis being higher than that for UFH-PS-trans.

47 at enoxaparin may potentially substitute for UFH as adjunctive therapy in fibrin-specific thrombolyti

48 on for UFH-PS-cis being higher than that for UFH-PS-trans.

49 easuring limit and thus of limited value for UFH monitoring.

50 f 0.12 life-years relative to patients given UFH.

51 lus a glycoprotein IIb/IIIa inhibitor (GPI) (UFH+GPI; n = 1,802).

52 lood products did not differ between groups (UFH=2.7+/-6.5 U and enoxaparin=2.3+/-4.5 U; P=NS).

53 collaboration with United Family Healthcare (UFH), we study the potential effectiveness improvement o

54 T-HB3, detected unfractionated free heparin (UFH) as low as 39ng/ml (equivalent to approximately 0.1U

55 -dose TNK and either unfractionated heparin (UFH) (bolus 60 U/kg; infusion 12 U/kg per hour) or enoxa

56 abrupt cessation of unfractionated heparin (UFH) among patients with acute coronary syndromes.

57 e their limitations, unfractionated heparin (UFH) and bivalirudin remain standard-of-care parenteral

58 Unfractionated heparin (UFH) and enoxaparin (Enox) were substituted with a photo

59 esired attributes of unfractionated heparin (UFH) and low-molecular-weight heparin: Potent activity a

60 to complexes between unfractionated heparin (UFH) and platelet factor 4 (PF4) that form over a narrow

61 arin was superior to unfractionated heparin (UFH) and that tirofiban was better than placebo in patie

62 evention strategies, unfractionated heparin (UFH) and the low-molecular-weight heparin (LMWH) daltepa

63 anticoagulation with unfractionated heparin (UFH) and the use of antiplatelet agents including aspiri

64 aparin compared with unfractionated heparin (UFH) as adjunctive therapy for fibrinolysis in patients

65 ENOX) is superior to unfractionated heparin (UFH) as adjunctive therapy for patients with ST-segment

66 s or weight-adjusted unfractionated heparin (UFH) before percutaneous coronary intervention.

67 Adjunctive unfractionated heparin (UFH) during thrombolytic therapy for acute myocardial in

68 s of bivalirudin and unfractionated heparin (UFH) for carotid artery stenting.

69 tive alternatives to unfractionated heparin (UFH) for management of unstable angina/non-Q-wave myocar

70 ween bivalirudin and unfractionated heparin (UFH) have not been well described.

71 nd increasing use of unfractionated heparin (UFH) in hospitalized patients.

72 aparin (ENOX) versus unfractionated heparin (UFH) in patients with ST-segment elevation myocardial in

73 of enoxaparin versus unfractionated heparin (UFH) in the SYNERGY (Superior Yield of the New Strategy

74 Unfractionated heparin (UFH) is a widely used anticoagulant that has long been k

75 Unfractionated heparin (UFH) is an effective antithrombotic during surgery but h

76 Monitoring unfractionated heparin (UFH) is crucial to prevent over- or under-anticoagulatio

77 Unfractionated heparin (UFH) is currently used during CPB but can lead to seriou

78 Unfractionated heparin (UFH) is frequently administered early in ST-segment elev

79 Unfractionated heparin (UFH) is the most widely used antithrombin during percuta

80 r of advantages over unfractionated heparin (UFH) leading to their increasing use for thrombotic vasc

81 of dalteparin versus unfractionated heparin (UFH) on the activated clotting time (ACT), and to determ

82 eived abciximab with unfractionated heparin (UFH) or bivalirudin during percutaneous coronary interve

83 Patients given unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH) for prophyla

84 n (n = 1,800) versus unfractionated heparin (UFH) plus a glycoprotein IIb/IIIa inhibitor (GPI) (UFH+G

85 d polyanions such as unfractionated heparin (UFH) that bind to each other primarily through electrost

86 of concentrations of unfractionated heparin (UFH), enoxaparin, 6-O-desulfated UFH, and 6-O-desulfated

87 olving enoxaparin or unfractionated heparin (UFH), in combination with tirofiban or placebo for 2 to

88 eraction of PF4 with unfractionated heparin (UFH), its 16-, 8-, and 6-mer subfractions, low-molecular

89 perior efficacy over unfractionated heparin (UFH), its longer activity, and its subcutaneous route of

90 d either therapeutic unfractionated heparin (UFH), low molecular weight heparin (LMWH) or normal sali

91 ts received aspirin, unfractionated heparin (UFH), or enoxaparin and early catheterization; clopidogr

92 ical advantages over unfractionated heparin (UFH).

93 patients exposed to unfractionated heparin (UFH).

94 noclonal antibody or unfractionated heparin (UFH).

95 LMWH) enoxaparin for unfractionated heparin (UFH).

96 ffects the dosing of unfractionated heparin (UFH).

97 al ingredient (API) unfractionated heparins (UFHs) from six different manufacturers and one USP stand

98 e anticoagulants to unfractionated heparins (UFHs).

99 Increasing UFH weight-indexed dose was independently associated wit

100 ng time (ACT); (2) other factors influencing UFH effect; (3) the agreement between the assays; and (4

101 arin plus a glycoprotein IIb/IIIa inhibitor (UFH+GPI) can be fully attributed to reduced bleeding.

102 LMWH is as effective and safe as intravenous UFH in the management of patients with acute coronary sy

103 with UA/NQMI were randomized to intravenous UFH for >/=3 days followed by subcutaneous placebo injec

104 wever, the optimal parameters for monitoring UFH in children are not well established.

105 kg rNAPc2 with half-dose UFH (n = 26) and no UFH (n = 26).

106 point occurred in 10.7% of ENOX and 13.8% of UFH patients (0.77 relative risk; p < 0.001).

107 s in neutralizing anti-Factor Xa activity of UFH and enoxaparin added to normal plasma in vitro, and

108 The amount of UFH to achieve the first ACT >/=300 seconds was signific

109 No association of UFH dose or effect with clinical outcome could be observ

110 n ACT >/=300 seconds after a single bolus of UFH met this end point in 160 of 168 patients (95%).

111 was derived to calculate the first bolus of UFH required to achieve an ACT >/=300 seconds, and this

112 bin generation after the abrupt cessation of UFH may represent a drug-induced impairment of physiolog

113 ld at which lowering the acquisition cost of UFH favored prophylaxis with UFH.

114 The age-dependency of UFH effect was confirmed.

115 s demonstrated the following determinants of UFH effect: UFH dose, age, baseline antithrombin (for an

116 Higher doses of UFH (>5000 U, or up to 90 U/kg) were independently assoc

117 his data establishes the negative effects of UFH and LMWH during the critical period of postnatal lun

118 mbin fragment 1.2) was evident within 1 h of UFH cessation, increased progressively (by nearly two-fo

119 Hydrodynamic diameter, D(h), of UFH-PS decreased upon trans-cis photoisomerization, the

120 le anticoagulation, and a lower incidence of UFH-induced thrombocytopenia.

121 o had received a continuous i.v. infusion of UFH for 48 h were randomly assigned to: 1) abrupt cessat

122 the strategy of using enoxaparin instead of UFH as adjunctive therapy for fibrinolysis in patients w

123 farction when enoxaparin was used instead of UFH as adjunctive therapy for fibrinolysis in patients w

124 The interaction of UFH-PS with HSA, lysozyme, and protamine was studied wit

125 rayed in a lattice with several molecules of UFH may play a fundamental role in autoantibody formatio

126 dition to weight, are the only predictors of UFH dosage needed to achieve an ACT >/=300 seconds.

127 otential candidates for clinical reversal of UFH and LMWH in humans.

128 tigated and its efficacy compared to that of UFH using an uncoated system suitable for adult therapy.

129 d had similar or lower costs than the use of UFH.

130 Notably, the influence of age on UFH effect was dose-dependent.

131 to bivalirudin (switch group, n = 1,178) or UFH plus a glycoprotein IIb/IIIa inhibitor (control grou

132 pared with VKA (39%), LMWH and VKA (23%), or UFH and VKA (34%).

133 VKA (16%; RAR: 3.1; 95% CI: 1.2 to 7.5), or UFH and VKA (16%; RAR: 3.1; 95% CI: 1.5 to 7.1).

134 May 2005 and March 2012 using bivalirudin or UFH.

135 h increasing concentrations of dalteparin or UFH.

136 nd those who were treated with enoxaparin or UFH or both.

137 or at least 3 days with either enoxaparin or UFH.

138 of ENOX throughout index hospitalization or UFH for at least 48 h, with blinded study drug to contin

139 oxaparin, enoxaparin plus tirofiban, UFH, or UFH plus tirofiban.

140 ation appears to be the major advantage over UFH.

141 have practical and clinical advantages over UFH and can be considered an effective alternative in th

142 nd potential pharmacological advantages over UFH in multiple applications but have not been systemati

143 time point while exhibiting advantages over UFH with respect to ischemic events through 30 days.

144 have a number of theoretical advantages over UFH.

145 r bleeding) favored treatment with ENOX over UFH, either with concomitant clopidogrel (absolute risk

146 ion and dissociated preformed ultralarge PF4-UFH (antigenic) complexes (ULCs), dissociated ULICs comp

147 3 to $76,139) for 1862 patients who received UFH (incremental cost, -$1297 [IQR, -$4398 to $1404]; P

148 rved in patients within minutes of receiving UFH, despite adequate inhibition by aspirin prior to hep

149 -11 and 67+/-11 years for patients receiving UFH and enoxaparin, respectively (P=0.005).

150 pectively, and in 5.6% of patients receiving UFH.

151 pectively, and in 3.8% of patients receiving UFH.

152 Seventy-five percent of those receiving UFH and 64% of those receiving enoxaparin (P<0.005) were

153 rates of VTE were similar in those receiving UFH or LMWH compared to those not receiving chemoprophyl

154 ario, Canada, since 2006, involved replacing UFH with low-molecular-weight heparin (LMWH) for prophyl

155 nclusion, all assays reflected a significant UFH dose-effect relationship, however, with poor agreeme

156 d using maximum variation sampling targeting UFH-dominant vs LMWH-dominant approaches in hospitalized

157 less in-hospital postprocedure bleeding than UFH but similar rates of in-hospital and 30-day ischemic

158 rin, not all have shown better efficacy than UFH.

159 mixaban reduced F1+2 significantly more than UFH at the highest dose regimen, whereas no significant

160 ieved a 5-to-7-fold lower bleeding time than UFH/bivalirudin.

161 We observed that UFH and tetrameric PF4 formed ultralarge (> 670 kDa) com

162 nt were 1.84% (95% CrI, 1.33%-2.51%) for the UFH-vitamin K antagonist combination and 1.30% (95% CrI,

163 7.9% in the enoxaparin group and 3.7% in the UFH group (adjusted hazard ratio=2.6, P=0.03).

164 curred by 8 days in 14.5% of patients in the UFH group and 12.4% of patients in the enoxaparin group

165 enoxaparin group versus 9.8% and 9.1% in the UFH group.

166 INR, ACT, and weight were predictors of the UFH dosage to achieve an ACT >/=300 seconds.

167 .00; P=0.048) and by 43 days in 19.7% of the UFH group and 17.3% of the enoxaparin group (OR 0.85; 95

168 A derived equation predicted the UFH dosage to achieve an ACT >/=300 seconds.

169 However, findings suggest that the UFH-vitamin K antagonist combination is associated with

170 combination, a treatment strategy using the UFH-vitamin K antagonist combination was associated with

171 t PCI through 30 days in the ENOX versus the UFH group (22.8% vs. 24.2%; p = 0.027).

172 entially treated with IV dalteparin and then UFH.

173 ed to enoxaparin, enoxaparin plus tirofiban, UFH, or UFH plus tirofiban.

174 a smaller degree of variance as compared to UFH.

175 ajor bleeding is approximately equivalent to UFH, but minor hemorrhage is clearly increased, especial

176 t both human and murine platelets exposed to UFH, either in solution or immobilized onto artificial s

177 FH demonstrated that M118 was noninferior to UFH at preventing percutaneous coronary intervention-rel

178 ave a similar safety and efficacy profile to UFH and may be an alternative treatment.

179 event included diabetes and randomization to UFH+GPI (vs. bivalirudin).

180 less death or MI than patients randomized to UFH (adjusted p = 0.041) with a trend toward increased b

181 occurred in 31.1% of patients randomized to UFH and in 22.7%, 28.3%, and 30.1% of patients randomize

182 lytic therapy followed by PCI is superior to UFH and provides a seamless transition from the medical

183 Enoxaparin is superior to UFH for reducing a composite of death and serious cardia

184 therapy with enoxaparin might be superior to UFH in reducing death or nonfatal MI, with a modest exce

185 Unlike UFH, Ir-CPI did not promote bleeding.

186 with combination therapy, it was 5.2% using UFH and 8.5% with enoxaparin.

187 Clinical variables, UFH doses, and ACT values were recorded.

188 n patients treated with LMWH (n=1429) versus UFH (n=1431) in CLARITY-TIMI 28, a randomized trial of c

189 t comparative analysis of bivalirudin versus UFH for non-ST-segment-elevation myocardial infarction t

190 ry PCI were randomized to bivalirudin versus UFH+GPI.

191 ifferences in major bleeding for ENOX versus UFH (1.4% vs. 1.6%; p = NS).

192 through 30 days was compared for ENOX versus UFH among the patients who underwent subsequent PCI (n =

193 y managed patients randomized to ENOX versus UFH in the ExTRACT-TIMI 25 (Enoxaparin and Thrombolysis

194 risk of TIMI major bleeding with ENOX versus UFH was numerically but not statistically significantly

195 to show noninferiority of enoxaparin versus UFH with regard to infarct-related artery patency.

196 points between the pooled M118 groups versus UFH demonstrated that M118 was noninferior to UFH at pre

197 for the first trimester, followed by a VKA (UFH and VKA).

198 s, incremental cost-effectiveness of LMWH vs UFH during the period of hospitalization, and sensitivit

199 ermine Safety and Efficacy of Bivalrudin vs. UFH [BRAVO-2/3]; NCT01651780).

200 The mechanism by which UFH elicits these platelet-activating effects, however,

201 d proliferation of murine fibroblasts, while UFH-PS-cis decreased the viability of these cells.

202 hemorrhage with full-dose TNK was 2.4% with UFH and 1.9% with enoxaparin; with combination therapy,

203 herapy, the rate of TIMI 3 flow was 48% with UFH and 47% to 58% with enoxaparin.

204 tion therapy group, the rates were 6.5% with UFH and 5.5% with enoxaparin.

205 f HPR on clinical outcomes in abciximab with UFH versus bivalirudin treated non-ST-segment elevation

206 For abciximab with UFH, the incidence of the efficacy endpoint was similar

207 icacy profiles as compared to abciximab with UFH.

208 Additionally, factors associated with UFH use were fear of decompensation and misperceptions r

209 evidence of adverse effects associated with UFH.

210 To compare bivalirudin with UFH, propensity score matching and instrumental variable

211 th the highest otamixaban dose compared with UFH (-0.3 versus -0.2 ng/mL, P=0.008).

212 e available on the use of ENOX compared with UFH as adjunctive therapy in STEMI patients treated with

213 rates of hemorrhagic outcomes compared with UFH during the index hospitalization for carotid artery

214 farction, and recurrent angina compared with UFH in non-reperfused STEMI patients.

215 preoperative use of enoxaparin compared with UFH in patients presenting with an ACS who undergo open-

216 ectiveness ratio of enoxaparin compared with UFH was $5,700 per life-year gained, with 99.9% of boots

217 When compared with UFH+GPI, bivalirudin resulted in lower 3-year rates of m

218 yocardial ischemia, or stroke, compared with UFH, both in patients (n = 2,173) treated with clopidogr

219 clinical and economic benefits compared with UFH, with no increase in major bleeding complications.

220 0.57 [0.36-0.89]; P=0.01) when compared with UFH-treated patients.

221 ty in outcomes with enoxaparin compared with UFH.

222 cal and economic benefits in comparison with UFH in the management of unstable angina/ non-ST-segment

223 t, explained by the greater use of GPIs with UFH.

224 ull-dose TNK group in 15.9% of patients with UFH and 4.4% with enoxaparin (P=0.005).

225 isition cost of UFH favored prophylaxis with UFH.

226 flow was reversed rapidly by suffusion with UFH, provided flow had not already stopped.

227 ,357 patients from HORIZONS-AMI treated with UFH before enrollment according to their subsequent rand

228 on patients who receive early treatment with UFH, switching to bivalirudin before primary percutaneou

229 occurred in 5 of 26 patients treated without UFH, but none in the half-dose UFH group (19% vs. 0%; p