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

11 the comparison of the pooled enoxaparin and UFH groups.

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

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

14 ding was observed between the otamixaban and UFH groups.

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

16 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

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

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

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

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

21 d ACT all showed good discrimination between UFH doses.

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

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

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

25 bition of thrombin-induced clot formation by UFH.

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

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

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

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

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

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

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

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

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

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

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

37 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 ical advantages over unfractionated heparin (UFH).

74 noclonal antibody or unfractionated heparin (UFH).

75 LMWH) enoxaparin for unfractionated heparin (UFH).

76 ffects the dosing of unfractionated heparin (UFH).

77 patients exposed to unfractionated heparin (UFH).

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

79 e anticoagulants to unfractionated heparins (UFHs).

80 Increasing UFH weight-indexed dose was independently associated wit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 The age-dependency of UFH effect was confirmed.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

110 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).

111 May 2005 and March 2012 using bivalirudin or UFH.

112 h increasing concentrations of dalteparin or UFH.

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

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

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

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

117 ation appears to be the major advantage over UFH.

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

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

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

121 have a number of theoretical advantages over UFH.

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

123 3 to $76,139) for 1862 patients who received UFH (incremental cost, -$1297 [IQR, -$4398 to $1404]; P

124 -11 and 67+/-11 years for patients receiving UFH and enoxaparin, respectively (P=0.005).

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

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

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

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

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

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

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

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

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

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

135 7.9% in the enoxaparin group and 3.7% in the UFH group (adjusted hazard ratio=2.6, P=0.03).

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

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

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

139 .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

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

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

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

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

144 entially treated with IV dalteparin and then UFH.

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

146 a smaller degree of variance as compared to UFH.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

177 icacy profiles as compared to abciximab with UFH.

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

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

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

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

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

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

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

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

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

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

188 0.57 [0.36-0.89]; P=0.01) when compared with UFH-treated patients.

189 ty in outcomes with enoxaparin compared with UFH.

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

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

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

193 isition cost of UFH favored prophylaxis with UFH.

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

195 ,357 patients from HORIZONS-AMI treated with UFH before enrollment according to their subsequent rand

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

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