ライフサイエンスコーパス: anticoagulant therapy

1 deep-vein thrombosis despite treatment with anticoagulant therapy.

2 , as well as intermittent discontinuation of anticoagulant therapy.

3 eded to improve selection of AF patients for anticoagulant therapy.

4 g was performed after three to six months of anticoagulant therapy.

5 reased PIVKA-II in adults not receiving oral anticoagulant therapy.

6 oembolism (VTE) would affect the duration of anticoagulant therapy.

7 bility of using 6A6 as an antidote for D3H44 anticoagulant therapy.

8 Current treatment relies primarily on anticoagulant therapy.

9 erformed safely after only a short period of anticoagulant therapy.

10 ve results on helical CT who did not receive anticoagulant therapy.

11 nd indicates which patients may benefit from anticoagulant therapy.

12 th mechanical heart valves require long-term anticoagulant therapy.

13 re observed in neonates and patients on oral anticoagulant therapy.

14 potential application of these inhibitors in anticoagulant therapy.

15 bin time, which may complicate management of anticoagulant therapy.

16 icoagulant therapy and those who received no anticoagulant therapy.

17 e), older age, and the absence of aspirin or anticoagulant therapy.

18 permanent AF, underlining the importance of anticoagulant therapy.

19 among patients receiving direct-acting oral anticoagulant therapy.

20 ions; and (6) identify future directions for anticoagulant therapy.

21 on with either aspirin or no antiplatelet or anticoagulant therapy.

22 if the patient is receiving antiplatelet or anticoagulant therapy.

23 The risk of stroke in AF is reduced by anticoagulant therapy.

24 trial fibrillation during the early phase of anticoagulant therapy.

25 opulations, including the subgroup receiving anticoagulant therapy.

26 risk of recurrence after discontinuation of anticoagulant therapy.

27 t venous thromboembolism and bleeding during anticoagulant therapy.

28 r testing is positive 1 month after stopping anticoagulant therapy.

29 making regarding the discontinuation of oral anticoagulant therapy.

30 eferences for specific benefits and risks of anticoagulant therapy.

31 disorders, particularly in association with anticoagulant therapy.

32 who would benefit from treatment with early anticoagulant therapy.

33 r bleeding with and without antiplatelet and anticoagulant therapy.

34 t been described among patients on effective anticoagulant therapy.

35 due to casting in the POT-CAST trial) or no anticoagulant therapy.

36 within 2 years after the withdrawal of oral anticoagulant therapy.

37 explore the development of antiplatelet and anticoagulant therapies.

38 ars, PAR1 has become an appealing target for anticoagulant therapies.

39 Anticoagulant therapy (ACT) is commonly prescribed in ch

40 are desirable pharmacological properties of anticoagulant therapy administered for acute indications

41 igned 822 patients who had completed initial anticoagulant therapy after a first episode of unprovoke

42 the data supporting various antiplatelet and anticoagulant therapies and their combinations in patien

43 ts (DOACs) represent a major advance in oral anticoagulant therapy and have replaced the vitamin K an

44 By simplifying long-term anticoagulant therapy and improving its safety, the DOAC

45 adults receiving long-term (>3 months) oral anticoagulant therapy and that compared PST or PSM with

46 ese procedures between patients who received anticoagulant therapy and those who received no anticoag

47 ac rupture after thrombolytic and adjunctive anticoagulant therapy and to identify possible associati

48 th acquired thrombotic risk factors includes anticoagulant therapy and, if possible, resolution of th

49 f stroke risk factors, antiplatelet therapy, anticoagulant therapy, and carotid endarterectomy have a

50 in 418 patients with spontaneous ICH without anticoagulant therapy, and hematoma expansion was calcul

51 Thrombin is the main target of anticoagulant therapy, and major efforts have led to the

52 nclude epidural hematoma in association with anticoagulant therapy, and neural toxicity in associatio

53 er, we estimated VTE recurrence, bleeding on anticoagulant therapy, and survival and tested cancer an

54 ive whole-leg CUS result who did not receive anticoagulant therapy, and were followed up at least 90

55 Discontinuation of anticoagulant therapy appears to be safe after successfu

56 Anticoagulant therapy appears to have a protective effec

57 Normal D-dimer levels after withdrawal of anticoagulant therapy are associated with a reduced risk

58 untreated because the risks associated with anticoagulant therapy are felt to exceed its benefits.

59 ed D-dimer level 1 month after discontinuing anticoagulant therapy are useful parameters in identifyi

60 that employ combinations of antiplatelet and anticoagulant therapies as well as strategies aimed at r

61 Anticoagulant therapy-associated bleeding and pathologic

62 thromboembolism, and therapeutic control of anticoagulant therapy at 6 months.

63 tients with cardiovascular disease as use of anticoagulant therapy becomes more widespread.

64 safety and cost-effectiveness of continuing anticoagulant therapy beyond the acute treatment period

65 ften considered an indication for indefinite anticoagulant therapy, but it is uncertain if this pract

66 LY trial (Randomized Evaluation of Long-Term Anticoagulant Therapy) compared dabigatran 150 and 110 m

67 chemic event while receiving antiplatelet or anticoagulant therapy, compared with 36 of 75 patients (

68 Patients receiving warfarin anticoagulant therapy concomitantly with capecitabine sh

69 ory abnormality after three to six months of anticoagulant therapy correlate with poor outcomes of th

70 Further, as the field of antiplatelet and anticoagulant therapy evolves, potential drug combinatio

71 n when it is given to patients after initial anticoagulant therapy for a first episode of unprovoked

72 After 3 months of anticoagulant therapy for a first episode of unprovoked

73 nsin receptor blocker use, beta-blocker use, anticoagulant therapy for atrial fibrillation, cardiac r

74 Risk schemes can help target anticoagulant therapy for patients at highest risk for A

75 Unfractionated heparin has been the primary anticoagulant therapy for percutaneous coronary interven

76 been shown to be noninferior to conventional anticoagulant therapy for prevention of recurrence and a

77 as been shown to be as effective as standard anticoagulant therapy for the treatment of deep-vein thr

78 ovide reassuring data that women taking oral anticoagulant therapy for venous thromboembolism (VTE) m

79 Oral anticoagulant therapy for venous thromboembolism is very

80 reatment regimen, including antiplatelet and anticoagulant therapies, for these high-risk patients wi

81 Peripheral blood was collected before anticoagulant therapy from cancer patients with acute de

82 e rivaroxaban group and 2149 in the standard anticoagulant therapy group.

83 By 90 days, oral anticoagulant therapy had been prescribed for more patie

84 cardial infarction (STEMI) patients, in whom anticoagulant therapy has been of particular interest.

85 Limitations of current anticoagulant therapies have led us to develop two disti

86 patients with cirrhosis and PVT who receive anticoagulant therapy have increased recanalization and

87 boembolic death were lack of antiplatelet or anticoagulant therapy (hazard ratio [HR], 91.6; P=0.0041

88 47), mitral valve involvement (HR 1.29), and anticoagulant therapy (HR 1.31).

89 resent opportunities to improve evidence for anticoagulant therapies in pediatric VTE through future

90 ombus resolution following standard-duration anticoagulant therapy in as many as 50% of patients.

91 esults is not low enough to justify stopping anticoagulant therapy in men but may be low enough to ju

92 The safety of anticoagulant therapy in patients undergoing bevacizumab

93 Previous studies suggest underuse of anticoagulant therapy in patients with AF.

94 risk ratio for recurrent VTE after stopping anticoagulant therapy in patients with an anticardiolipi

95 Guidelines for anticoagulant therapy in patients with atrial fibrillati

96 , experience-informed approach for tailoring anticoagulant therapy in patients with cancer-associated

97 nd meta-analysis to determine the effects of anticoagulant therapy in patients with cirrhosis and PVT

98 argatroban, a direct thrombin inhibitor, as anticoagulant therapy in patients with HIT or HIT with t

99 d reduce reocclusion when used as adjunctive anticoagulant therapy in patients with ST segment elevat

100 ing or thrombosis and to monitor response to anticoagulant therapy in patients.

101 ism and should influence the decision to use anticoagulant therapy in persons with AF.

102 cal trials comparing thrombolytic therapy vs anticoagulant therapy in pulmonary embolism patients.

103 s, risk for adverse outcome, and efficacy of anticoagulant therapy in the setting of blunt and caroti

104 all controlled study showing the efficacy of anticoagulant therapy in this disease.

105 Besides vitamin K, candidate targets for anticoagulant therapy include thrombin, a key prothrombo

106 0.1%) had received long-term antiplatelet or anticoagulant therapy, including 18 (12.6%) who did not

107 Optimized antiplatelet and anticoagulant therapy--including aspirin, clopidogrel, a

108 Oral anticoagulant therapy is effective antithrombotic treatm

109 An extended duration of anticoagulant therapy is often recommended for obese or

110 Chronic oral anticoagulant therapy is recommended (class I) in patien

111 of recurrent VTE in the first 2 years after anticoagulant therapy is stopped.

112 g 353 patients, that assessed the effects of anticoagulant therapy (low-weight heparin or warfarin vs

113 , these patients can recover, but indefinite anticoagulant therapy may be appropriate to prevent recu

114 Prolonged anticoagulant therapy may be required in patients with r

115 Antiplatelet or anticoagulant therapy may reduce the risk of ischemic ev

116 In addition to antiplatelet therapy, anticoagulant therapy might be indicated for stroke prev

117 their preferences for benefits and risks of anticoagulant therapy: nonfatal stroke, nonfatal myocard

118 Systemic anticoagulant therapy of patients with a clinical diagno

119 should be advised of the potential effect of anticoagulant therapy on menstrual bleeding at the time

120 patients are treated conservatively or with anticoagulant therapy only.

121 lteration in the type or duration of initial anticoagulant therapy or the use of long-term prophylact

122 ntervention, long-term antithrombotic and/or anticoagulant therapy, or possibly aggressive lipid lowe

123 Following a minimum of 3 months of anticoagulant therapy, patients with VTE in association

124 With proliferating treatment options for anticoagulant therapy, physicians and patients must choo

125 one of these factors after standard-duration anticoagulant therapy predict a poor outcome in children

126 mbotic drugs, which include antiplatelet and anticoagulant therapies, prevent and treat many cardiova

127 and observational studies of antiplatelet or anticoagulant therapy, published in any language and rep

128 negative D-dimer results and did not restart anticoagulant therapy, rates of recurrent VTE were 6.7%

129 The Randomized Evaluation of Long-Term Anticoagulant Therapy (RE-LY) trial randomized 18 113 pa

130 (Randomized Evaluation of Long Term Anticoagulant Therapy [RE-LY] With Dabigatran Etexilate;

131 Antiplatelet and anticoagulant therapy reduce the risk of stroke in other

132 sought to determine whether antiplatelet or anticoagulant therapy reduces ischemic complications in

133 Anticoagulant therapy reduces the risk of stroke, and th

134 In the Randomized Evaluation of Long-Term Anticoagulant Therapy (RELY) trial, dabigatran, with app

135 agement of patients receiving long-term oral anticoagulant therapy remains a common but difficult cli

136 However, anticoagulant therapy remains underused, particularly in

137 critical, and transitory discontinuation of anticoagulant therapy should be considered.

138 risk determines how and when postprocedural anticoagulant therapy should be resumed.

139 To prevent recurrence, anticoagulant therapy should be started as soon as possi

140 4% vs. 0%; p = 0.12); all were resolved with anticoagulant therapy, suggesting a thrombotic etiology.

141 as FLIN-Q3 may represent a superior form of anticoagulant therapy than either the native zymogen or

142 In patients selected for oral anticoagulant therapy, the absolute risk difference was

143 The choice of anticoagulant therapy, the degree of monitoring, and the

144 C levels are low, as in early stages of oral anticoagulant therapy, the reduction in protein C would

145 ng the basis for the use of antiplatelet and anticoagulant therapies to optimize procedural success a

146 Rs greater than 4.0 to 5.0, tight control of anticoagulant therapy to maintain the INR between 2.0 an

147 idelines are needed on whether or not to use anticoagulant therapy to prevent stroke in patients with

148 These include optimal duration of anticoagulant therapy, treatment of recurrent VTE, and t

149 he RE-LY (Randomized Evaluation of Long Term Anticoagulant Therapy) trial, we used a previously devel

150 Nevertheless, anticoagulant therapies typically fail to protect humans

151 domly selected from the 1994 registry of the anticoagulant-therapy unit (222 controls).

152 e published literature on real-world data on anticoagulant therapy use, the risks and risk factors of

153 atients' preferences for various outcomes of anticoagulant therapy vary and depend on their previous

154 017, for studies that assessed the effect of anticoagulant therapy vs no treatment in patients with c

155 Despite anticoagulant therapy, VTE recurs frequently in the firs

156 ior vena cava filter insertion compared with anticoagulant therapy was associated with a lower risk o

157 We recorded whether (and for how long) anticoagulant therapy was interrupted preprocedure, whet

158 For example, oral anticoagulant therapy was recommended for 188 who curren

159 Anticoagulant therapy was stopped if D-dimer test result

160 g 186,570 AF patients not on antiplatelet or anticoagulant therapy, we evaluated males with a CHA2DS2

161 ions or contraindications to antiplatelet or anticoagulant therapy were randomly assigned to receive

162 parin bridging therapy, to minimize time off anticoagulant therapy, while the procedural bleed risk d

163 increased use of aggressive antiplatelet and anticoagulant therapies will alter our current understan

164 al trials have compared various durations of anticoagulant therapy with a vitamin K antagonist (ie, w

165 The risk of thrombosis during anticoagulant therapy with these treatments is not well

166 Oral anticoagulant therapy with warfarin sodium is the prefer

167 In no prospective study was anticoagulant therapy withheld without further testing f

168 The duration of anticoagulant therapy would vary depending on the specif