ライフサイエンスコーパス: antiplatelet agent

1 ent) and in atherosclerosis (when used as an antiplatelet agent).

2 he improved synthesis of (S)-clopidogrel (an antiplatelet agent).

3 sease, and aspirin is the most commonly used antiplatelet agent.

4 edictive of clinical utility as a once-daily antiplatelet agent.

5 g x kg(-1) x min(-1) (EPILOG regimen) of the antiplatelet agent.

6 s is the first specific antidote against any antiplatelet agent.

7 et reactivity, and reduced responsiveness to antiplatelet agents.

8 hould not be treated with antithrombotic and antiplatelet agents.

9 n (325 mg/day for > or =7 days) and no other antiplatelet agents.

10 owering lipid levels, and the routine use of antiplatelet agents.

11 hieved, influences the response to different antiplatelet agents.

12 /IIIa inhibitors, which are much more potent antiplatelet agents.

13 ractions between the newer anticoagulant and antiplatelet agents.

14 little actionable pharmacogenetic data with antiplatelet agents.

15 ional adjustment for the longitudinal use of antiplatelet agents.

16 l drug-drug interaction between morphine and antiplatelet agents.

17 d with a delayed onset of action of the oral antiplatelet agents.

18 that MRP4 might serve as a target for novel antiplatelet agents.

19 as the potential to differentiate from other antiplatelet agents.

20 ple--and in blood from patients treated with antiplatelet agents.

21 dosing and monitoring of anticoagulation and antiplatelet agents.

22 hypertension, controlling lipids and use of antiplatelet agents.

23 and an expanding array of anticoagulant and antiplatelet agents.

24 hypertension, warfarin anticoagulation, and antiplatelet agents.

25 ns: warfarin (33.3%), insulins (13.9%), oral antiplatelet agents (13.3%), and oral hypoglycemic agent

26 cium channel blockers, 3 of 3 RCTs (100%) of antiplatelet agents, 2 of 2 RCTs (100%) of statins, 1 of

27 ly higher than it was for patients taking no antiplatelet agents (3.9% vs. 1.6%, p = 0.078).

28 participants were receiving aspirin or other antiplatelet agents, 33% were receiving beta-blockers, 1

29 r cerebrovascular disease to 76.2% for CAD), antiplatelet agents (78.6% overall; range: 53.9% for > o

30 e warfarin (6 trials, 2900 participants) and antiplatelet agents (8 trials, 4876 participants) reduce

31 tched for stroke risk factors and the use of antiplatelet agents (85% of subjects in each group).

32 that lipid-modifying agents (e.g., statins), antiplatelet agents (acetylsalicylic acid, thienopyridin

33 st, and much of the rationale for the use of antiplatelet agents after endovascular peripheral revasc

34 ombolytic agents; and new antithrombotic and antiplatelet agents all offer the potential for improved

35 ventive therapy, but the potential for other antiplatelet agents alone or in combination is explored.

36 Use of antiplatelet agents and angiotensin-converting enzyme in

37 plasma-borne molecules and, second, whether antiplatelet agents and anticoagulants that perturb thro

38 intervention (or fibrinolysis), advances in antiplatelet agents and anticoagulants, and greater use

39 ugs is a high-gain strategy for yielding new antiplatelet agents and could have particular benefit in

40 This loss was sensitive to well-established antiplatelet agents and genetic manipulation of platelet

41 for new molecules being fully efficacious as antiplatelet agents and having a reduced propensity to c

42 ted that P2Y1 antagonists are efficacious as antiplatelet agents and may offer a safety advantage ove

43 The drug-drug interaction between antiplatelet agents and PPIs at the enzymatic level does

44 drug-drug interactions between the available antiplatelet agents and proton pump inhibitors (PPIs).

45 mark randomized studies showing advantage of antiplatelet agents and risk factor modification, and a

46 f medical therapy will be administered using antiplatelet agents and statins, as well as measures to

47 ma, in addition to acquired causes including antiplatelet agents and the new oral anticoagulants.

48 ns for the understanding of new and existing antiplatelet agents and their potential risks.

49 us treatment with oral anticoagulants and/or antiplatelet agents and with higher blood HCQ concentrat

50 iews platelet function, molecular targets of antiplatelet agents, and clinical indications for antipl

51 Statins, antiplatelet agents, and coronary vasodilators protect a

52 ntervention, the use of drug-eluting stents, antiplatelet agents, and embolic protection devices may

53 Treatment options include antiplatelet agents, anticoagulants, surgical closure, o

54 tudy sought to evaluate the relation between antiplatelet agent (APA) use and survival and morbidity

55 ased in nontargeted, low-risk groups in whom antiplatelet agents are appropriate.

56 Antiplatelet agents are emerging as some of the newest a

57 tion with rivaroxaban plus either one or two antiplatelet agents are uncertain.

58 Antiplatelet agents are used to prevent cardiovascular e

59 Antiplatelet agents are widely used to reduce these comp

60 Furthermore, the antiplatelet agent aspirin inhibited platelet-mediated a

61 The antiplatelet agents aspirin, ticlopidine, and the combin

62 Among antiplatelet agents, aspirin and clopidogrel have a simi

63 Therapeutic anticoagulation and use of antiplatelet agents at present focus on the older child.

64 coagulation (OAC) is far more effective than antiplatelet agents at reducing stroke risk in patients

65 Anticoagulants are more effective than antiplatelet agents at reducing stroke risk in patients

66 angioplasty and use of glycoprotein IIb/IIIa antiplatelet agents at the time of angiography were disc

67 Aspirin is the most widely used antiplatelet agent because it is safe, efficient, and in

68 Dense granules also are targeted by antiplatelet agents because of their role in thrombus fo

69 ocumented contraindication to all medicines (antiplatelet agent, beta-blocker, and statin).

70 ld be considered for lipid lowering therapy, antiplatelet agents, beta-blockers, and control of hyper

71 2008 and 2009 in appropriate prescription of antiplatelet agents, beta-blockers, angiotensin-converti

72 hrombosis, as well as its shared (with other antiplatelet agents) bleeding liability.

73 at in vivo c7E3 Fab functions not only as an antiplatelet agent but also as an anticoagulant; direct

74 , and this provides a situation in which new antiplatelet agents can be evaluated.

75 Clopidogel (Plavix), a newer antiplatelet agent, can increase the risk of bleeding.

76 The antiplatelet agent clopidogrel adds to the benefit of as

77 carotid artery injuries (by CTA and DSA) on antiplatelet agent developed stroke related to carotid a

78 Exposure to antiplatelet agents during the at-risk period was associ

79 d the corresponding maintenance doses of the antiplatelet agents during the following 24 hours and un

80 antiinflammatory drugs (NSAIDs) or selected antiplatelet agents (e.g., NSAID prescription in a patie

81 Dual antiplatelet agents, evaluation for ischemia, and close

82 Aspirin is the most widely used antiplatelet agent for preventing and treating vascular

83 nesium in myocardial infarction, calcium and antiplatelet agents for prevention of preeclampsia), whe

84 ished randomized trials of anticoagulants or antiplatelet agents for stroke prevention provide solid

85 cy of anticoagulation is superior to that of antiplatelet agents for stroke prophylaxis in AF, the op

86 24 randomised controlled trials, evaluating antiplatelet agents, for the prevention of pre-eclampsia

87 of stroke, we tested the effects of a potent antiplatelet agent given both before and after the onset

88 ew evaluates and interprets the role of oral antiplatelet agents, glycoprotein IIb-IIIa inhibitors, a

89 or recent gastrointestinal bleed, used dual antiplatelet agents, had a medical condition requiring p

90 Although the use of more powerful antiplatelet agents has been associated with increased r

91 Ticagrelor, a novel reversible antiplatelet agent, has a Food and Drug Administration (

92 strating their benefits in patient outcomes, antiplatelet agents have become paramount in the prevent

93 the development of novel stent scaffolds and antiplatelet agents holds much promise for reducing the

94 ded that (i) Ap(s)pCHClpp(s)A is a promising antiplatelet agent; (ii) it is resistant to blood phosph

95 rrently, eptifibatide is used as the adjunct antiplatelet agent in the majority of patients undergoin

96 ow determination of the effectiveness of new antiplatelet agents in humans.

97 ickle cell anemia, which suggests a role for antiplatelet agents in modifying disease events.

98 Data for antiplatelet agents in persons with CKD are frequently d

99 the use of less intensive anticoagulation or antiplatelet agents in some patient subsets, anticoagula

100 a loading dose of the currently recommended antiplatelet agents in ST-segment-elevation myocardial i

101 ental and clinical models suggest a role for antiplatelet agents in the prevention of thrombosis.

102 ghlighting the need for clinical research of antiplatelet agents in this population.

103 n = 50), (2) healthy volunteers treated with antiplatelet agents in vitro (n = 10), and (3) patients

104 logical concentrations of antithrombotic and antiplatelet agents in vitro.

105 ompare clopidogrel with ticagrelor, a potent antiplatelet agent, in patients with peripheral artery d

106 unfractionated heparin (UFH) and the use of antiplatelet agents including aspirin, thienopyridines,

107 As the availability of more effective antiplatelet agents increases, it is time to revisit the

108 sting that previous observations with potent antiplatelet agents indicating differential results are

109 r those exposed to both an anticoagulant and antiplatelet agent (IRR, 10.48; 95% CI, 8.16-13.45), 140

110 6.5; 95% CI, 25.9-27.0) for those exposed to antiplatelet agents (IRR, 1.31; 95% CI, 1.29-1.33).

111 isease is unresolved, and commonly, a single antiplatelet agent is added to oral anticoagulation.

112 Dilazep, an antiplatelet agent, is an adenosine uptake inhibitor kno

113 the potentially significant interaction with antiplatelet agents, leading to impaired inhibition of p

114 activation, and in turn PMC formation, with antiplatelet agents may prove beneficial in developing a

115 all, inconclusive trials have suggested that antiplatelet agents may reduce thrombosis of new fistula

116 Antiplatelet agents must also be considered in the perio

117 Compared with controls not taking antiplatelet agents (n = 255), the combination of aspiri

118 f percutaneous coronary intervention, making antiplatelet agents necessary components of the pharmaco

119 atelet inhibition with combined early use of antiplatelet agents needs further evaluation in prospect

120 Antiplatelet agents or anticoagulants were not used in 5

121 tionship between aspirin dose and the potent antiplatelet agent prasugrel in the TRITON-TIMI 38 (Tria

122 Choice of initial antiplatelet agent (prasugrel or clopidogrel).

123 included male sex, filling beta-blocker and antiplatelet agent prescriptions, and attending cardiac

124 Antiplatelet agents presently used in the secondary prev

125 ns with stable or no cardiovascular disease, antiplatelet agents prevented myocardial infarction but

126 Adjusted-dose warfarin and antiplatelet agents reduce stroke by approximately 60% a

127 emoglobin and reduced creatinine clearance), antiplatelet agent-related factors (higher on-treatment

128 After risk adjustment, prior use of antiplatelet agents remained associated with higher odds

129 ical outcomes in patients requiring a single antiplatelet agent remains unknown.

130 In vivo testing of novel antiplatelet agents requires informative biomarkers.

131 tients require a monitored setting and their antiplatelet agents restarted immediately.

132 in alone, and group 4 (n=20) received 3 oral antiplatelet agents: ridogrel, ketanserin, and clopidogr

133 beta-blockers, statins, and antiplatelet agents should be considered for all patient

134 Program that promoted antiplatelet agents, statins, angiotensin-converting enz

135 Use of clopidogrel, a more potent antiplatelet agent than aspirin, appears to decrease rec

136 reas rejection and clopidogrel treatment, an antiplatelet agent that has been associated with immunol

137 discovery of 4 (SCH 530348), a potent, oral antiplatelet agent that is currently undergoing Phase-II

138 n of GPIb-IX, and also suggest a new type of antiplatelet agent that may be potentially useful in pre

139 Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellula

140 itric oxide (NO) is a potent vasodilator and antiplatelet agent that suppresses vascular smooth muscl

141 tformin exemplifies a promising new class of antiplatelet agents that are highly effective at inhibit

142 The anticoagulants and antiplatelet agents that patients are receiving preopera

143 affect human cells, (ii) glucocorticoid and antiplatelet agents that together suppress the productio

144 Among users of antiplatelet agents, the rates were 5.3% per year and 5.

145 ion between high-dose aspirin and the potent antiplatelet agent ticagrelor.

146 al imaging, genetically engineered mice, and antiplatelet agents to determine how variations in the e

147 should facilitate the development of better antiplatelet agents to treat cardiovascular diseases.

148 3 antagonists, the first rationally designed antiplatelet agents, to prevent and treat thrombotic car

149 Despite the use of antiplatelet agents, usually aspirin, in patients who ha

150 th commonly used cardiovascular medications: antiplatelet agents, warfarin, statins, beta-blockers, d

151 Additive effects of antiplatelet agents were readily detectable with both he

152 ypothesis, the effects of c7E3 Fab and other antiplatelet agents were tested in a thrombin generation

153 had an IC50 of 0.24 microM and was a potent antiplatelet agent when dosed intravenously in a canine

154 nalising therapies, including combination of antiplatelet agents with intravenous thrombolysis, bridg

155 y 0.3% per year while on treatment with >/=1 antiplatelet agent, with increased risk independently as

156 escriptions for statins, BBs, ACEIs/ARBs, or antiplatelet agents within 30 days after discharge.