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 r to clopidogrel, or by reducing the dose of antiplatelet agents.

15 little actionable pharmacogenetic data with antiplatelet agents.

16 ional adjustment for the longitudinal use of antiplatelet agents.

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

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

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

20 as the potential to differentiate from other antiplatelet agents.

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

22 dosing and monitoring of anticoagulation and antiplatelet agents.

23 hypertension, controlling lipids and use of antiplatelet agents.

24 and an expanding array of anticoagulant and antiplatelet agents.

25 hypertension, warfarin anticoagulation, and antiplatelet agents.

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

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

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

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

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

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

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

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

34 ification of anticoagulation, addition of an antiplatelet agent, adjunctive treatment for thrombosis,

35 he roles of anticoagulation alone or with an antiplatelet agent after transcatheter aortic-valve impl

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

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

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

39 -dose aspirin remains the most commonly used antiplatelet agent among patients with atherosclerotic c

40 Use of antiplatelet agents and angiotensin-converting enzyme in

41 ecommendations for the evidence-based use of antiplatelet agents and anticoagulant agents after strok

42 Antiplatelet agents and anticoagulants are a mainstay fo

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

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

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

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

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

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

49 exposure to and dosing regimens of edoxaban, antiplatelet agents and other concomitant medications of

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

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

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

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

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

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

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

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

58 Statins, antiplatelet agents, and coronary vasodilators protect a

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

60 associated with a widely prescribed class of antiplatelet agents, and highlight differences between h

61 indication for antithrombotic therapy, i.e. antiplatelet agents, anticoagulant drugs, or their combi

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

63 nd premature PAD received comparatively less antiplatelet agents, any statin, and HIS.

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

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

66 Antiplatelet agents are emerging as some of the newest a

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

68 Antiplatelet agents are used to prevent cardiovascular e

69 Antiplatelet agents are widely used to reduce these comp

70 (an anticoagulant agent) or eptifibatide (an antiplatelet agent) are unclear.

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

72 The antiplatelet agents aspirin, ticlopidine, and the combin

73 Among antiplatelet agents, aspirin and clopidogrel have a simi

74 as having continued either a single or dual antiplatelet agent at the time of device surgery.

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

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

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

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

79 Adult patients taking at least one antiplatelet agent based on presenting history and docum

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

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

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

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

84 2008 and 2009 in appropriate prescription of antiplatelet agents, beta-blockers, angiotensin-converti

85 bed oral anticoagulant and/or thienopyridine antiplatelet agents between January 1, 2016, and Decembe

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

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

88 cation for bridging therapy with intravenous antiplatelet agents, but management is guided primarily

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

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

91 The antiplatelet agent clopidogrel adds to the benefit of as

92 models relative to the clinically important antiplatelet agent clopidogrel and provide a potential o

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

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

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

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

97 Dual antiplatelet agents, evaluation for ischemia, and close

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

99 extracellular vesicles, and the potential of antiplatelet agents for cancer treatment.

100 change clinical practice through addition of antiplatelet agents for HZ and initiatives to increase H

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

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

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

104 24 randomised controlled trials, evaluating antiplatelet agents, for the prevention of pre-eclampsia

105 , blood pressure-lowering, antidiabetic, and antiplatelet agents from October 1, 2013, until January

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

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

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

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

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

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

112 However, some antiplatelet agents have shown a differential treatment

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

114 thromboembolic events was also observed with antiplatelet agents (HR: 0.54; 95% CI: 0.32 to 0.92) but

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

116 Indobufen is used as an alternative antiplatelet agent in some countries, despite an absence

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

118 latelet cross-talk with effective and atoxic antiplatelet agents in combination with anticancer drugs

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

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

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

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

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

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

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

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

127 logical concentrations of antithrombotic and antiplatelet agents in vitro.

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

129 oint inhibitor therapies in combination with antiplatelet agents, in patients with PD-L1 negative tum

130 and appropriate dosing of anticoagulant and antiplatelet agents, in secondary prevention strategies

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

132 inical studies where it may be combined with antiplatelet agents, including aspirin and/or clopidogre

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

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

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

136 6.5; 95% CI, 25.9-27.0) for those exposed to antiplatelet agents (IRR, 1.31; 95% CI, 1.29-1.33).

137 rocedural cangrelor is an effective and safe antiplatelet agent, irrespective of BMI.

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

139 The use of a single antiplatelet agent is commonly recommended for the long-

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

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

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

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

144 Antiplatelet agents must also be considered in the perio

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

146 on in platelet count that is not affected by antiplatelet agents, nearly normal responses to platelet

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

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

149 The effects of antiplatelet agents on the cerebral metastasis formation

150 Antiplatelet agents or anticoagulants were not used in 5

151 efficacy of prevention strategies, including antiplatelet agents, oral anticoagulants or left atrial

152 blockers (P value for interaction = .76), or antiplatelet agents (P value for interaction = .49).

153 han 100 x 103/muL, including those receiving antiplatelet agents, platelet transfusion is not recomme

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

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

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

157 Antiplatelet agents presently used in the secondary prev

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

159 does not seem to exacerbate with the use of antiplatelet agents, provided successful obliteration of

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

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

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

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

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

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

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

167 ming of revascularization, pretreatment with antiplatelet agents, selection of vascular access, choic

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

169 AF, anticoagulation has to be combined with antiplatelet agents (so called, dual pathway antithrombo

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

171 tion can be achieved by discontinuation of 1 antiplatelet agent, switching from a potent P2Y12 inhibi

172 iments of whole blood perfusion with various antiplatelet agents targeting COX-1, P2Y1, or the IP rec

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

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

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

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

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

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

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

180 The anticoagulants and antiplatelet agents that patients are receiving preopera

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

182 e development of numerous anticoagulants and antiplatelet agents, the mortality rate associated with

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

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

185 hermore, there is confusion over alternative antiplatelet agents to be used in these patients.

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

187 myocardial revascularization and the use of antiplatelet agents to limit thrombosis.

188 ntive medications such as lipid-lowering and antiplatelet agents to reduce the risk for cardiovascula

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

190 3 antagonists, the first rationally designed antiplatelet agents, to prevent and treat thrombotic car

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

192 The clinical efficacy and safety of antiplatelet agents vary among patients.

193 ymptomatic severe aortic valve stenosis; and antiplatelet agents vorapaxar and prasugrel for reducing

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

195 cribed oral anticoagulant and thienopyridine antiplatelet agents was divided into development and val

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

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

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

199 athway inhibition strategies that combine an antiplatelet agent with an anticoagulant drug.

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

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

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