ライフサイエンスコーパス: antiplatelet

1 larization (15% vs. 34%) and to receive dual antiplatelet (26% vs. 43%), statin (16% vs. 26%), or oth

2 botic effect during a window of limited oral antiplatelet action.

3 Onset of antiplatelet activity was determined by the rate and ext

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

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

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

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

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

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

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

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

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

13 6.5; 95% CI, 25.9-27.0) for those exposed to antiplatelet agents (IRR, 1.31; 95% CI, 1.29-1.33).

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

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

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

17 Antiplatelet agents and anticoagulants are a mainstay fo

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

19 Antiplatelet agents are widely used to reduce these comp

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

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

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

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

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

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

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

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

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

29 Alternative strategies with new drugs, both antiplatelet and anticoagulant agents, and new coronary

30 Antiplatelet and anticoagulant medications are the corne

31 y a central role in stroke pathogenesis, and antiplatelet and anticoagulant therapies are central to

32 on cascade, forming the basis for the use of antiplatelet and anticoagulant therapies to optimize pro

33 Data on antiplatelet and antithrombotic therapy were collected.

34 ationale and clinical evidence for combining antiplatelet and oral anticoagulant therapy in patients

35 etylation of COX-2 and may contribute to its antiplatelet and other pharmacologic effects.

36 a single dose of IV desmopressin (DDAVP) for antiplatelet-associated intracranial hemorrhage based on

37 DDAVP treatment at recognition of antiplatelet-associated intracranial hemorrhage versus n

38 analyzing DDAVP effectiveness and safety in antiplatelet-associated intracranial hemorrhage.

39 lus aspirin [75 to 100 mg] once daily) or an antiplatelet-based strategy (clopidogrel [75 mg] plus as

40 rombotic strategy was more effective than an antiplatelet-based strategy in preventing subclinical le

41 ations and a higher risk of bleeding than an antiplatelet-based strategy.

42 tions and a higher risk of bleeding than the antiplatelet-based strategy.

43 number of secondary prevention medications (antiplatelets, beta-blockers, statins, and renin-angiote

44 est when a VKA was used concurrently with an antiplatelet drug (low-dose aspirin and a VKA: 3.6% of c

45 is prototype can act as a real-time assay of antiplatelet drug pharmacokinetics.

46 enetic test results significantly influenced antiplatelet drug prescribing; however, almost half of C

47 roup) or no genotyping (usual care) to guide antiplatelet drug selection.

48 r therapy with a vitamin K antagonist and an antiplatelet drug, 1.28 (95% CI, 1.13-1.44) for therapy

49 erapy of a direct oral anticoagulant with an antiplatelet drug, 3.73 (95% CI, 3.23-4.31) for vitamin

50 associated with combined use of a VKA and an antiplatelet drug.

51 troke, or myocardial infarction treated with antiplatelet drugs (mainly aspirin based, without routin

52 In a stability analysis excluding antiplatelet drugs from the exposure definition, more me

53 Antiplatelet drugs induce only a moderate relative risk

54 h established CAD, secondary prevention with antiplatelet drugs is an asset of pharmacological strate

55 , be considered for the development of novel antiplatelet drugs to fight cardiovascular diseases in h

56 the evidence for the efficacy and safety of antiplatelet drugs, and to provide practicing cardiologi

57 n of antithrombotic therapy with more potent antiplatelet drugs, dual antiplatelet therapy, or vitami

58 Y12 inhibitors are among the most successful antiplatelet drugs, however, show remarkable variability

59 ay competing risk models (sex, age, smoking, antiplatelet drugs, previous vascular disease, diabetes

60 the ensuing thrombosis) relative to current antiplatelet drugs.

61 are concerns with ticagrelor, as with other antiplatelet drugs.

62 We show that rivaroxaban's antiplatelet effect is plasma dependent but independent

63 Therefore, rivaroxaban exerts an antiplatelet effect that together with its well-known po

64 those with diabetes, may not have an optimal antiplatelet effect.

65 studies have shown that morphine blunts the antiplatelet effects of oral adenosine diphosphate recep

66 The antiplatelet effects of ticagrelor cannot be reversed wi

67 ided immediate and sustained reversal of the antiplatelet effects of ticagrelor, as measured by multi

68 Aspirin exerts antiplatelet effects through irreversible inhibition of

69 efore, as NOX1 inhibitors are likely to have antiplatelet effects without associated bleeding risks,

70 ous P2Y(12) inhibitor with prompt and potent antiplatelet effects.

71 ndrome patients, to allow dissipation of its antiplatelet effects.

72 Dairy polar lipids (PL) seem to exhibit antiplatelet effects.

73 udy, data were collected including age, sex, antiplatelet factor 4/heparin enzyme-linked immunosorben

74 n release assay and 80 patients had positive antiplatelet factor 4/heparin enzyme-linked immunosorben

75 If antiplatelet factor 4/heparin enzyme-linked immunosorben

76 A total of 135 patients had 4Ts, antiplatelet factor 4/heparin enzyme-linked immunosorben

77 as noted in nine of 11 patients (81.8%) with antiplatelet factor 4/heparin enzyme-linked immunosorben

78 parin-induced thrombocytopenia and underwent antiplatelet factor 4/heparin enzyme-linked immunosorben

79 urred in the rivaroxaban group and 38 in the antiplatelet group (5.8 and 3.4 per 100 person-years, re

80 oxaban group and in 33 of 102 (32.4%) in the antiplatelet group (difference, -20.0 percentage points;

81 p, as compared with 11 of 101 (10.9%) in the antiplatelet group (difference, -8.8 percentage points;

82 rivaroxaban group and in 78 patients in the antiplatelet group (incidence rates, 9.8 and 7.2 per 100

83 dose of 75 mg daily for the first 3 months) (antiplatelet group).

84 ress this critical gap, TAILOR-PCI (Tailored Antiplatelet Initiation to Lessen Outcomes due to Decrea

85 ext of contemporary pharmacotherapy, optimal antiplatelet management with percutaneous coronary inter

86 ties, 772 (18%) were taking anticoagulant or antiplatelet medication, and alcohol was contributory in

87 nts (heparins, phenprocoumon, apixaban), and antiplatelet medication.

88 Whereas antiplatelet medications have been the preferred therapy

89 g cardiovascular outcomes of antidiabetic or antiplatelet medications.

90 that the effect of aspirin is related to an antiplatelet mode of action.

91 y lower in the PFO closure group than in the antiplatelet-only group (22 patients [5.7%] vs. 20 patie

92 higher in the PFO closure group than in the antiplatelet-only group (4.6% vs. 0.9%, P=0.02).

93 re group and in 27.8% of the patients in the antiplatelet-only group (P=0.22).

94 p) or to receive antiplatelet therapy alone (antiplatelet-only group).

95 s why dual pathway inhibition is superior to antiplatelet or anticoagulant therapy alone, (3) compare

96 nts with previous ulcer bleeding who require antiplatelet or anticoagulant therapy for cardiovascular

97 aspirin and those who were already receiving antiplatelet or anticoagulant therapy were excluded.

98 s using a rapid turnaround test would change antiplatelet prescribing following percutaneous coronary

99 ntervention (PVI), there are limited data on antiplatelet prescribing patterns post-procedure.

100 The antiplatelet response to low-dose aspirin can be markedl

101 induced a profound, rapid, and dose-related antiplatelet response.

102 idence interval [CI], 0.80-0.94), nonaspirin antiplatelets (RR=0.83; 95% CI, 0.75-0.91), beta blocker

103 patient specific benefit/risk of holding an antiplatelet should be carefully considered.

104 o guide their choice of the most appropriate antiplatelet strategy for the individual patient present

105 Routine antiplatelet strategy was DAPT for 3 months post procedu

106 telet receptor could be harnessed as a novel antiplatelet strategy.

107 file, we have therefore turned to PAR4 as an antiplatelet target.

108 Advances in antiplatelet therapies for patients with cardiovascular

109 Sex-specific differences in response to antiplatelet therapies have been described.

110 Antiplatelet therapies have been proposed for the treatm

111 trials evaluating the risks and benefits of antiplatelet therapies in patients with atherosclerosis.

112 gh-content chemical library screening of new antiplatelet therapies.

113 gh-content screening of new more efficacious antiplatelet therapies.

114 hematologists about the 2 most commonly used antiplatelet therapies: Could the patient be aspirin "re

115 of major bleeding by 40% compared with dual antiplatelet therapy (1.97% versus 3.13%; hazard ratio [

116 [4%] of 224) than among those receiving dual antiplatelet therapy (31 [15%] of 208; p<0.0001); NOACs

117 Most patients receiving antiplatelet therapy (3613 of 4527 [80%]) received low-d

118 OAC (58.0% versus 60.7%), had similar use of antiplatelet therapy (44.0% versus 41.3%) after catheter

119 short-term oral anticoagulation (OAC) versus antiplatelet therapy (APT) following LAAC.

120 Antiplatelet therapy (APT; aspirin/clopidogrel, ticagrel

121 ticoagulation, empirical treatment with dual antiplatelet therapy (aspirin plus clopidogrel) for 3 to

122 compare the safety and efficacy of intensive antiplatelet therapy (combined aspirin, clopidogrel, and

123 agrelor monotherapy following one-month dual antiplatelet therapy (DAPT) after percutaneous coronary

124 effect of 30 months versus 12 months of dual antiplatelet therapy (DAPT) after percutaneous coronary

125 The optimal duration of dual antiplatelet therapy (DAPT) after percutaneous coronary

126 es the associations between patterns of dual antiplatelet therapy (DAPT) cessation and adverse events

127 ermine the impact of baseline anemia on dual antiplatelet therapy (DAPT) cessation patterns <=2 years

128 The benefits and harms of dual antiplatelet therapy (DAPT) continuation beyond 1 year a

129 treatment guidance endorsing shortened dual antiplatelet therapy (DAPT) duration in high bleeding ri

130 aneous coronary intervention to 1-month dual antiplatelet therapy (DAPT) followed by 23-month ticagre

131 been validated in patients treated with dual antiplatelet therapy (DAPT) following percutaneous coron

132 ent guidelines suggesting a benefit for dual antiplatelet therapy (DAPT) following peripheral vascula

133 Dual antiplatelet therapy (DAPT) is prescribed to millions of

134 Dual antiplatelet therapy (DAPT) reduced stroke risk in high-

135 The dual-antiplatelet therapy (DAPT) score was developed to ident

136 ommend that these patients also receive dual antiplatelet therapy (DAPT) to reduce the risk of ischem

137 Dual antiplatelet therapy (DAPT) with aspirin plus a P2Y12 in

138 1, n=709); rivaroxaban 2.5 mg bid plus dual antiplatelet therapy (DAPT; Group 2, n=709); and warfari

139 , with aspirin or a P2Y(12) inhibitor), dual antiplatelet therapy (eg, aspirin combined with a P2Y(12

140 uch antithrombotic strategies include single antiplatelet therapy (eg, with aspirin or a P2Y(12) inhi

141 1, n=709); rivaroxaban 2.5 mg bid plus dual antiplatelet therapy (group 2, n=709); and warfarin plus

142 apy (group 2, n=709); and warfarin plus dual antiplatelet therapy (group 3, n=706).

143 ng or MI rate, compared with continuation of antiplatelet therapy (HR, 0.32 [95% CI, 0.11-0.92]; P=0.

144 0.71%) or were not (0.69%) treated with dual antiplatelet therapy (HR, 1.02; 95% CI, 0.54-1.95).

145 ference in the likelihood of prescription of antiplatelet therapy (odds ratio [OR], 0.94 [95% CI, 0.6

146 AD and CAD were more likely to be prescribed antiplatelet therapy (odds ratio [OR]: 2.6; 95% confiden

147 in a 2:1 ratio, to undergo PFO closure plus antiplatelet therapy (PFO closure group) or to receive a

148 ternative noncontraindicated treatment or to antiplatelet therapy (randomization groups 2 and 3).

149 with a novel oral anticoagulant plus single antiplatelet therapy (SAPT) reduces bleeding or cardiova

150 ct of an experimental strategy (1-month dual antiplatelet therapy [DAPT] followed by 23-month ticagre

151 In the debate about the duration of dual antiplatelet therapy after drug-eluting stent implantati

152 ndation ("may be considered") to extend dual antiplatelet therapy after drug-eluting stent implantati

153 ontinuation of the aspirin component of dual antiplatelet therapy after percutaneous coronary interve

154 tcomes of HBR patients receiving 30-day dual antiplatelet therapy after percutaneous coronary interve

155 inclusion/exclusion criteria and 30-day dual antiplatelet therapy after percutaneous coronary interve

156 et therapy (PFO closure group) or to receive antiplatelet therapy alone (antiplatelet-only group).

157 f PFO closure plus antiplatelet therapy with antiplatelet therapy alone was performed with combined d

158 the comparison of oral anticoagulation with antiplatelet therapy alone was performed with combined d

159 gulants and in 7 of 174 patients assigned to antiplatelet therapy alone.

160 latelet therapy than among those assigned to antiplatelet therapy alone; however, PFO closure was ass

161 were diagnosed on CT (252 assigned to start antiplatelet therapy and 255 assigned to avoid antiplate

162 m patients with bleeding risk factors (e.g., antiplatelet therapy and anticoagulation or coagulation

163 Despite modest increases in antiplatelet therapy and coronary revascularization afte

164 rs of premature discontinuation or switch of antiplatelet therapy and their association with major ad

165 apid and useful approach for monitoring both antiplatelet therapy and traumatic bleeding risk.

166 vent occurrences further solidified the dual antiplatelet therapy approach.

167 0.55%) or were not (0.52%) treated with dual antiplatelet therapy at hospital discharge (HR, 1.04; 95

168 De-escalation of antiplatelet therapy at the time of BARC 3 bleeding coul

169 De-escalation of antiplatelet therapy at the time of BARC 3 bleeding was

170 latelet agents, and clinical indications for antiplatelet therapy before focusing on a frequent quest

171 bosis, any bleeding, and major bleeding with antiplatelet therapy compared with none ranged from 0.26

172 uld play a role in these late bleedings, and antiplatelet therapy could be a precipitating factor.

173 Concomitant antiplatelet therapy doubled the risk of CSH during devi

174 -phase cardiovascular benefit of potent dual antiplatelet therapy driven largely by reducing de novo

175 eluting stents, which require prolonged dual antiplatelet therapy due to the increased risk of late a

176 nted to further define optimal management of antiplatelet therapy during anticoagulation in surgical

177 For patients on dual antiplatelet therapy followed for 1 year, the hazard rat

178 asis on reduced duration and/or intensity of antiplatelet therapy following percutaneous coronary int

179 clinical and genetic factors when selecting antiplatelet therapy following percutaneous coronary int

180 receiving either routine anticoagulation or antiplatelet therapy for existing conditions prior to be

181 sion, diabetes mellitus and lipid disorders, antiplatelet therapy for high vascular risk patients, an

182 Ticagrelor is an effective antiplatelet therapy for patients with coronary atherosc

183 ifically the selection of anticoagulation vs antiplatelet therapy for secondary prevention.

184 ded, randomized placebo-controlled trials of antiplatelet therapy for the prevention of ischemic even

185 equired brain MRI protocol (122 in the start antiplatelet therapy group and 132 in the avoid antiplat

186 iplatelet therapy group and 132 in the avoid antiplatelet therapy group).

187 Net costs were calculated between antiplatelet therapy groups according to level of ischem

188 However, dual antiplatelet therapy has been preliminarily associated w

189 on and symptoms of claudication was low: any antiplatelet therapy in 35.7% (standard error [SE]: 2.7%

190 ble evidence about the risk-benefit ratio of antiplatelet therapy in adults with ET is highly uncerta

191 evidence of heterogeneity in the effects of antiplatelet therapy in any exploratory subgroup analyse

192 ctiveness of 1-month DAPT followed by single antiplatelet therapy in HBR patients undergoing percutan

193 attractive alternative to blocking PAR1 for antiplatelet therapy in humans.

194 d therapy was superior to warfarin plus dual antiplatelet therapy in lowering bleeding outcomes regar

195 Myocardial Infarction in Patients on Modern Antiplatelet Therapy in the Swedish Web System for Enhan

196 Tailoring antiplatelet therapy intensity to patient risk may impro

197 aspirin, we aimed to establish whether dual antiplatelet therapy involving cilostazol is safe and ap

198 ts prospectively and prescribing alternative antiplatelet therapy is beneficial.

199 ntion of coronary artery disease (CAD), oral antiplatelet therapy is essential.

200 ase of coronary intervention, temporary dual antiplatelet therapy is mandatory as well.

201 Antiplatelet therapy is preferred for lesions characteri

202 Although dual antiplatelet therapy is recommended, single antiplatelet

203 ed with biolimus-A9 followed by 1-month dual antiplatelet therapy is safer and more effective than a

204 Antiplatelet therapy is the mainstay for the treatment o

205 Anticoagulant or antiplatelet therapy is the preferred treatment option f

206 More potent and longer antiplatelet therapy may be beneficial for patients unde

207 from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent

208 als in the UK that assessed whether starting antiplatelet therapy might reduce the risk of recurrent

209 for shortening the minimum duration of dual antiplatelet therapy needed after coronary intervention.

210 s to: (1) evaluate the effect of concomitant antiplatelet therapy on CSH, and (2) understand the rela

211 ally or statistically significant hazards of antiplatelet therapy on recurrent intracerebral haemorrh

212 lude all but a very modest harmful effect of antiplatelet therapy on recurrent intracerebral haemorrh

213 sought to examine the effect of more potent antiplatelet therapy on the basis of the timing and etio

214 time of stroke, 37674 (39.9%) were receiving antiplatelet therapy only, and 28583 (30.3%) were not re

215 cannot tolerate or have contraindications to antiplatelet therapy or in the setting of a subarachnoid

216 to oral anticoagulation and used only single antiplatelet therapy or nothing.

217 antiplatelet therapy is recommended, single antiplatelet therapy or oral anticoagulation is frequent

218 is, any bleeding, and major bleeding without antiplatelet therapy ranged from 5 to 110 (median, 20),

219 Dual antiplatelet therapy reduces ischemic events in cardiova

220 More intensive antiplatelet therapy reduces the risk of VTE.

221 mptomatic atherosclerosis and more intensive antiplatelet therapy reduces VTE risk beyond aspirin mon

222 Postdischarge antiplatelet therapy regimen rates were determined (none

223 Triple antiplatelet therapy should not be used in routine clini

224 (The Dual Antiplatelet Therapy Study [DAPT Study]; NCT00977938).

225 those assigned to PFO closure combined with antiplatelet therapy than among those assigned to antipl

226 ntaneous Cerebral Hemorrhage Associated With Antiplatelet Therapy trial, our results suggest no hemos

227 Meta-analysis of dual antiplatelet therapy versus monotherapy with P2Y12 inhib

228 randomly assigned to either anticoagulant or antiplatelet therapy versus placebo or no treatment.

229 eding use of therapeutic warfarin, NOACs, or antiplatelet therapy was associated with lower odds of m

230 By contrast, intensive antiplatelet therapy was associated with more, and more

231 Antiplatelet therapy was used in 67.9% of the population

232 on, and patients with an indication for dual antiplatelet therapy were excluded.

233 The observation that dual antiplatelet therapy with acetylsalicylic acid and clopi

234 The comparison of PFO closure plus antiplatelet therapy with antiplatelet therapy alone was

235 Dual antiplatelet therapy with aspirin and a P2Y(12) inhibito

236 Although dual antiplatelet therapy with aspirin and clopidogrel reduce

237 d in the ADAPT-DES study (Assessment of Dual Antiplatelet Therapy With Drug-Eluting Stents) according

238 ADAPT-DES (Assessment of Dual Antiplatelet Therapy With Drug-Eluting Stents) was a pro

239 ticenter ADAPT-DES study (Assessment of Dual Antiplatelet Therapy With Drug-Eluting Stents) were stra

240 ROMETHEUS, ADAPT-DES [the Assessment of Dual AntiPlatelet Therapy with Drug-Eluting Stents], THIN [Th

241 rial comparing point-of-care genotype-guided antiplatelet therapy with routine care to determine whet

242 Intensive antiplatelet therapy with three agents might be more eff

243 tation after loading and maintenance of dual antiplatelet therapy with ticagrelor and the influence o

244 reased risk of bleeding compared with single antiplatelet therapy without significant ischemic benefi

245 of the patients (all of them in patients on antiplatelet therapy).

246 eding were 1.13 (95% CI, 1.06-1.19) for dual antiplatelet therapy, 1.82 (95% CI, 1.76-1.89) for thera

247 eceived coronary revascularization, 22% dual-antiplatelet therapy, and 71% high-dose statin therapy v

248 ted with the decision for DAPT versus single antiplatelet therapy, and further study is required to u

249 otensin system blockers, beta-blockers, dual antiplatelet therapy, and long-term cardiovascular event

250 Options for management include antiplatelet therapy, carotid endarterectomy and carotid

251 In 682 patients not treated with antiplatelet therapy, circulating PCSK9 and 11-dh-TxB2 w

252 des cardiovascular risk reduction and use of antiplatelet therapy, depending on myeloproliferative ne

253 d myocardial infarctions with prolonged dual antiplatelet therapy, findings that support the new Clas

254 etes and a history of PCI who have tolerated antiplatelet therapy, have high ischaemic risk, and low

255 tiplatelet therapy and 255 assigned to avoid antiplatelet therapy, of whom one withdrew and was not a

256 py with more potent antiplatelet drugs, dual antiplatelet therapy, or vitamin K antagonists further r

257 d to identify patients with ACS who, despite antiplatelet therapy, remain at high cardiovascular risk

258 n receptor blockers, beta-blockers, and dual antiplatelet therapy, respectively.

259 f patients with 0, 1, 2, or 3 factors (i.e., antiplatelet therapy, thrombopenia [< 150 G/L], and prev

260 tion (both NOACs and warfarin), but not dual antiplatelet therapy, was effective in prevention or tre

261 tive patients were planned for 12-month dual antiplatelet therapy, whereas troponin-negative patients

262 n, but their use necessitates prolonged dual antiplatelet therapy, which increases costs and bleeding

263 Perioperative management of antiplatelet therapy, which necessitates concomitant eva

264 r monotherapy compared with traditional dual antiplatelet therapy.

265 patients with early discontinuation of dual antiplatelet therapy.

266 of approaches using anticoagulants on top of antiplatelet therapy.

267 ative patients were planned for 1-month dual antiplatelet therapy.

268 acerebral haemorrhage compared with avoiding antiplatelet therapy.

269 ardiovascular risk factors and unaffected by antiplatelet therapy.

270 acerebral haemorrhage compared with avoiding antiplatelet therapy.

271 brain imaging features modify the effects of antiplatelet therapy.

272 ional, and clinical sciences in the field of antiplatelet therapy.

273 d dipyridamole) with that of guideline-based antiplatelet therapy.

274 cker treatment, and a neutral effect of dual antiplatelet therapy.

275 tent (DCS) or a BMS followed by 1-month dual antiplatelet therapy.

276 h MV score could benefit from a personalized antiplatelet therapy.

277 .9% and 89.3% of patients were taking single antiplatelet therapy.

278 cagrelor plus ASA following 3 months of dual antiplatelet therapy.

279 l risk of ischaemic events despite receiving antiplatelet therapy.

280 ommon reason for premature cessation of dual antiplatelet therapy.

281 with those discharged on single-agent or no antiplatelet therapy.

282 Antithrombotic (anticoagulant or antiplatelet) therapy is withheld from some patients wit

283 (130-149mmHg vs <130mmHg; open label) and to antiplatelet treatment (aspirin/clopidogrel vs aspirin/p

284 patients with intracerebral hemorrhage under antiplatelet treatment and follow-up CT at 24 +/- 12 hou

285 60 minutes of intracerebral hemorrhage under antiplatelet treatment diagnosis on brain imaging.

286 ARTEMIS trial (Affordability and Real-World Antiplatelet Treatment Effectiveness After Myocardial In

287 Lifelong antiplatelet treatment is recommended after ischaemic va

288 The effect of single as compared with dual antiplatelet treatment on bleeding and thromboembolic ev

289 Data on optimal antiplatelet treatment regimens in patients who undergo

290 regation and (2) novel molecular targets for antiplatelet treatment strategies.

291 ransfusion in intracerebral hemorrhage under antiplatelet treatment.

292 say clot biomechanics associated with common antiplatelet treatments and bleeding disorders.

293 n activator, direct thrombin inhibitors, and antiplatelet treatments.

294 and major vascular events as defined by the Antiplatelet Trialists' Collaboration (APTC).

295 Antiplatelet Trialists' Collaboration adverse events (de

296 Antiplatelet Trialists' Collaboration vascular events oc

297 .01), preextracorporeal membrane oxygenation antiplatelet use (7 vs 0; p = 0.03), and a higher day 1

298 Antiplatelet use (versus nonuse) was associated with CSH

299 In multivariable analysis, adjusting for antiplatelet use, there was no significant difference in

300 c <=9% in diabetic patients, statin use, and antiplatelet use-termed optimal medial therapy (OMT) was