ライフサイエンスコーパス: antiplatelet

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

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

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

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

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

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

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

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

9 6.5; 95% CI, 25.9-27.0) for those exposed to antiplatelet agents (IRR, 1.31; 95% CI, 1.29-1.33).

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

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

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

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

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

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

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

17 Antiplatelet agents are widely used to reduce these comp

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

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

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

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

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

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

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

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

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

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

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

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

30 little actionable pharmacogenetic data with antiplatelet agents.

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

32 ostasis has played in the development of new antiplatelet and anticoagulant drugs.

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

34 antithrombotic treatment regimen, including antiplatelet and anticoagulant therapies, for these high

35 Antiplatelet and direct antithrombin agents may be usefu

36 isk factors, but only 203 (54.4%) were on an antiplatelet and only 166 (44.5%) were on a statin.

37 were divided into 3 groups: anticoagulation, antiplatelet, and no therapy cohorts.

38 whether breast milk of ITP mothers contained antiplatelet antibodies causing persistent thrombocytope

39 Thus, transfer of antiplatelet antibodies from ITP mothers by breastfeedin

40 We found increased levels of antiplatelet antibodies of the immunoglobulin A type in

41 immune thrombocytopenia (ITP) commonly have antiplatelet antibodies that cause thrombocytopenia thro

42 aging scanning (0.31% per quarter; P=0.013), antiplatelet/anticoagulant use (-0.20% per quarter; P<0.

43 Nitric oxide (NO) exerts vasodilatatory, antiplatelet, antioxidant, and antiproliferative effects

44 cell-neutralizing (anti-NK 1.1 antibody) or antiplatelet (aspirin/Plavix [clopidogrel bisulfate]; As

45 Prophylaxis with antiplatelets (aspirin, ticlopidine [alone or in combina

46 Olaratumab is a human antiplatelet-derived growth factor receptor alpha monocl

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

48 , the method was applied to the synthesis of antiplatelet drug n-butyl phthalide and cytotoxic agonis

49 Among patients in whom antiplatelet drug use was discontinued at least 2 days b

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 port the inhibition of GPR17 by the marketed antiplatelet drugs cangrelor and ticagrelor, previously

53 with a previous ICH treated with warfarin or antiplatelet drugs in comparison with no antithrombotic

54 The relative safety and efficacy of some antiplatelet drugs in women has been disputed.

55 mportant for patients who take warfarin with antiplatelet drugs or nonselective nonsteroidal anti-inf

56 ctive effect for warfarin patients not using antiplatelet drugs or NSAIDs (HR, 0.86; 95% CI, 0.70-1.0

57 Among patients concurrently using antiplatelet drugs or NSAIDs, those without PPI co-thera

58 t reduction occurred in patients also taking antiplatelet drugs or NSAIDs.

59 ment options now include the next-generation antiplatelet drugs prasugrel and ticagrelor, and, in ter

60 Antiplatelet drugs provide first-line antithrombotic the

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

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

63 nticoagulants (OAC) and 762 (28.6%) received antiplatelet drugs.

64 and ticagrelor exerted a high and consistent antiplatelet effect (68.2% and 62.2% of platelet inhibit

65 Suboptimal antiplatelet effect during and after primary percutaneou

66 ed of onset, variable response, and a modest antiplatelet effect.

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

68 on, and consequently, more prompt and potent antiplatelet effects compared with whole tablet ingestio

69 Aspirin exerts antiplatelet effects through irreversible inhibition of

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

71 Ticagrelor, beyond its antiplatelet efficacy, exerts cardioprotective effects b

72 nts were defined as those with both positive antiplatelet factor 4/heparin enzyme-linked immunosorben

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

74 ecent increased caution encouraging a higher antiplatelet factor 4/heparin enzyme-linked immunosorben

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

76 If antiplatelet factor 4/heparin enzyme-linked immunosorben

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

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

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

80 urves demonstrated a significant benefit for antiplatelet, lipid-lowering, and beta-blocker therapy i

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

82 15(17.6%) had a contraindication to a common antiplatelet medication and 737 (6.5%) of these patients

83 Receipt of an oral anticoagulant or antiplatelet medication.

84 reduced the rate of high-risk prescribing of antiplatelet medications and NSAIDs and may have improve

85 ents with contraindications to commonly used antiplatelet medications during and after PCI, defined i

86 Several antiplatelet medications used during and after percutane

87 dergoing PCI had contraindications to common antiplatelet medications.

88 aspirin therapy and those with no additional antiplatelet medications.

89 Patient groups included antiplatelet (n = 181), anticoagulation (n = 91), and no

90 gs, including 514 participants (44.1%) using antiplatelets only, 77 (6.6%) using anticoagulants only,

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 ke occurred in 14 of the 235 patients in the antiplatelet-only group (hazard ratio, 0.03; 95% confide

94 roup and in 12 of 223 patients (5.4%) in the antiplatelet-only group (hazard ratio, 0.23; 95% confide

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

96 closure group), antiplatelet therapy alone (antiplatelet-only group), or oral anticoagulation (antic

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

98 Associations between use of antiplatelet or anticoagulant drugs and hemorrhage were

99 At baseline, 608 participants (52.2%) used antiplatelet or anticoagulant drugs, including 514 parti

100 Participants were interviewed for use of antiplatelet or anticoagulant drugs.

101 Randomized and observational studies of antiplatelet or anticoagulant therapy, published in any

102 arin in comparison with either aspirin or no antiplatelet or anticoagulant therapy.

103 f hematuria even if the patient is receiving antiplatelet or anticoagulant therapy.

104 ; these hemorrhages were not associated with antiplatelet or anticoagulant use at baseline (P = 0.28)

105 ng participants with hypertension (n = 807), antiplatelet or anticoagulant use was associated with a

106 Among all CATT participants, antiplatelet or anticoagulant use was not associated sig

107 sociated with the type, dose, or duration of antiplatelet or anticoagulant use.

108 Hemorrhage was present in 64.5% of antiplatelet or anticoagulant users and in 59.6% of nonu

109 Aspirin represents the sine qua non for antiplatelet pharmacotherapy in patients with cardiovasc

110 and allowed for a personalized 1-month dual antiplatelet regimen.

111 describing reticulated platelets can predict antiplatelet response to thienopyridine loading compared

112 m, IPC may become the preferred predictor of antiplatelet response to thienopyridine treatment.

113 ependent platelet count-derived predictor of antiplatelet response to thienopyridine treatment.

114 describing reticulated platelets can predict antiplatelet response to thienopyridines.

115 t reticulated platelets significantly affect antiplatelet response to thienopyridines.

116 These results highlight an antiplatelet strategy centered on blocking or desensitiz

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

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

119 nists could potentially be useful adducts in antiplatelet therapies and may provide a promising persp

120 elopment of strategies to improve on current antiplatelet therapies and to reduce cardiovascular dise

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

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

123 A limitation of current antiplatelet therapies is their inability to separate th

124 s of platelet dysfunction and currently used antiplatelet therapies provide a framework for understan

125 th diabetes often show hyporesponsiveness to antiplatelet therapies, and it has been suggested that h

126 ts with acute coronary syndrome on different antiplatelet therapies.

127 splay adverse thrombotic events with current antiplatelet therapies.

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

129 [4%] of 224) than among those receiving dual antiplatelet therapy (31 [15%] of 208; p<0.0001); NOACs

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

131 ate of sICH was higher in patients receiving antiplatelet therapy (5.0% vs 3.7%).

132 loading doses and then 30 days of intensive antiplatelet therapy (combined aspirin 75 mg, clopidogre

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

134 recent studies, the optimum duration of dual antiplatelet therapy (DAPT) after coronary drug-eluting

135 The appropriate duration of dual-antiplatelet therapy (DAPT) after drug-eluting stent (DE

136 The optimal duration of dual antiplatelet therapy (DAPT) after implantation of newer-

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

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

139 se of proton pump inhibitors (PPIs) and dual antiplatelet therapy (DAPT) for cardiovascular outcomes.

140 ice guidelines recommend post-operative dual antiplatelet therapy (DAPT) in patients who undergo coro

141 nged (24 months) vs short (</=6 months) dual antiplatelet therapy (DAPT) in patients with PAD undergo

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

143 Prolonged dual antiplatelet therapy (DAPT) is recommended after an acut

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

145 g patients with DM participating in the Dual Antiplatelet Therapy (DAPT) Study as a prespecified anal

146 analysis is derived from data from the Dual Antiplatelet Therapy (DAPT) Study, a multicenter trial i

147 In the Dual Antiplatelet Therapy (DAPT) Study, continuation of dual

148 lation with a vitamin K antagonist plus dual antiplatelet therapy (DAPT) with a P2Y12 inhibitor and a

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

150 Dual antiplatelet therapy (DAPT), aspirin plus a P2Y12 inhibi

151 with a vitamin K antagonist (VKA) plus dual antiplatelet therapy (DAPT), yet this treatment leads to

152 tinal (GI) events in patients requiring dual antiplatelet therapy (DAPT).

153 stents (BMS) under similar durations of dual-antiplatelet therapy (DAPT).

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

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

156 to transcatheter PFO closure plus long-term antiplatelet therapy (PFO closure group), antiplatelet t

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

158 More intensive antiplatelet therapy (vorapaxar and ticagrelor pooled) s

159 rapy with P2Y12 inhibitors alone versus dual-antiplatelet therapy after acute coronary syndromes or c

160 etween those who were and were not receiving antiplatelet therapy after adjustment (8.0% vs 6.6%; AOR

161 The benefit and need for prolonged dual antiplatelet therapy after bioresorbable scaffold implan

162 trial, compared 30 versus 12 months of dual antiplatelet therapy after coronary stenting.

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

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

165 Dual antiplatelet therapy after percutaneous coronary interve

166 rm antiplatelet therapy (PFO closure group), antiplatelet therapy alone (antiplatelet-only group), or

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

168 re combined with antiplatelet therapy versus antiplatelet therapy alone on the risks of recurrent str

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

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

171 latelet therapy than among those assigned to antiplatelet therapy alone.

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

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

174 Continued dual antiplatelet therapy and optimal medical therapy (OMT) i

175 years; 65% men; 75% diabetic) received dual antiplatelet therapy as a single loading dose (ticagrelo

176 dherence patients described missing doses of antiplatelet therapy at least twice a week after percuta

177 wever, many patients may have been receiving antiplatelet therapy before acute ischemic stroke and co

178 istry patients, 38844 (45.7%) were receiving antiplatelet therapy before admission; 46 228 patients (

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

180 inferior to standard care for people taking antiplatelet therapy before intracerebral haemorrhage.

181 reated with intravenous tPA, those receiving antiplatelet therapy before the stroke had a higher risk

182 Prestroke antiplatelet therapy before tPA administration for acute

183 t Therapy (DAPT) Study, continuation of dual antiplatelet therapy beyond 12 months after coronary ste

184 patient benefit and harm from continued dual antiplatelet therapy beyond assessment of MI history alo

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

186 ts with recent cerebral ischaemia, intensive antiplatelet therapy did not reduce the incidence and se

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

188 tool (DAPT score) aids prescription of dual antiplatelet therapy duration in patients with or withou

189 e ischemic and bleeding risks to inform dual antiplatelet therapy duration showed modest accuracy in

190 neration and BMS, thus allowing shorter dual antiplatelet therapy duration.

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

192 In patients treated with dual antiplatelet therapy for at least 1 year after coronary

193 l haemorrhage symptom onset if they had used antiplatelet therapy for at least 7 days beforehand and

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

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

196 latelet therapy group, 1540 in the guideline antiplatelet therapy group) were recruited from 106 hosp

197 3096 participants (1556 in the intensive antiplatelet therapy group, 1540 in the guideline antipl

198 However, patients receiving antiplatelet therapy had a greater risk-adjusted likelih

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

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

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

202 ctical strategies for managing perioperative antiplatelet therapy in patients following percutaneous

203 clinical trials comparing anticoagulation to antiplatelet therapy in secondary stroke prevention.

204 Antiplatelet therapy is of proven benefit in coronary ar

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

206 Anticoagulant or antiplatelet therapy is the preferred treatment option f

207 er OMT modifies the treatment effect of dual antiplatelet therapy is unknown.

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

209 The benefits and risks of prolonged dual antiplatelet therapy may be different for patients with

210 y intracerebral haemorrhage in people taking antiplatelet therapy might reduce death or dependence by

211 e comparison of the current standard of dual antiplatelet therapy of aspirin with clopidogrel versus

212 assess the effect of extended duration dual antiplatelet therapy on mortality by doing a meta-analys

213 botic therapy (27.1% [95% CI, 26.6%-27.7%]), antiplatelet therapy only (24.8% [95% CI, 24.3%-25.3%]),

214 rombotic therapy (9.3% [95% CI, 8.9%-9.6%]), antiplatelet therapy only (8.1% [95% CI, 7.8%-8.3%]), or

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

216 extended duration versus short duration dual antiplatelet therapy or aspirin alone.

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

218 ly been studied in addition to aspirin; dual-antiplatelet therapy proved superiority compared with as

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

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 e comparable benefit from intensification of antiplatelet therapy remains uncertain.

223 Triple antiplatelet therapy should not be used in routine clini

224 New data from long-term dual antiplatelet therapy studies and investigations of antic

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

226 The Dual Antiplatelet Therapy Study, a randomized double-blind, p

227 (The Dual Antiplatelet Therapy Study; NCT00977938).

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

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

230 er intracerebral haemorrhage associated with antiplatelet therapy use.

231 lusions regarding the safety and efficacy of antiplatelet therapy varied depending on analytic techni

232 ated the effect of PFO closure combined with antiplatelet therapy versus antiplatelet therapy alone o

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

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

235 Extended duration dual antiplatelet therapy was not associated with a differenc

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

237 Patients receiving antiplatelet therapy were older (median [25th-75th perce

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

239 Dual antiplatelet therapy with aspirin and a P2Y12 inhibitor

240 Dual-antiplatelet therapy with aspirin and clopidogrel after

241 t (DES) implantation require additional dual antiplatelet therapy with aspirin and clopidogrel.

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

243 rformed in the ADAPT-DES (Assessment of Dual Antiplatelet Therapy With Drug-Eluting Stents) registry.

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

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

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

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

248 investigation includes evaluation of single-antiplatelet therapy with P2Y12 inhibitors alone versus

249 The optimal duration of dual antiplatelet therapy with prasugrel after TAXUS Liberte

250 Intensive antiplatelet therapy with three agents might be more eff

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

252 of this study was to determine the effect of antiplatelet therapy with ticagrelor on recurrent ischem

253 ronary stenting and completed 1 year of dual antiplatelet therapy without major bleeding or ischemic

254 The DAPT (Dual Antiplatelet Therapy) study enrolled patients after coro

255 The DAPT (Dual Antiplatelet Therapy) Study, a double-blind trial, rando

256 nts (1:1; stratified by hospital and type of antiplatelet therapy) to receive either standard care or

257 In the DAPT Study (Dual Antiplatelet Therapy), after percutaneous coronary inter

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

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

260 t era of drug-eluting stents, prolonged dual antiplatelet therapy, and potent P2Y12 inhibitors are no

261 ned to 1 of 3 groups, that is, no treatment, antiplatelet therapy, and warfarin.

262 in what has come to be commonly called dual antiplatelet therapy, are a mainstay of treatment for pa

263 erapy refers to the contemporary approach of antiplatelet therapy, blood pressure control, low-densit

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

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

266 risk of VTE by 29% compared with background antiplatelet therapy, from 0.93% to 0.64% at 3 years (ha

267 occurred in patients who had suspended dual antiplatelet therapy, in 6 cases prematurely.

268 ssist device support; yet, their relation to antiplatelet therapy, including aspirin (ASA) dosing, is

269 ed duration versus no or short duration dual antiplatelet therapy, published before Oct 1, 2014.

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

271 he proportion of visits with medication use (antiplatelet therapy, statins, angiotensin-converting en

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

273 e than adults without diabetes, yet standard antiplatelet therapy, which is the cornerstone for prima

274 n receptor blockers, beta-blockers, and dual antiplatelet therapy.

275 erent risks and benefits with prolonged dual antiplatelet therapy.

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

277 closure or anticoagulation, as compared with antiplatelet therapy.

278 s comprehensive risk factor modification and antiplatelet therapy.

279 l outcomes than those who were not receiving antiplatelet therapy.

280 feasible approach for patients needing dual antiplatelet therapy.

281 ed with aspirin alone or short duration dual antiplatelet therapy.

282 ted patients and 25.7 for patients receiving antiplatelet therapy.

283 participants to different durations of dual antiplatelet therapy.

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

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

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

287 runs, earlier date of procedure, and no dual antiplatelet therapy; high pre-TAVR aortic peak gradient

288 on test be used to guide the dose or type of antiplatelet therapy?

289 (130-149mmHg vs <130mmHg; open label) and to antiplatelet treatment (aspirin/clopidogrel vs aspirin/p

290 ubanalysis of the randomized Prolonging Dual Antiplatelet Treatment After Grading Stent-Induced Intim

291 trials comparing aggressive management (dual antiplatelet treatment for 90 days followed by aspirin m

292 All patients were recommended to take dual antiplatelet treatment for at least 6 months.

293 sk, time course, and outcomes of bleeding on antiplatelet treatment for secondary prevention in patie

294 Lifelong antiplatelet treatment is recommended after ischaemic va

295 ; NNH, 147) and 2397 patients receiving dual antiplatelet treatment of aspirin and clopidogrel (AOR,

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

297 ETATION: In patients receiving aspirin-based antiplatelet treatment without routine PPI use, the long

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

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

300 icant after adjustment for anticoagulant and antiplatelet use in patients >/=66 years old.