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1 5 to 277) to 241 (194 to 275) (p < 0.001 vs. prasugrel).
2 t of aspirin dose on the clinical effects of prasugrel.
3 ved placebo received a 60-mg loading dose of prasugrel.
4 yocardial infarction, 26.0% of whom received prasugrel.
5 with either 100 mg (n=47) or 60 mg (n=35) of prasugrel.
6  risk reduction appeared to be enhanced with prasugrel.
7 ged ACS patients treated with clopidogrel or prasugrel.
8 opidogrel or replacement of clopidogrel with prasugrel.
9  the dose of clopidogrel or were switched to prasugrel.
10  syndrome, and in this group, 17.2% received prasugrel.
11 entify the proportion likely to benefit from prasugrel.
12 7.9% lower risk to an 11.2% higher risk with prasugrel.
13 tly higher platelet inhibition compared with prasugrel.
14 rial (2008 to 2011) comparing clopidogrel vs prasugrel.
15  increasing bleeding time to 16 vs 9 min for Prasugrel.
16 e investigated the PK/PD effects of crushing prasugrel.
17  absorption with crushed compared with whole prasugrel.
18 who were randomized to either clopidogrel or prasugrel.
19 t reactivity rates were reduced with crushed prasugrel.
20 ation drug-eluting stents and 19.5% received prasugrel.
21 ose aspirin, and 2 patients were also taking prasugrel.
22 ated with aspirin and risk-adjusted doses of prasugrel.
23 7; P=0.007) were both reduced with prolonged prasugrel.
24 cts of switching patients from ticagrelor to prasugrel.
25 absolute reduction in the ischemia risk with prasugrel=1.5+/-3.0%, ranging from an 8.4% increased ris
26      Rates of mild bleeding were higher with prasugrel 10 mg but similar for prasugrel 5 mg versus cl
27 s was noninferior to the 75th percentile for prasugrel 10 mg in HBW patients (primary endpoint) and m
28 eight (LBW) patients would be noninferior to prasugrel 10 mg in higher-body-weight (HBW) patients as
29 63 +/- 14%; p < 0.001) in VE but higher than prasugrel 10 mg in NE (46 +/- 12%; p < 0.001).
30 el 5 mg in VE versus the 75th percentile for prasugrel 10 mg in NE, using a pre-specified 1-sided 97.
31 re-specified noninferiority criterion versus prasugrel 10 mg in NE, with significantly better PD resp
32 e primary PD noninferiority criterion versus prasugrel 10 mg in NE.
33                         Within HBW patients, prasugrel 10 mg lowered MPA more than clopidogrel (-16.9
34 ed to receive either ticagrelor 90 mg BID or prasugrel 10 mg OD with a 15-day treatment period.
35 ombolysis In Myocardial Infarction 38) study prasugrel 10 mg reduced ischemic events versus clopidogr
36 ndomized to continue ticagrelor or switch to prasugrel 10-mg once-daily MD, with or without a 60-mg L
37 ized to receive clopidogrel (75 mg daily) or prasugrel (10 mg daily) for 10 days and crossed over aft
38  evaluated up to 30 months of treatment with prasugrel (10 mg daily) versus clopidogrel (75 mg daily)
39  mitigate the bleeding risk of standard-dose prasugrel (10 mg/d).
40 =75 years of age, n=2083) were randomized to prasugrel (10 mg/d; 5 mg/d for those >/=75 or <75 years
41           Those with HTPR were randomized to prasugrel (10 mg/day) or high-dose clopidogrel (150 mg/d
42                          Aspirin with either prasugrel (10 or 5 mg/d) or clopidogrel (75 mg/d); those
43                                   At hour 2, prasugrel 100 mg over 60 mg loading dose significantly r
44 e interval [CI]: 18.7 to 47.2) compared with prasugrel (101.3 PRU, 95% CI: 86.8 to 115.7) with a leas
45 use mortality was significantly reduced with prasugrel (2.31%) compared with 8.67% with clopidogrel (
46 h at day 5 it was lower with ticagrelor than prasugrel (25.6 PRU, 95% CI 12.3-38.9 versus 50.3 PRU, 9
47 een patients randomized to ticagrelor versus prasugrel (257.3 P2Y12 reaction unit [PRU], 95% CI 230.8
48                    Among patients prescribed prasugrel, 28.3% (n=2614) received the medication for in
49 eated with clopidogrel (39.93), but not with prasugrel (3.87).
50                       For clopidogrel 600 mg/prasugrel 30 mg (least squares mean PRU, 53.9), the diff
51 stenting to loading with clopidogrel 600 mg, prasugrel 30 mg, or prasugrel 60 mg.
52  prasugrel 60 mg, or clopidogrel 600 mg plus prasugrel 30 mg.
53 rwent PCI; 1,394 received pre-treatment with prasugrel (30-mg loading dose), and 1,376 received place
54 elor was more effective than genotyping with prasugrel ($30 200 per QALY relative to clopidogrel).
55 ctive metabolite pharmacokinetics (PKs) with prasugrel 5 and 10 mg and clopidogrel 75 mg in a 3-perio
56 oronary artery disease (CAD) taking aspirin, prasugrel 5 and 10 mg and clopidogrel 75 mg were adminis
57                        Median MPA by LTA for prasugrel 5 mg in LBW patients was noninferior to the 75
58  confirm prior modeling data suggesting that prasugrel 5 mg in low-body-weight (LBW) patients would b
59      In aspirin-treated stable CAD patients, prasugrel 5 mg in VE attenuated platelet inhibition whil
60                                              Prasugrel 5 mg in VE met the primary PD noninferiority c
61 t aggregation (MPA) comparing the median for prasugrel 5 mg in VE versus the 75th percentile for pras
62                                              Prasugrel 5 mg resulted in fewer VE poor responders than
63  higher with prasugrel 10 mg but similar for prasugrel 5 mg versus clopidogrel 75 mg.
64                                          For prasugrel 5 mg, MPA was significantly lower (57 +/- 14%)
65                                     Low-dose prasugrel (5 mg/d) is recommended for younger, lower-bod
66 ignificantly lower with ticagrelor than with prasugrel (52 [32-72] versus 83 [63-103]; least-square m
67  clopidogrel (600 mg, n=13 or 900 mg, n=12), prasugrel 60 mg (n=10), or ticagrelor 180 mg (n=10) were
68 acebo/prasugrel 60 mg and clopidogrel 600 mg/prasugrel 60 mg (primary outcome) was 22.2 (-11.0 to 55.
69 fidence interval) difference between placebo/prasugrel 60 mg and clopidogrel 600 mg/prasugrel 60 mg (
70                     Platelet reactivity with prasugrel 60 mg LD added to clopidogrel 600 mg LD was no
71 as not significantly different compared with prasugrel 60 mg LD alone in acute coronary syndrome pati
72              The pharmacodynamic response of prasugrel 60 mg ld alone was compared with prasugrel 60
73                         At 6 hours after the prasugrel 60 mg LD, the least squares mean (95% confiden
74 lor 180 mg loading followed by 90 mg bid, or prasugrel 60 mg loading followed by 10 mg od for 5 days.
75 f prasugrel 60 mg ld alone was compared with prasugrel 60 mg or 30 mg added 24 hours to clopidogrel 6
76 ding dose of intravenous LA 450 mg plus oral prasugrel 60 mg or loading dose of aspirin 300 mg plus p
77 60 mg or loading dose of aspirin 300 mg plus prasugrel 60 mg orally in a crossover fashion after a 2-
78  randomized to 3 LD strategies: placebo plus prasugrel 60 mg, clopidogrel 600 mg plus prasugrel 60 mg
79 lus prasugrel 60 mg, clopidogrel 600 mg plus prasugrel 60 mg, or clopidogrel 600 mg plus prasugrel 30
80 s 3.9 (-28.2 to 36.1; P=0.81) versus placebo/prasugrel 60 mg.
81 with clopidogrel 600 mg, prasugrel 30 mg, or prasugrel 60 mg.
82 rgoing PPCI (n = 52) who were treated with a prasugrel 60-mg loading dose (LD) either as whole or cru
83 ry disease were randomly assigned to receive prasugrel (60 mg loading dose [LD]/10 mg maintenance dos
84  patients treated initially in-hospital with prasugrel, 751 (11.5%) were discharged on clopidogrel.
85   Patients were randomly assigned to receive prasugrel (a 30-mg loading dose) before the angiography
86 ere predicted to experience net benefit with prasugrel, a rate that increased if patients more strong
87 l duration of dual antiplatelet therapy with prasugrel after TAXUS Liberte paclitaxel-eluting stent r
88    Genotyping with prasugrel was superior to prasugrel alone, with an ICER of $35 800 per QALY relati
89 rimary end point) suggested a lower risk for prasugrel among patients under the age of 75 years (haza
90 latelet function substudy: 1286 treated with prasugrel and 1278 treated with clopidogrel.
91 for economic reasons was 34.1% (n = 216) for prasugrel and 44.4% (n = 265) for ticagrelor (p = 0.003)
92                                              Prasugrel and aspirin continued for 30 months reduced is
93                               Treatment with prasugrel and aspirin improves outcomes compared with cl
94 obability of treatment weighting adjustment, prasugrel and clopidogrel had similar major adverse card
95                             (A Comparison of Prasugrel and Clopidogrel in Acute Coronary Syndrome Sub
96 ding risk were observed between reduced-dose prasugrel and clopidogrel in elderly patients.
97          (The Influence of Smoking Status on Prasugrel and Clopidogrel Treated Subjects Taking Aspiri
98 ifference in predicted bleeding risk between prasugrel and clopidogrel was calculated for each patien
99 d point rates were similar with reduced-dose prasugrel and clopidogrel.
100 sk for major ischemia and bleeding with both prasugrel and clopidogrel.
101 ss the offset of the antiplatelet effects of prasugrel and clopidogrel.
102 ght to evaluate the impact of treatment with prasugrel and high-dose clopidogrel on the basis of plat
103  not show any significant difference between prasugrel and ticagrelor (2.7% and 2.5%, respectively; o
104 oint did not differ between groups receiving prasugrel and ticagrelor (4.0% and 4.1%, respectively; o
105 zation may improve the cost-effectiveness of prasugrel and ticagrelor after percutaneous coronary int
106                  It has been documented that prasugrel and ticagrelor are able to provide effective p
107 s in acute coronary syndrome have shown that prasugrel and ticagrelor are more effective than standar
108                                              Prasugrel and ticagrelor are similarly effective during
109 ts defined by VerifyNow were similar between prasugrel and ticagrelor at 30 minutes and 2 hours post-
110 gometry, and Multiplate were similar between prasugrel and ticagrelor at each time point, including a
111              This head-to-head comparison of prasugrel and ticagrelor does not support the hypothesis
112   In patients with acute coronary syndromes, prasugrel and ticagrelor further reduce cardiovascular i
113 e 217 (12 to 279) and 275 (88 to 305) in the prasugrel and ticagrelor groups, respectively (p = NS),
114  PRU <240 was 3 +/- 2 h and 5 +/- 4 h in the prasugrel and ticagrelor groups, respectively.
115 latelet reactivity rate between the combined prasugrel and ticagrelor groups.
116 signed to compare the efficacy and safety of prasugrel and ticagrelor in acute myocardial infarction
117   This study sought to compare the action of prasugrel and ticagrelor in ST-segment elevation myocard
118  of patients in the PRAGUE-18 (Comparison of Prasugrel and Ticagrelor in the Treatment of Acute Myoca
119                               (Comparison of Prasugrel and Ticagrelor in the Treatment of Acute Myoca
120 t reactivity reduced significantly with both prasugrel and ticagrelor LD and maintenance dose.
121 ever, the pharmacodynamic measurements after prasugrel and ticagrelor LD have been provided by assess
122 e (P < 0.001) and without difference between prasugrel and ticagrelor patients.
123                                              Prasugrel and ticagrelor provide a superior anti-ischemi
124                                              Prasugrel and ticagrelor reduce thrombotic complications
125  analyses of pivotal clinical trials testing prasugrel and ticagrelor versus clopidogrel showed DM pa
126 clude the next-generation antiplatelet drugs prasugrel and ticagrelor, and, in terms of anticoagulant
127                                              Prasugrel and ticagrelor, new P2Y12-adenosine diphosphat
128           Next-generation P2Y12 antagonists, prasugrel and ticagrelor, overcome these limitations and
129 ermined by VerifyNow P2Y12 at 1 week between prasugrel and ticagrelor.
130  a comparison of efficacy and safety between prasugrel and ticagrelor; and 2) the risk of major ische
131 t with a thienopyridine drug (clopidogrel or prasugrel) and aspirin, patients were randomly assigned
132 th ticagrelor) or prasugrel (genotyping with prasugrel) and noncarriers receiving clopidogrel.
133 asugrel received an additional 30-mg dose of prasugrel, and those who received placebo received a 60-
134           The P2Y12 inhibitors, clopidogrel, prasugrel, and ticagrelor, are administered in fixed dos
135  for clopidogrel 600 mg, clopidogrel 900 mg, prasugrel, and ticagrelor, respectively; P for trend <0.
136 ed antithrombotic drugs such as clopidogrel, prasugrel, and ticagrelor.
137 ns obtained thus far from subgroup analyses, prasugrel appears to provide higher anti-ischemic protec
138                              Clopidogrel and prasugrel are not uncommonly switched in-hospital in pat
139  with clopidogrel, antiplatelet responses to prasugrel are not uniform.
140 yndrome (ACS) is complicated: Ticagrelor and prasugrel are novel alternatives to clopidogrel, patient
141 efficacy, safety, and antiplatelet effect of prasugrel as compared with clopidogrel in patients with
142                               Data regarding prasugrel as part of triple therapy are not available.
143 e CBFV ratio was higher with ticagrelor than prasugrel at 50, 80, and 110 mug/kg per minute but not a
144 effect of administering the P2Y12 antagonist prasugrel at the time of diagnosis versus administering
145 mized, double-blind ACCOAST (A Comparison of prasugrel at the time of percutaneous Coronary intervent
146 seline without therapy, at 1 week with 10 mg prasugrel, at 2 weeks with 10 mg prasugrel plus 75 mg as
147   Bleeding outcomes tended to be higher with prasugrel but did not differ significantly between treat
148         MI rates increased within 90 days of prasugrel cessation after both 12 and 30 months treatmen
149 fidence interval </=45), although PRU in the prasugrel cohort was lower at 7 days than at 24 or 48 h.
150 hemic or bleeding outcomes with reduced-dose prasugrel compared with clopidogrel in elderly patients.
151 odynamic properties and clinical efficacy of prasugrel compared with clopidogrel, antiplatelet respon
152 503 +/- 378 ml; p = 0.050) was observed with prasugrel compared with clopidogrel, without significant
153 tivity was lower 24 h after the last dose of prasugrel compared with clopidogrel.
154 ing occurred significantly more often in the prasugrel compared with the clopidogrel group (6 [28.6%)
155 TIMI 38, the safety and efficacy outcomes of prasugrel compared with those of clopidogrel were direct
156                             (A Comparison of Prasugrel [CS-747] and Clopidogrel in Acute Coronary Syn
157 o undergo catheterization, pretreatment with prasugrel did not reduce the rate of major ischemic even
158  P2Y12 inhibitor and, unlike clopidogrel and prasugrel, does not require metabolic activation.
159 ess the pharmacodynamic effects of different prasugrel dosing regimens in patients on maintenance pra
160 luding the prodrugs clopidogrel (Plavix) and prasugrel (Effient) that are metabolized and bind covale
161 s coronary intervention, both ticagrelor and prasugrel exhibit an initial delay in the onset of their
162 cute coronary syndrome patients treated with prasugrel experience fewer ischemic complications, but m
163  These findings suggest that substitution of prasugrel for clopidogrel in patients needing triple the
164 r ticagrelor (genotyping with ticagrelor) or prasugrel (genotyping with prasugrel) and noncarriers re
165 risis events per person-year was 2.30 in the prasugrel group and 2.77 in the placebo group (rate rati
166 eached the primary endpoint was lower in the prasugrel group than in the clopidogrel group for those
167 ay PRU values were 139 (IQR, 86-203) for the prasugrel group vs 209 (IQR, 148-283) for the clopidogre
168 n PRU values were 164 (IQR, 105-216) for the prasugrel group vs 222 (IQR, 148-268) for the clopidogre
169 ity unit values and lower weight only in the prasugrel group, there was a nonsignificant treatment-by
170 emained significantly higher in the combined prasugrel groups versus the ticagrelor group (least-squa
171 eactivity were higher at 24 and 48 h in both prasugrel groups.
172                                        After prasugrel, &gt;/=75% of patients returned to baseline react
173 and bleeding outcomes (1.18; 0.77-1.80), but prasugrel had a lower rate of stent thrombosis (0.51; 0.
174 Regardless of low- or high-dose aspirin use, prasugrel had lower rates of the primary efficacy endpoi
175 < 0.0001), and patients who were switched to prasugrel had similar outcomes (HR: 0.90; 95% CI: 0.44 t
176 urs after the standard 60 mg loading dose of prasugrel has been described.
177 of the efficacy and safety of ticagrelor and prasugrel has been published in the 7 years since the hi
178    The oral P2Y12 antagonists ticagrelor and prasugrel have higher recommendations than clopidogrel,
179 4.17; p = 0.04) than in patients switched to prasugrel (HR: 0.45; 95% CI: 0.11 to 1.91; p = 0.28).
180 of the primary endpoint whether treated with prasugrel (HR: 0.82) or clopidogrel (HR: 0.91; p for int
181                           (Ticagrelor Versus Prasugrel in Acute Coronary Syndromes After Percutaneous
182        The clinical impact of treatment with prasugrel in patients with ACS who have high platelet re
183 ing RPs strongly correlates with response to prasugrel in patients with STEMI treated with PCI.
184 ing compared with the known P2Y12 antagonist prasugrel in rabbit efficacy/bleeding models.
185        Ticagrelor did not appear superior to prasugrel in reducing PR during the first 24 hours of ST
186     There are no data on contemporary use of prasugrel in routine clinical practice.
187 e efficacy between high-dose clopidogrel and prasugrel in the 18 (56.3%) CYP2C19*2 noncarriers (HTPR
188 duced platelet reactivity in comparison with prasugrel in the acute and chronic phases of treatment,
189 pirin dose and the potent antiplatelet agent prasugrel in the TRITON-TIMI 38 (Trial to Assess Improve
190 let reactivity compared with oral aspirin on prasugrel-inhibited platelets.
191 alicylate (LA) compared with oral aspirin on prasugrel-inhibited platelets.
192          Twenty-one patients (5.6%) received prasugrel instead of clopidogrel.
193 PR is successfully abolished by therapy with prasugrel irrespective of CYP2C19 genotype.
194                                              Prasugrel is a recently approved thienopyridine for use
195 s study sought to determine whether crushing prasugrel is associated with more favorable drug bioavai
196 s study was to determine whether response to prasugrel is associated with the proportion of circulati
197 monotherapy were randomized to receive 60 mg prasugrel LD (n = 25) or 180 mg ticagrelor LD (n = 25).
198 asugrel LD, and 2, 6, 24, and 72 hours after prasugrel LD in 149 patients with evaluable platelet fun
199 2Y12 Reaction Units (PRU) immediately before prasugrel LD, and 2, 6, 24, and 72 hours after prasugrel
200   In STEMI patients undergoing PPCI, crushed prasugrel leads to faster drug absorption, and consequen
201         Compared with whole tablets, crushed prasugrel led to reduced P2Y12 reaction units by 30 min
202                                     Adding a prasugrel loading dose (LD) to a clopidogrel LD could be
203 ransferring From Clopidogrel Loading Dose To Prasugrel Loading Dose In Acute Coronary Syndrome Patien
204 pharmacodynamic (PD) response to the reduced prasugrel maintenance dose of 5 mg in very elderly (VE)
205  who weighed less than 60 kg received a 5-mg prasugrel maintenance dose.
206        This study sought to evaluate whether prasugrel may serve as an alternative to clopidogrel in
207 ial heterogeneity of the treatment effect of prasugrel (mean absolute reduction in the ischemia risk
208                              Clopidogrel and prasugrel metabolite levels, cytochrome P450 1A2 activit
209 neous coronary intervention receiving either prasugrel (n = 95) or ticagrelor (n = 205) loading dose
210 ance dose of aspirin and clopidogrel (n=45), prasugrel (n=6), or ticagrelor (n=3).
211 ect of maintenance dose of ticagrelor versus prasugrel on coronary blood flow velocity (CBFV) during
212 6 574) and 17% (n=9247) of patients received prasugrel on hospital discharge.
213    There was no impact of pre-treatment with prasugrel on the presence of thrombus before PCI or on o
214 te Coronary Syndromes) trial of aspirin plus prasugrel or clopidogrel following ACS.
215        Choice of initial antiplatelet agent (prasugrel or clopidogrel).
216 aspirin and oral anticoagulation with either prasugrel or clopidogrel.
217 nemia were randomly assigned to receive oral prasugrel or placebo for 9 to 24 months.
218 nts that occurred while patients were taking prasugrel or placebo, and of discontinuations due to pra
219 l or placebo, and of discontinuations due to prasugrel or placebo, did not differ significantly betwe
220                                   The use of prasugrel or ticagrelor eliminated bleeding differences
221 ous coronary intervention were randomized to prasugrel or ticagrelor with an intended treatment durat
222  randomly assigned across 14 sites to either prasugrel or ticagrelor, which was initiated before perc
223 d the progressive switch from clopidogrel to prasugrel or ticagrelor.
224   Patients with HPR (>46 U) were switched to prasugrel or treated with high-dose clopidogrel, and tho
225 t with a potent P2Y12 inhibitor (ticagrelor, prasugrel, or cangrelor) without the planned use of glyc
226 e trilemma of selecting between clopidogrel, prasugrel, or ticagrelor.
227             The endpoint occurred in 6.6% of prasugrel patients and in 5.7% of ticagrelor patients (h
228 lus 75 mg aspirin, and at 3 weeks with 10 mg prasugrel plus 300 mg aspirin.
229  with 10 mg prasugrel, at 2 weeks with 10 mg prasugrel plus 75 mg aspirin, and at 3 weeks with 10 mg
230  12 months of thienopyridine (clopidogrel or prasugrel) plus aspirin, eligible patients remained on a
231 ter treatment adjustments in those with HPR, prasugrel provided significantly more potent platelet in
232                  In 212 patients assigned to prasugrel, PRU decreased from 245 (225 to 273) (median [
233 CI, patients who received pre-treatment with prasugrel received an additional 30-mg dose of prasugrel
234 ents with ACS who have HPR to treatment with prasugrel reduces thrombotic and bleeding events to a le
235 ossed-over to, respectively, clopidogrel and prasugrel, repeating the P2Y12 assay at the end of each
236 PRU) were 46.2% and 34.6% for ticagrelor and prasugrel, respectively, decreased significantly thereaf
237 r (100 mg) than the standard loading dose of prasugrel results in greater and more consistent platele
238 reactivity index, and PK by plasma levels of prasugrel's active metabolite.
239                      In patients with STEMI, prasugrel showed to be noninferior as compared with tica
240 cally meaningful interaction of aspirin with prasugrel, suggesting that previous observations with po
241 significantly lower among those who received prasugrel than among those who received placebo.
242 ion were randomly assigned to clopidogrel or prasugrel.The primary endpoint was cardiovascular death,
243 threatening bleeding with pre-treatment with prasugrel; the same trends persisted in patients who had
244 grelor therapy, switching from ticagrelor to prasugrel therapy was associated with an increase in pla
245                  For patients on maintenance prasugrel therapy, a 60 mg dosing strategy is associated
246 and pharmacodynamics (PD) of clopidogrel and prasugrel therapy.
247 l dosing regimens in patients on maintenance prasugrel therapy.
248  Among patients who had angiography who took prasugrel there were fewer cardiovascular deaths, myocar
249  clopidogrel, 2125 (5.2%) were discharged on prasugrel; this frequency steadily increased from 0% to
250 comes by Optimizing Platelet Inhibition With Prasugrel-Thrombolysis in Myocardial Infarction 38 (TRIT
251 comes by Optimizing Platelet Inhibition with Prasugrel-Thrombolysis in Myocardial Infarction 38 (TRIT
252 comes by Optimizing Platelet Inhibition With Prasugrel-Thrombolysis In Myocardial Infarction 38) stud
253 comes by Optimizing Platelet InhibitioN with Prasugrel-Thrombolysis In Myocardial Infarction 38) stud
254 comes by Optimizing Platelet Inhibition with Prasugrel-Thrombolysis In Myocardial Infarction 38), in
255 ifferent oral P2Y12 inhibitors (clopidogrel, prasugrel, ticagrelor) has enabled physicians to contemp
256 Y12 inhibitor (eg, ticlopidine, clopidogrel, prasugrel, ticagrelor) reduces the risk of stent thrombo
257 rategies were examined: generic clopidogrel, prasugrel, ticagrelor, and genotyping for polymorphisms
258 trials of potent P2Y12 inhibitors, including prasugrel, ticagrelor, and intravenous cangrelor.
259 ensitivity troponin assays, a preference for prasugrel/ticagrelor and fondaparinux for anticoagulatio
260 dial approach was used in 21.3% of patients, prasugrel/ticagrelor was used in 18.1% of patients, and
261 f ADP receptor inhibitor (clopidogrel versus prasugrel/ticagrelor).
262  at discharge were associated with switching prasugrel to clopidogrel.
263 h TAXUS Liberte paclitaxel-eluting stent and prasugrel to the Dual Antiplatelet Therapy Study (DAPT)
264 ks (increased bleeding) to support targeting prasugrel to those who benefit most from treatment.
265 ia-related hospitalizations was noted in the prasugrel-treated patients when analyses were performed
266 e was higher for ticagrelor-treated than for prasugrel-treated patients, with a least squares mean di
267 ly lower in clopidogrel-treated smokers than prasugrel-treated smokers (least squares mean treatment
268  MI was significantly reduced with prolonged prasugrel treatment (1.9% versus 7.1%; HR, 0.255; P<0.00
269 e) was lower with 30 compared with 12 months prasugrel treatment (3.7% versus 8.8%; hazard ratio [HR]
270 ater antiplatelet effects were present after prasugrel treatment regardless of smoking status (p < 0.
271 d with increased platelet reactivity despite prasugrel treatment.
272 cked, and stratified by use of ticagrelor or prasugrel, type of acute coronary syndrome (ST-segment e
273 tment with aspirin and either clopidogrel or prasugrel, underwent isolated CABG (N = 346).
274 se findings support deferring treatment with prasugrel until a decision is made about revascularizati
275                  We assessed the patterns of prasugrel use among 55 821 patients who underwent percut
276                                              Prasugrel use in patients with known contraindications i
277         Using instrumental variable methods, prasugrel use was associated with a lower rate of the ma
278                 A steady, linear increase in prasugrel use was seen during the study period, with dis
279 rction at 6 months occurred in no patient on prasugrel versus 1 on clopidogrel.
280           The expected benefits and risks of prasugrel versus clopidogrel depend highly on patient ch
281  absolute increase in the bleeding risk with prasugrel versus clopidogrel was 1.3+/-1.4% and ranged f
282 ly greater at 24 and 48 h after switching to prasugrel versus continued therapy with ticagrelor, alth
283 int was platelet reactivity after 14 days of prasugrel versus high-dose clopidogrel.
284                          Those discharged on prasugrel (versus clopidogrel) had a slightly higher lik
285 , no significant differences existed between prasugrel vs clopidogrel in the occurence of the primary
286                                              Prasugrel was associated with greater active metabolite
287                     Switching clopidogrel to prasugrel was associated with high-risk angiographic cha
288                                The offset of prasugrel was consistent with current guidelines regardi
289                                Withdrawal of prasugrel was followed by an increase in MI after both 1
290 atment group at the time of PCI and 60 mg of prasugrel was given in the control group.
291 en PCI was indicated, an additional 30 mg of prasugrel was given in the pretreatment group at the tim
292                           Pre-treatment with prasugrel was not associated with decreases in any ische
293 ng of acute coronary syndrome (ACS) and PCI, prasugrel was not superior to clopidogrel in medically t
294                              Genotyping with prasugrel was superior to prasugrel alone, with an ICER
295                              Genotyping with prasugrel was the preferred therapy among patients who c
296 HPR with high-dose clopidogrel, but not with prasugrel, was an independent predictor of the composite
297  primary percutaneous intervention (PCI) and prasugrel were tested for platelet reactivity using puri
298 relor augments CBFV to a greater extent than prasugrel when incremental doses of adenosine are admini
299 ere has been a steady increase in the use of prasugrel with the drug being used in approximately 22%
300 e directly compared genotyping strategies or prasugrel with ticagrelor.
301 rvention, who received either clopidogrel or prasugrel within 24 hours of admission at 361 US hospita

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