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1 re included, including 3,237 (34%) receiving aspirin.
2 let and non-platelet eicosanoids affected by aspirin.
3 mg twice daily) plus aspirin or placebo plus aspirin.
4 iratory disease-like (ptges1(-/-)) mice with aspirin.
5 mg aspirin daily or rivaroxaban placebo plus aspirin.
6 min K antagonist (VKA) and with placebo than aspirin.
7 riptions for 90 or more consecutive doses of aspirin.
8 dopt preventive strategies, such as low-dose aspirin.
9 l patients were on clopidogrel 75 mg/day and aspirin.
10 REDS2 participants, 1198 (49.9%) were taking aspirin.
11 asurably lower in cardiology patients taking aspirin.
12    These patients are generally treated with aspirin.
13 75 to 100 mg daily) or matching placebo plus aspirin.
14 most famous being salicin, the progenitor of aspirin.
15  them to anti- and pro-thrombotic effects of aspirin.
16  (2001-2020) that studied discontinuation of aspirin 1 to 3 months after PCI with continued P2Y(12) i
17 were randomized (1:1:1) to receive 100 mg of aspirin 1, 2, or 3 times daily for 2 weeks.
18 eeding was observed for recent initiators of aspirin (1.40; 1.13-1.72;p = 0.002) but not for those co
19  with GFR >=60 ml/min (2.9% rivaroxaban plus aspirin, 1.6% aspirin alone, HR: 1.81; 95% CI: 1.44 to 2
20  daily plus aspirin 100 mg once daily versus aspirin 100 mg once daily reduced the primary major adve
21 PI) with rivaroxaban 2.5 mg twice daily plus aspirin 100 mg once daily versus aspirin 100 mg once dai
22 cts of rivaroxaban (2.5 mg twice daily) plus aspirin (100 mg daily) versus placebo plus aspirin in pa
23        Routine perioperative use of low-dose aspirin (100 mg/d) does not decrease cardiovascular even
24  Patients who were starting to take low-dose aspirin (14,205 patients) were identified by their first
25 e with GFR <60 ml/min (3.9% rivaroxaban plus aspirin, 2.7% aspirin alone, HR: 1.47, 95% CI: 1.05 to 2
26 initial concentration 70 mg/L, using 2000 mg aspirin, (2) carbamazepine, initial concentration 35 mg/
27  2016, respectively, from 57.3% to 64.3% for aspirin, 3.6% to 24.8% for clopidogrel, and 36.2% to 77.
28 ing dose followed by 90 mg twice daily) plus aspirin (300 to 325 mg on the first day followed by 75 t
29 s were randomly assigned to receive low-dose aspirin (5990 women) or placebo (5986 women).
30  significantly between users and nonusers of aspirin (7.8% and 6.9%, respectively; difference, 0.9 pe
31 de, and 10 mg of ramipril) or placebo daily, aspirin (75 mg) or placebo daily, and vitamin D or place
32 hrombotic strategy (rivaroxaban [10 mg] plus aspirin [75 to 100 mg] once daily) or an antiplatelet-ba
33 let-based strategy (clopidogrel [75 mg] plus aspirin [75 to 100 mg] once daily).
34 G to ticagrelor or placebo added to standard aspirin (80 mg or 100 mg).
35 masked, placebo-controlled trial of low-dose aspirin (81 mg daily) initiated between 6 weeks and 0 da
36  naproxen (95% CI: 0.85, 1.35), and 1.05 for aspirin (95% CI: 0.81, 1.35), as compared with nonuse of
37 telet activation as an efficacious target of aspirin, a widely available and affordable host-directed
38 ntieth century, coincident with marketing of aspirin-a signature event in the history of modern drug
39  whether the anti-inflammatory activities of aspirin (acetylsalicylic acid [ASA]) could protect again
40 lts explain why increasing aspirin dosage or aspirin addition to other drugs may lessen antithromboti
41 oronary syndrome, in whom discontinuation of aspirin after 1 to 3 months reduced bleeding by 50% (1.7
42 n making on the ideal duration of the use of aspirin after an acute coronary syndrome or percutaneous
43  is commonly used as a short-term adjunct to aspirin after endovascular revascularization.
44  data support the addition of rivaroxaban to aspirin after lower extremity revascularization regardle
45 ge >40 years, coronary artery bypass, and no aspirin after LT as independent risk factors for early o
46 of coronary artery calcium (CAC) for guiding aspirin allocation for primary prevention by using 2019
47 e cardiovascular events (MACE) compared with aspirin alone after percutaneous coronary intervention (
48 tal of 331 patients were assigned to receive aspirin alone and 334 were assigned to receive aspirin p
49 nt occurred in 76 patients (23.0%) receiving aspirin alone and in 104 (31.1%) receiving aspirin plus
50 nt occurred in 50 patients (15.1%) receiving aspirin alone and in 89 (26.6%) receiving aspirin plus c
51 in resistance than all patients treated with aspirin alone and TCT decreased the frequency of aspirin
52 alone as compared with matching placebo, for aspirin alone as compared with matching placebo, and for
53                    Ticagrelor and aspirin or aspirin alone in acute ischemic stroke or TIA.
54  with rivaroxaban 2.5 mg plus aspirin versus aspirin alone in those with GFR >=60 ml/min (2.9% rivaro
55  anticoagulation, in a 1:1 ratio, to receive aspirin alone or aspirin plus clopidogrel for 3 months.
56  was lower with ticagrelor-aspirin than with aspirin alone, but the incidence of disability did not d
57  ml/min (3.9% rivaroxaban plus aspirin, 2.7% aspirin alone, HR: 1.47, 95% CI: 1.05 to 2.07).
58  ml/min (2.9% rivaroxaban plus aspirin, 1.6% aspirin alone, HR: 1.81; 95% CI: 1.44 to 2.28) and simil
59 thout a previous PCI treated with DPI versus aspirin alone.
60 ke, or death from cardiovascular causes than aspirin alone.
61 igher with rivaroxaban and aspirin than with aspirin alone.
62 coronary intervention and the withholding of aspirin among patients with both CCS and atrial fibrilla
63 ere reported in 36 participants who received aspirin and 36 participants who received placebo.
64  or placebo; 427 (50%) participants received aspirin and 434 (50%) placebo.
65 ccurred in 668 (11.6%) of the women who took aspirin and 754 (13.1%) of those who took placebo (RR 0.
66               Dual antiplatelet therapy with aspirin and a P2Y(12) inhibitor has been shown to reduce
67 et count that can be partially reversed with aspirin and a P2Y12 antagonist.
68                                  Concomitant aspirin and anticoagulation in critically ill surgical p
69 matic thrombosis occurred and resolved under aspirin and anticoagulation therapy.
70                   In conclusion, patients on aspirin and clopidogrel had a higher incidence of aspiri
71      Although dual antiplatelet therapy with aspirin and clopidogrel reduces early recurrence of isch
72 utcome except for reduced co-prescription of aspirin and clopidogrel without gastro-protection in pat
73       Results showed that in patients taking aspirin and clopidogrel, the incidence of aspirin resist
74 report clinical benefit when desensitized to aspirin and maintained on daily aspirin therapy.
75 tion, such that a strong association between aspirin and major bleeding was observed for recent initi
76 disease without safety concerns around using aspirin and meeting trial eligibility criteria.
77 by chronic rhinosinusitis and intolerance of aspirin and other COX1 inhibitors.
78  develop bronchospasm after the ingestion of aspirin and other nonsteroidal anti-inflammatory drugs,
79 us triple therapy (vitamin K antagonist plus aspirin and P2Y12 inhibitor) in patients with nonvalvula
80 events during the intervention phase between aspirin and placebo groups were similar, and no signific
81 s to 6 months with apixaban and VKA and with aspirin and placebo.
82 ll surgical patients may receive concomitant aspirin and therapeutic anticoagulation postoperatively,
83 , all 3 of our patients were taking low-dose aspirin and/or clopidogrel as secondary cardiovascular p
84 redient (ibuprofen, acetaminophen, naproxen, aspirin) and cumulative monthly dose.
85 relor Compared to Placebo on a Background of Aspirin), and FOURIER (Further Cardiovascular Outcomes R
86 AREDS participants, 1049 (28.1%) were taking aspirin, and of the 2403 eligible AREDS2 participants, 1
87 ry syndrome were randomly assigned to DPI or aspirin, and, of these, 9862 (59.6%) had previous PCI (m
88 ose tissue of OSA patients receiving statin, aspirin, and/or RAS inhibitors was comparable to non-OSA
89 cent studies have highlighted the utility of aspirin as a host-directed therapy modulating the inflam
90  matching placebo, and for the polypill plus aspirin as compared with double placebo.
91 ated fatty acids (omega-3 PUFA) and low-dose aspirin (ASA) have been proposed as a host modulation re
92 .5 mg twice daily plus acetylsalicylic acid (aspirin; ASA) 100 mg reduced the risk of cardiovascular
93 r the first 3 months) (rivaroxaban group) or aspirin at a dose of 75 to 100 mg daily (with clopidogre
94 e rivaroxaban at a dose of 10 mg daily (with aspirin at a dose of 75 to 100 mg daily for the first 3
95                            Intervention with aspirin, atorvastatin or renin-angiotensin system (RAS)
96 afety of a four-component polypill including aspirin, atorvastatin, hydrochlorothiazide, and either e
97 linical benefit of low-dose rivaroxaban plus aspirin, but at the expense of increased bleeding risk i
98        The antiplatelet response to low-dose aspirin can be markedly improved by shortening the dosin
99               From randomization to 30 days, aspirin caused more severe bleeding (absolute risk diffe
100  and aspirin-tolerant (n = 82) who underwent aspirin challenge from May 2014 to May 2018.
101 203769 attenuated AHR induced by allergen or aspirin challenge of wild-type or ptges1(-/-) mice, resp
102 Although it cannot replace the gold-standard aspirin challenge test, the implementation of the ANN mi
103 up Report provides a comprehensive review of aspirin challenges, aspirin desensitizations, and mainte
104 tality through colonoscopic surveillance and aspirin chemoprevention; it also enables cascade testing
105   We examined temporal changes in the use of aspirin, clopidogrel, and statins and 1-year cause-speci
106 ) inhibitor), dual antiplatelet therapy (eg, aspirin combined with a P2Y(12) inhibitor), and dual-pat
107 rs (n=14 005) who were discharged alive with aspirin combined with either clopidogrel (60.2%) or tica
108 inhibitor), and dual-pathway inhibition (eg, aspirin combined with the vascular dose of the direct or
109                  The primary outcome for the aspirin comparison occurred in 116 participants (4.1%) i
110    The primary outcome for the polypill-plus-aspirin comparison occurred in 59 participants (4.1%) in
111                                      For the aspirin comparison, the primary outcome was death from c
112     For the polypill-alone and polypill-plus-aspirin comparisons, the primary outcome was death from
113 rios, including early discontinuation of the aspirin component of dual antiplatelet therapy after per
114 ly 5% of MESA participants would qualify for aspirin consideration for primary prevention according t
115                               After 30 days, aspirin continues to increase bleeding without significa
116 ome were randomly assigned to receive 600 mg aspirin daily or placebo.
117 o rivaroxaban 2.5 mg twice daily plus 100 mg aspirin daily or rivaroxaban placebo plus aspirin.
118  comprehensive review of aspirin challenges, aspirin desensitizations, and maintenance aspirin therap
119     40 (9%) of 427 participants who received aspirin developed colorectal cancer compared with 58 (13
120                                      Mice on aspirin developed lower fibrosis and extent compared wit
121 ntibody (82.3 vs. 69.2 AU; P < 0.07) but not aspirin dialuminate (82.1 vs. 79.5 AU; P > 0.05).
122 rial, the addition of ticagrelor to standard aspirin did not reduce SVG occlusion at 1 year after CAB
123 ong aspirin users and 8.3% among nonusers of aspirin (difference, -4.3 percentage points; 95% confide
124                   The safety and efficacy of aspirin discontinuation on a background of a P2Y12 inhib
125  stroke (i.e., rates were not increased with aspirin discontinuation prior to anticoagulation).
126         These results explain why increasing aspirin dosage or aspirin addition to other drugs may le
127 tion of a computable phenotype in ADAPTABLE (Aspirin Dosing: a Patient-Centric Trial Assessing Benefi
128                     Here, we have shown that aspirin dramatically reduced lung metastasis through inh
129                                              Aspirin-exacerbated respiratory disease (AERD) is a mech
130                                              Aspirin-exacerbated respiratory disease (AERD) is charac
131                                              Aspirin-exacerbated respiratory disease (AERD) is charac
132       The cause of severe nasal polyposis in aspirin-exacerbated respiratory disease (AERD) is unknow
133 enhanced LTC(4) synthesis similar to that in aspirin-exacerbated respiratory disease, completely bloc
134 ssociated bronchoconstriction by challenging aspirin-exacerbated respiratory disease-like (ptges1(-/-
135  properties of desensitization to aspirin in aspirin-exacerbated respiratory disease.
136 l anti-inflammatory drugs, a disorder termed aspirin-exacerbated respiratory disease.
137 ), a similar trial treating with clopidogrel-aspirin for 21 days and showing no increase in major hem
138 n in acute stroke; early or first aid use of aspirin for chest pain; control of life-threatening blee
139                                              Aspirin for primary atherosclerotic cardiovascular disea
140 vascular disease, the efficacy and safety of aspirin for primary prevention has become uncertain.
141        Monotherapy with a P2Y12 inhibitor or aspirin for secondary prevention in patients with establ
142 l clinical trial testing the optimal dose of aspirin for secondary prevention of atherosclerotic card
143 tor targets, indicating that the efficacy of aspirin for secondary prevention of CCS may similarly ha
144  raise some uncertainty as to the primacy of aspirin for the lifelong management of all patients with
145                      Whether the benefits of aspirin for the primary prevention of cardiovascular dis
146 irin group and in 345 patients (6.3%) in the aspirin group (hazard ratio, 0.79; 95% CI, 0.68 to 0.93;
147 irin group and in 362 patients (6.6%) in the aspirin group (hazard ratio, 0.83; 95% confidence interv
148 d significantly reduced overall risk for the aspirin group (HR=0.63, 0.43-0.92; p=0.018).
149 spirin group and in 7 patients (0.1%) in the aspirin group (P = 0.001).
150 erwent randomization (5523 in the ticagrelor-aspirin group and 5493 in the aspirin group).
151                            5780 women in the aspirin group and 5764 in the placebo group were evaluab
152 n occurred in 116 participants (4.1%) in the aspirin group and in 134 (4.7%) in the placebo group (ha
153 red in 276 patients (5.0%) in the ticagrelor-aspirin group and in 345 patients (6.3%) in the aspirin
154 red in 303 patients (5.5%) in the ticagrelor-aspirin group and in 362 patients (6.6%) in the aspirin
155 rred in 28 patients (0.5%) in the ticagrelor-aspirin group and in 7 patients (0.1%) in the aspirin gr
156 om 861 agreed to be randomly assigned to the aspirin group or placebo; 427 (50%) participants receive
157 the ticagrelor-aspirin group and 5493 in the aspirin group).
158  multiple blood-pressure-lowering drugs, and aspirin has been proposed to reduce the risk of cardiova
159           A total of 95 asthma patients with aspirin hypersensitivity underwent sputum induction.
160 sults support a more complex pathobiology of aspirin hypersensitivity.
161                                       Use of aspirin immediately and for up to 30 days results in an
162 tigated whether ticagrelor added to standard aspirin improves SVG patency at 1 year after CABG.
163 therapeutic properties of desensitization to aspirin in aspirin-exacerbated respiratory disease.
164 llenging the previously unquestioned role of aspirin in CCS have come from recent trials where aspiri
165                  The safety of discontinuing aspirin in favor of P2Y(12) inhibitor monotherapy remain
166                               The Effects of Aspirin in Gestation and Reproduction Trial (2006-2012)
167 ase for prevention of colorectal cancer with aspirin in Lynch syndrome is supported by our results.
168  to consistently demonstrate net benefit for aspirin in patients treated to optimal contemporary card
169 s aspirin (100 mg daily) versus placebo plus aspirin in patients with diabetes mellitus versus withou
170 evious trial, ticagrelor was not better than aspirin in preventing vascular events or death after str
171  in a more personalized, safer allocation of aspirin in primary prevention.
172 cohort equations to inform the allocation of aspirin in primary prevention.
173 thy older adults using data from the ASPREE (Aspirin in Reducing Events in the Elderly) trial.
174 her study of the universal need for lifelong aspirin in secondary prevention for all adults with CCS,
175 rials: the NAVIGATE ESUS (Rivaroxaban Versus Aspirin in Secondary Prevention of Stroke and Prevention
176 aboration, solidified the historical role of aspirin in secondary prevention.
177                      Although the benefit of aspirin in the immediate phase after a myocardial infarc
178 e the first trial suggesting the efficacy of aspirin in the secondary prevention of myocardial infarc
179 m assessment of the effect of taking regular aspirin in this high-risk population.
180 CE was not observed after discontinuation of aspirin, including in patients with acute coronary syndr
181 ng airway PGE2 biosynthesis in allergen- and aspirin-induced asthma.
182 e older patients who are at highest risk for aspirin-induced bleeding.
183 of prostaglandin E(2) (PGE(2)) contribute to aspirin-induced hypersensitivity.
184  prostaglandin D(2) metabolite levels during aspirin-induced reactions in the study population as a w
185 o therapeutic concentration in 460 min while aspirin infusion reduces that time to 330 min.
186 he physiologic response to subsequent lysine-aspirin inhalation challenges, as well as increases in l
187 income and middle-income countries, low-dose aspirin initiated between 6 weeks and 0 days of gestatio
188 out established CAD, primary prevention with aspirin is not routinely advocated because of its increa
189                                     Low-dose aspirin is recommended for prophylaxis in high-risk popu
190 estigated the possibility that the effect of aspirin is related to an antiplatelet mode of action.
191                          Once-daily low-dose aspirin is the recommended antithrombotic regimen, but a
192 outweigh the risks of bleeding, and low-dose aspirin is uniformly recommended in this setting.
193      Combined treatment with a polypill plus aspirin led to a lower incidence of cardiovascular event
194         However, the non-platelet actions of aspirin limit its antithrombotic effects.
195 use of preventive pharmacotherapies, such as aspirin, lipid-lowering mediations, and cardiometabolic
196 eded about the long-term effects of low-dose aspirin (&lt;=160 mg) on incident hepatocellular carcinoma,
197 ocation for primary prevention by using 2019 aspirin meta-analysis data on cardiovascular disease rel
198 0.45-0.83]), and short-term DAPT followed by aspirin monotherapy (absolute risk difference, -6.1 inci
199 on to conventional 12-month DAPT followed by aspirin monotherapy in the reduction of the primary comp
200  with midterm or short-term DAPT followed by aspirin monotherapy, with the exception that short-term
201 olled trials including 165,502 participants (aspirin n = 83,529, control n = 81,973) were available f
202      Patients on chronic once-daily low-dose aspirin (n = 245) were randomized (1:1:1) to receive 100
203 an plus aspirin (n=9152) versus placebo plus aspirin (n=9126) in patients both with (n=6922) and with
204 ion was seen for benefit of rivaroxaban plus aspirin (n=9152) versus placebo plus aspirin (n=9126) in
205 Benefit/harm calculations were restricted to aspirin-naive participants <70 years of age not at high
206 ention agents that have been studied include aspirin, nonaspirin nonsteroidal anti-inflammatory drugs
207 s related to the following variables: use of aspirin/NSAIDs/anti-coagulants/anti-platelets, pathologi
208 of ticagrelor monotherapy vs ticagrelor with aspirin on major bleeding and cardiovascular events in p
209  effect of the combination of ticagrelor and aspirin on prevention of stroke has not been well studie
210 therapy regimen rates were determined (none, aspirin only, P2Y12 inhibitor only, and DAPT).
211 nclude single antiplatelet therapy (eg, with aspirin or a P2Y(12) inhibitor), dual antiplatelet thera
212 ubstudy within the TWILIGHT (Ticagrelor With Aspirin or Alone in High-Risk Patients After Coronary In
213                               Ticagrelor and aspirin or aspirin alone in acute ischemic stroke or TIA
214 tening bleeding compared with treatment with aspirin or clopidogrel alone in patients at high risk fo
215           The combination of cilostazol with aspirin or clopidogrel had a reduced incidence of ischae
216                                  Conversely, aspirin or lack of systemic COX-1 activity decreased the
217 pared short-term (<6-month) DAPT followed by aspirin or P2Y12 inhibitor monotherapy; midterm (6-month
218 P2Y(12) inhibitor were randomized to blinded aspirin or placebo and to open-label apixaban or VKA for
219 eceive rivaroxaban (2.5 mg twice daily) plus aspirin or placebo plus aspirin.
220 men with previous pregnancy loss to low dose aspirin or placebo prior to conception.
221 ssigned (1:1, stratified by site) to receive aspirin or placebo tablets of identical appearance, via
222 deline-directed medical therapies, including aspirin (p < 0.001), statin (p < 0.001), and beta-blocke
223 icoagulation for atrial fibrillation, use of aspirin, perimenopausal hormone therapy, and psychosocia
224 xaban vs Vitamin K Antagonist and Aspirin vs Aspirin Placebo in Patients With Atrial Fibrillation and
225 g aspirin alone and in 104 (31.1%) receiving aspirin plus clopidogrel (difference, -8.2 percentage po
226 ng aspirin alone and in 89 (26.6%) receiving aspirin plus clopidogrel (risk ratio, 0.57; 95% confiden
227 icantly less frequent with aspirin than with aspirin plus clopidogrel administered for 3 months.
228  in a 1:1 ratio, to receive aspirin alone or aspirin plus clopidogrel for 3 months.
229 pirin alone and 334 were assigned to receive aspirin plus clopidogrel.
230 n stable atherosclerosis, the combination of aspirin plus rivaroxaban 2.5 mg twice daily provided a s
231 e patients would benefit from treatment with aspirin plus ticagrelor.
232                                              Aspirin-precipitated bronchoconstriction is associated w
233 nsteroidal anti-inflammatory drug use except aspirin prescribed for secondary prevention of cardiovas
234                                              Aspirin prevents thrombosis by inhibiting platelet cyclo
235 n those with previous PCI, DPI compared with aspirin produced consistent (robust) reductions in MACE
236       Regardless of previous PCI, DPI versus aspirin produced consistent reductions in MACE (PCI: 4.0
237                            DPI compared with aspirin produced consistent reductions in MACE and morta
238   In the VOYAGER PAD trial, rivaroxaban plus aspirin reduced the risk of adverse cardiovascular and l
239     In conclusion, the currently recommended aspirin regimen of 75 to 100 once daily for cardiovascul
240 blind trial to investigate the efficacy of 3 aspirin regimens in optimizing platelet COX-1 inhibition
241                             The incidence of aspirin resistance in aspirin-treated patients or platel
242 rin alone and TCT decreased the frequency of aspirin resistance in this group.
243 in and clopidogrel had a higher incidence of aspirin resistance than all patients treated with aspiri
244 ng aspirin and clopidogrel, the incidence of aspirin resistance was significantly decreased from 40%
245                                Compared with aspirin, rivaroxaban increased TIMI major bleeding simil
246 esolvins and AT-lipoxins may explain some of aspirin's broad anticancer activity.
247  the risk of severe bleeding was higher with aspirin than placebo (absolute risk difference, 1.25% [9
248 ath within 30 days was lower with ticagrelor-aspirin than with aspirin alone, but the incidence of di
249 as significantly higher with rivaroxaban and aspirin than with aspirin alone.
250 1 year were significantly less frequent with aspirin than with aspirin plus clopidogrel administered
251                           Discontinuation of aspirin therapy 1 to 3 months after PCI significantly re
252  studies evaluating the clinical efficacy of aspirin therapy after desensitization as well as a discu
253 ization, and recommendations for maintenance aspirin therapy following desensitization are reviewed.
254                              The benefits of aspirin therapy for the secondary prevention of cardiova
255 s, aspirin desensitizations, and maintenance aspirin therapy in patients with AERD.
256  Guidelines recommended considering low-dose aspirin therapy only among adults 40 to 70 years of age
257 ernal care and possible chemoprevention (eg, aspirin therapy) to prevent preeclampsia, a disease that
258 ensitized to aspirin and maintained on daily aspirin therapy.
259 ch may help focus the use of rivaroxaban and aspirin therapy.
260                      The overall NNT(5) with aspirin to prevent 1 cardiovascular disease event was 47
261                    Meta-analyses of low-dose aspirin to prevent pre-eclampsia suggest that the incide
262 ls have evaluated the use of clopidogrel and aspirin to prevent stroke after an ischemic stroke or tr
263 periority of rivaroxaban plus aspirin versus aspirin to reduce major cardiac and ischemic limb events
264 atabase of patients with N-ERD (n = 121) and aspirin-tolerant (n = 82) who underwent aspirin challeng
265  and lower respiratory tract disease than do aspirin-tolerant patients with CRSwNP.
266 ly different profile from global-COX-1-ko or aspirin-treated control mice, notably significantly high
267       The incidence of aspirin resistance in aspirin-treated patients or platelet inhibition in patie
268                            We also show that aspirin-triggered 15-epi-lipoxin A(4) (15-epi-LXA(4)) an
269 le Haemophilus influenzae, using 17-HDHA and aspirin-triggered-resolvin D1 (AT-RvD1) as adjuvants.
270 rough 2015 and who did not have a history of aspirin use (50,275 patients).
271 ciated with increased risk of EOCRC, whereas aspirin use and being overweight or obese (relative to n
272 uggested a differential relationship between aspirin use and major bleeding based on aspirin use in t
273 ween aspirin use and major bleeding based on aspirin use in the 7 days prior to anticoagulation, such
274                                              Aspirin use prior to anticoagulation did not modify the
275 se results suggest that limiting clopidogrel-aspirin use to 21 days may maximize benefit and reduce r
276 associated with increased risk of EOCRC, and aspirin use to be significantly associated with decrease
277              In secondary analyses, low-dose aspirin use was assessed within exposure periods of 5 or
278                                              Aspirin use was not associated significantly with progre
279 y artery bypass graft surgery (CABG) despite aspirin use.
280 amily history of CRC, smoking, diabetes, and aspirin use.
281 s index (BMI), diabetes, smoking status, and aspirin use.
282 pylori (H. pylori) eradication and long-term aspirin use.
283  = 0.002) but not for those continuing prior aspirin use.
284 ical prosthesis, bridging therapies, role of aspirin, use of fibrinolytic therapy for prosthetic valv
285 year liver-related mortality was 11.0% among aspirin users and 17.9% among nonusers (difference, -6.9
286 e of hepatocellular carcinoma was 4.0% among aspirin users and 8.3% among nonusers of aspirin (differ
287 s more frequent with rivaroxaban 2.5 mg plus aspirin versus aspirin alone in those with GFR >=60 ml/m
288 demonstrated superiority of rivaroxaban plus aspirin versus aspirin to reduce major cardiac and ische
289 (HR) of 0.65 (95% CI 0.43-0.97; p=0.035) for aspirin versus placebo.
290 me enrolled into a randomised trial of daily aspirin versus placebo.
291 ents) over time with apixaban versus VKA and aspirin versus placebo.
292 fety of Apixaban vs Vitamin K Antagonist and Aspirin vs Aspirin Placebo in Patients With Atrial Fibri
293                                              ASPIRIN was a randomised, multicountry, double-masked, p
294 roxaban at a dose of 2.5 mg twice daily plus aspirin was associated with a significantly lower incide
295 c viral hepatitis in Sweden, use of low-dose aspirin was associated with a significantly lower risk o
296 in in CCS have come from recent trials where aspirin was discontinued in specific clinical scenarios,
297                              In women taking aspirin, we also observed significant reductions in peri
298 withdrawal of acetylsalicylic acid (ASA), or aspirin, while maintaining P2Y(12) inhibition.
299                           Discontinuation of aspirin with continued P2Y(12) inhibitor monotherapy red
300 lower liver-related mortality than no use of aspirin, without a significantly higher risk of gastroin

 
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