ライフサイエンスコーパス: bleeding risk

1 -6 months) treatment in relation to baseline bleeding risk.

2 ion is controversial because of an increased bleeding risk.

3 observed benefits are influenced by baseline bleeding risk.

4 t eliminate thrombosis, and have substantial bleeding risk.

5 NSAID exposure was associated with increased bleeding risk.

6 nd thromboembolic stroke, without increasing bleeding risk.

7 olic or coronary risk, but notably increased bleeding risk.

8 thromboembolism (VTE) who had a significant bleeding risk.

9 secondary endpoint), without an increase in bleeding risk.

10 tithrombotic strategy with a potentially low bleeding risk.

11 h clopidogrel but are associated with higher bleeding risk.

12 ; 3) predict thrombotic risk; and 4) predict bleeding risk.

13 en by not only predominantly stroke but also bleeding risk.

14 (TIA) as a marker of increased intracranial bleeding risk.

15 urrent mainstream use cannot reliably assess bleeding risk.

16 of acquired TTP without evidence of a severe bleeding risk.

17 bocytopenia was not linked with an excessive bleeding risk.

18 isks of the use of OAC in patients with high bleeding risk.

19 nhibitor of FXI, with focus on assessment of bleeding risk.

20 hose associated with an intermediate or high bleeding risk.

21 olic events, but at the cost of an increased bleeding risk.

22 ation conjunctively used for MI with reduced bleeding risk.

23 e biopsy, and no increased cardiovascular or bleeding risk.

24 e metabolic pathways that may increase major bleeding risk.

25 vitamin K antagonists is closely related to bleeding risk.

26 reatment categories did platelet dose affect bleeding risk.

27 The use of warfarin has a well-known bleeding risk.

28 e second-generation APC mutants with reduced bleeding risk.

29 effect must be balanced against an increased bleeding risk.

30 hrombotic therapeutic potential with reduced bleeding risk.

31 in the absence of active bleeding or a high bleeding risk.

32 ng an elective procedure on a patient with a bleeding risk.

33 oncurrent systemic anticoagulation increased bleeding risk.

34 ts the abnormality nor reduces the perceived bleeding risk.

35 d in the identification of targets to reduce bleeding risk.

36 opidogrel therapy is costly and may increase bleeding risk.

37 ophylaxis in all ICU patients, regardless of bleeding risk.

38 tine testing has no benefit in assessment of bleeding risk.

39 induced thrombocytopenia, without increasing bleeding risk.

40 improve early IRA patency without increasing bleeding risk.

41 othetical cohort was stratified according to bleeding risk.

42 surgery in cirrhotic patients stratified by bleeding risk.

43 savings depended on the individual patient's bleeding risk.

44 variceal bleeding in cirrhosis regardless of bleeding risk.

45 risk of MI but was associated with increased bleeding risk.

46 d tomographic angiography, respectively) and bleeding risk.

47 alization, without a significant increase in bleeding risk.

48 ose with CVD risk factors that also increase bleeding risk.

49 use kidney biopsies are avoided due to their bleeding risk.

50 nts with hemodynamic decompensation and high bleeding risk.

51 lder without known CVD and without increased bleeding risk.

52 ivator) therapy may be required, despite its bleeding risk.

53 -platelet aggregation activities, with a low bleeding risk.

54 e creatinine clearance and procedure-related bleeding risk.

55 and little is known about their intraocular bleeding risk.

56 hromboembolism, with no apparent increase of bleeding risk.

57 concentrations, which significantly increase bleeding risk.

58 hosphate (ADP) are associated with increased bleeding risk.

59 ilter placement because of known significant bleeding risk.

60 tricular assist device support and increased bleeding risk.

61 es targeting them may be associated with low bleeding risks.

62 intravascular coagulation without increasing bleeding risks.

63 , is associated with increased mortality and bleeding risks.

64 iovascular benefits of warfarin outweigh the bleeding risks.

65 ention of ischemic events, despite increased bleeding risks.

66 sights into the balance between ischemic and bleeding risks.

67 cantly than empirical models when estimating bleeding risks.

68 S(2)-VASc score of 0 and moderately elevated bleeding risk (-1.7%/y).

69 ents into groups to distinguish ischemic and bleeding risk 12 to 30 months after PCI.

70 lopidogrel (n = 139) significantly increased bleeding risk (7.2% vs. 1.6%; p = 0.004).

71 Considering both ischemia and bleeding risk, a large proportion of TRITON participants

72 was associated with increased mortality and bleeding risks (adjusted ORs, 1.39 [95% CI, 1.33 to 1.46

73 at the time of injury can also contribute to bleeding risk after TBI.

74 a contraindicated medication with attendant bleeding risk, although this did not translate into sign

75 nown whether there are racial differences in bleeding risks among patients with ST-segment-elevation

76 clopidogrel therapy and its association with bleeding risks among those having "early" CABG < or =5 d

77 No association between postoperative bleeding risk and Caprini score was identified.

78 tified into deciles based on their predicted bleeding risk and compared with PCI indication.

79 din use in patients at intermediate and high bleeding risk and decreased use in lower-risk patients.

80 latelet inhibition appears to correlate with bleeding risk and drug tolerability.

81 of these findings might be useful to reduce bleeding risk and improve outcomes in ACS.

82 therapy for hemophilia B aims to ameliorate bleeding risk and provide endogenous factor IX (FIX) act

83 t bleeding history correlates with increased bleeding risk and should be considered in tailoring the

84 cava filter insertion for known significant bleeding risk and the outcomes of all-cause mortality, p

85 more effective than sucralfate in decreasing bleeding risk and transfusion requirements.

86 esent challenges in diagnosis, evaluation of bleeding risk and treatment.

87 ent in the preoperative period to assess for bleeding risks and anemia, with a goal to optimize a pat

88 idualized assessment of aspirin's effects on bleeding risks and expected benefits because absolute bl

89 omy, a clear understanding of its associated bleeding risks and management is mandatory.

90 xtensive acute iliofemoral DVT, low expected bleeding risk, and good functional status.

91 Such triple therapy confers an elevated bleeding risk, and its optimal duration is not known.

92 iximab reduced 30-day TVR without increasing bleeding risk, and primary stenting reduced 1-year TVR a

93 To reduce APC-associated bleeding risk, APC variants were engineered to lack >90%

94 Uncertainty remains as to which markers of bleeding risk are independent predictors.

95 mediating anticoagulant actions and related bleeding risks are distinct from those mediating cytopro

96 thrombotic complications, but also minimize bleeding risk, are well tolerated in patients with organ

97 TT should only be prescribed after thorough bleeding risk assessment of patients.

98 e prevention of ischaemic stroke, as well as bleeding risk assessment, mitigation and management.

99 To compare the ischemic and bleeding risks associated with glycoprotein IIb/IIIa inh

100 e therefore compared the acute mortality and bleeding risks associated with the initial use of 162 ve

101 confidence interval, 1.25-3.08; P<0.0001) or bleeding risk at 3 months (odds ratio, 1.92; 95% confide

102 men (OR 1.27, 95% CI 0.97 to 1.66); however, bleeding risk attributable to dosing was much higher in

103 Guidelines support weighting bleeding risk before the selection of treatment duration

104 There was no statistical difference in bleeding risk between patients continued on warfarin wit

105 dicted ischemia risk/difference in predicted bleeding risk between prasugrel and clopidogrel was calc

106 Furthermore, the relationships among bleeding risk, bleeding site, and mortality are unclear.

107 core not only is useful in the assessment of bleeding risk, but also shows some predictive value for

108 14-3-3zeta-deficient mice does not increase bleeding risk, but results in decreased thrombin generat

109 atory drugs (NSAIDs) are assumed to increase bleeding risk, but their actual relation to serious blee

110 Whether routine estimation of individualized bleeding risk can affect physicians' use of bivalirudin

111 Bleeding risk can be assessed by HAS-BLED score, whereas

112 Baseline prediction of bleeding risk can complement ischemic risk prediction fo

113 herapy is safe, and with proper precautions, bleeding risks can be minimized.

114 Key topics discussed include bleeding risk; cardiac complications, particularly atria

115 Among those with high bleeding risk, CHADS(2) stroke risk had a smaller impact

116 with roughly half of the reduction in annual bleeding risk: change in risk ratio from 7.5% to 4% for

117 Sorafenib was associated with increased bleeding risk compared to control for all grade bleeding

118 imilar ischemic risk and lower risk-adjusted bleeding risk compared with clopidogrel-GPIs.

119 gher baseline stroke risk and lower baseline bleeding risk compared with men.

120 that integrates patient-specific stroke and bleeding risk could result in significant gains in quali

121 individualized assessment of recurrence and bleeding risk, coupled with patient preference.

122 h low bleeding risk, whereas those with high bleeding risk demonstrate consistently lower use of OAC

123 ortality (risk difference, -0.8%; P=0.76) or bleeding (risk difference, 2.3%; P=0.33) and with signif

124 /- mice, a level that carries no significant bleeding risk, dramatically decreased adenoma formation

125 oprotective effects of APC while diminishing bleeding risk due to reduction in APC's anticoagulant an

126 t to assess whether incorporation of routine bleeding risk estimates affected the utilization of biva

127 ng after the incorporation of individualized bleeding risk estimates into clinical practice.

128 Beginning in July 2009, individualized bleeding risk estimates were provided immediately preced

129 tion prescribing patterns would suggest that bleeding risk estimation by clinicians is poor and that

130 was to compare the predictive performance of bleeding risk-estimation tools in a cohort of patients w

131 r gastrointestinal bleeding in patients with bleeding risk factors (1B); oral or enteral (if necessar

132 Several bleeding risk factors and CHA2DS2-VASc scores were lower

133 ch 11, 2015, that reported on AF and stroke, bleeding risk factors, and stroke prevention.

134 sted for previously identified mortality and bleeding risk factors.

135 postdischarge between groups, adjusting for bleeding risk factors.

136 D score should focus attention on reversible bleeding risk factors.

137 se outcomes, while controlling for available bleeding risk factors.

138 mia were independently associated with major bleeding risk; female sex and DBP <90 mm Hg were associa

139 Bleeding risk for NOACs may be increased in persons olde

140 the estimation of oral anticoagulant-related bleeding risk for use in clinical practice, supporting r

141 ypothetical patients into cardiovascular and bleeding risk groups on the basis of published data.

142 Bleeding risk >30 days was lowest in MRep versus MVRb an

143 YP2C9 genotype and anticoagulation status or bleeding risk has not been established.

144 mbotic events without excessive increases in bleeding risk has remained the same for decades.

145 Those at higher bleeding risk (HAS-BLED >/= 3) were also at highest risk

146 We compared patients with low-intermediate bleeding risk (HAS-BLED 0-2) and high risk (HAS-BLED >/=

147 thetic techniques are mainly associated with bleeding risks, hemodynamic side-effects, difficulties i

148 ogrel therapy was not associated with higher bleeding risks if CABG was delayed >5 days (adjusted OR

149 the CHA2DS2VASc scores and do not integrate bleeding risk in an explicit, quantitative manner.

150 yocardial infarction (MI) risk and increases bleeding risk in comparison with aspirin alone.

151 A significantly lower major bleeding risk in comparison with VKA was observed for ap

152 e coagulation tests are poor determinants of bleeding risk in critically ill patients with coagulopat

153 Furthermore, clopidogrel increased bleeding risk in early cardiac surgery.

154 These tests may be useful markers of future bleeding risk in ITP.

155 PURPOSE OF REVIEW: To assess the safety and bleeding risk in men on chronic oral anticoagulation, in

156 Our study aimed to estimate postoperative bleeding risk in older adults taking clopidogrel before

157 ere also associated with a somewhat elevated bleeding risk in patients receiving allogeneic stem cell

158 pies as well as strategies aimed at reducing bleeding risk in patients treated with these therapies.

159 dogrel therapy is associated with a variable bleeding risk in patients undergoing coronary artery byp

160 s that need to balance ischaemic benefit and bleeding risk in patients with acute coronary syndromes.

161 oke risk, but it is associated with a higher bleeding risk in patients with AF undergoing dialysis.

162 s demonstrated usefulness in assessing major bleeding risk in patients with AF.

163 concomitantly) has been suggested to assess bleeding risk in patients with atrial fibrillation (scor

164 nogen and platelets) correspond to increased bleeding risk in patients with liver cirrhosis in the in

165 ) is associated with heightened ischemic and bleeding risk in patients with prior myocardial infarcti

166 ors that have been developed so far increase bleeding risk in patients, likely because they interfere

167 eed to take into consideration the potential bleeding risk in sepsis patients who are already at incr

168 ficant 6% to 8% per year reduction in annual bleeding risk in UA/NSTEMI and elective PCI, but not in

169 are needed to establish the net benefit and bleeding risks in PAD.

170 wn about contemporary treatment patterns and bleeding risks in this population.

171 Major bleeding risk increased with age, but there were no diff

172 ic 0.715, 95% CI: 0.69 to 0.74) showed major bleeding risk increased with dabigatran exposure (p < 0.

173 bating thrombotic diseases without increased bleeding risk, indicating that polyphosphate drives thro

174 s presenting with VTE and with a significant bleeding risk, inferior vena cava filter insertion compa

175 gulants (DOACs) in the elderly, particularly bleeding risks, is unclear despite the presence of great

176 was observed in all strata of preprocedural bleeding risk (low: 1.62% vs 0.17%; risk difference, 1.4

177 ked to categorize their patients' stroke and bleeding risks: low risk (<3%); intermediate risk (3%-6%

178 lementation, for patients across 3 strata of bleeding risk (<1%, 1% to 3%, and >3%).

179 latelet counts, indicating that their excess bleeding risk may be because of factors other than plate

180 Increased bleeding risk may be minimized by reduction and weight-a

181 risks and expected benefits because absolute bleeding risk may vary considerably by patient.

182 e of mortality reduction related to baseline bleeding risk (MMRS <10, OR: 0.73 [95% CI: 0.62 to 0.86]

183 sing the newly revised CathPCI Registry((R)) bleeding risk model (c-index, 0.77) among 1292 National

184 by preprocedural risk assessed with the NCDR bleeding risk model (low risk, 0.72%; intermediate risk,

185 Anticoagulants will probably always increase bleeding risk, necessitating tailored treatment strategi

186 the benefit of anticoagulation outweighs the bleeding risk (net clinical benefit) has been shown to b

187 otic treatment was associated with increased bleeding risk (odds ratio, 1.40 [95% CI, 1.14-1.72] for

188 stable cardiovascular disease), however, the bleeding risk of dual therapy exceeds its potential bene

189 was undertaken to compare the periprocedural bleeding risk of patients in the Randomized Evaluation o

190 ith acute coronary syndromes to mitigate the bleeding risk of standard-dose prasugrel (10 mg/d).

191 e that further work is needed to clarify the bleeding risks of these DOACs in the elderly.

192 The impact of baseline bleeding risk on 30-day mortality and its relationship w

193 assessed the association between stroke and bleeding risk on rates of OAC.

194 Age >80 years (p = 0.008) and perceived bleeding risk (p = 0.022) were negative predictors of wa

195 ntermediate (27% to 35%, p < 0.001) and high bleeding risk patients (25% to 43%, p < 0.001), and decr

196 double-blind trial, we randomized 2,466 high bleeding risk patients to receive a drug-coated stent (D

197 to treat to prevent 1 bleeding event in high-bleeding risk patients was 68.

198 over BMS were maintained for 2 years in high bleeding risk patients.

199 anticoagulation prescribing does not reflect bleeding risk per se.

200 Three bleeding risk-prediction schemes have been derived for a

201 All 3 tested bleeding risk-prediction scores demonstrated only modest

202 al to demonstrate robust efficacy with a low bleeding risk profile.

203 -BLED score has been designed for predicting bleeding risk rather than thrombotic events per se, and

204 din-based regimens lowered the risk of major bleeding (risk ratio 0.62, 95% CI 0.49-0.78; p<0.0001),

205 Major bleeding (risk ratio, 0.82 [95% CI, 0.56, 1.21]; p=0.32;

206 7 [95% CI, 0.60, 1.25]; p=0.44; I=0%), major bleeding (risk ratio, 0.97 [95% CI, 0.75, 1.26]; p=0.83;

207 and nonsignificantly increased risk of major bleeding (risk ratio, 1.35; 95% confidence interval, 0.7

208 otic treatment was associated with increased bleeding risk regardless of admission INR level.

209 ay reduce ischemic events, but perioperative bleeding risk remains a major concern.

210 acute symptomatic VTE and known significant bleeding risk remains unclear.

211 y reperfuse some patients and the persistent bleeding risk represent areas for improvement in therapy

212 Bleeding risk represents a major concern in anticoagulat

213 The predictive value of several bleeding risk schema was assessed using the c-statistic

214 I) via the femoral approach over a validated bleeding risk score (BRS) of clinical and procedural var

215 The rate of major bleeding increased by bleeding risk score quintiles: 3.1% for those at very lo

216 OAC use fell slightly with increasing ATRIA bleeding risk score, from 81% for ATRIA=3 to 73% for ATR

217 y was to test the hypothesis that a specific bleeding risk score, HAS-BLED (hypertension, abnormal re

218 coagulated AF patients, a validated specific bleeding risk score, HAS-BLED, should be used for assess

219 ratified by trial, and developed a numerical bleeding risk score.

220 Although 17% (n=1749) had high ATRIA bleeding risk (score >/=5), only 7% (n=719) were conside

221 Risk Factors in Atrial Fibrillation (ATRIA) bleeding risk scores (>/=5).

222 d validate the predictive value of available bleeding risk scores (mOBRI, HEMORR2HAGES, Shireman, HAS

223 the discrimination performance of different bleeding risk scores and investigated if adding TTR woul

224 itantly (HAS-BLED) score against other older bleeding risk scores and the new Anticoagulation and Ris

225 risk was calculated by using modified Mehran bleeding risk scores in 348,689 PCI procedures performed

226 We hypothesised that predictive value of bleeding risk scores other than HAS-BLED could be improv

227 ation using HAS-BLED compared with all other bleeding risk scores tested.

228 ith age, sex, comorbid conditions, stroke or bleeding risk scores, follow-up interval, baseline LAA v

229 n the HAS-BLED score was compared with other bleeding risk scores, the net reclassification improveme

230 CHADS2 and CHA2DS2-VASc as a measure of high bleeding risk should be discouraged, given its inferior

231 ve an estimated thrombosis risk greater than bleeding risk should receive pharmacologic prophylaxis.

232 Of the contemporary bleeding risk stratification schemas, the new HAS-BLED s

233 to evaluate the predictive value of several bleeding risk stratification schemas.

234 factors have been incorporated into clinical bleeding risk stratification schemas.

235 ly patients, given an appropriate stroke and bleeding risk stratification.

236 oach to PCI may permit greater reductions in bleeding risk than have been achieved with pharmacologic

237 nt smokers, but it may also confer a greater bleeding risk than in nonsmokers.

238 tors of TF/FVIIa may be associated with less bleeding risk than other antithrombotic agents.

239 12 months had lower ischemic risk but higher bleeding risk than those treated with placebo and aspiri

240 mg (1.40, 1.04-1.90) and lower intracranial bleeding risks than VKA for dabigatran 150 mg (0.43, 0.2

241 it is important to understand any potential bleeding risks that may be associated with the use of en

242 associated with substantial stroke risks and bleeding risks that were similar among patients treated

243 y, the renally impaired, and those with high bleeding risk), the appropriate dose adjustment to achie

244 ssed pharmacological strategies for reducing bleeding risk, there is a mounting body of evidence sugg

245 itude of this effect was related to baseline bleeding risk; those at highest risk of bleeding complic

246 tine to rapidly regenerate ATP, may modulate bleeding risk through a dose-dependent inhibition of ADP

247 prediction rule assessing late ischemic and bleeding risks to inform dual antiplatelet therapy durat

248 The increased bleeding risk together with its long half-life and absen

249 rmal and impaired hemostasis, coupled with a bleeding risk tool, enables practitioners to make inform

250 vestigated the relationship between baseline bleeding risk, TRA utilization, and procedure-related ou

251 Among those with low bleeding risk, use of OAC increased significantly with i

252 Assessment of bleeding risk using the HAS-BLED score should focus atte

253 We estimated mortality and bleeding risk using validated models from the registry.

254 Bleeding risk was assessed by the HAS-BLED, ATRIA, ORBIT

255 Baseline bleeding risk was calculated by using modified Mehran bl

256 Thrombolysis in Myocardial Infarction major bleeding risk was increased with early eptifibatide in t

257 Coronary Arteries (GUSTO) moderate or severe bleeding risk was increased with vorapaxar and was not s

258 In patients taking aspirin alone (n = 536), bleeding risk was marginally higher than it was for pati

259 When compared to triple therapy, bleeding risk was nonsignificantly lower for OAC plus cl

260 The bleeding risk was significantly higher for dual-therapy

261 MI (HR: 1.11; 95% CI: 0.96 to 1.28), whereas bleeding risk was significantly increased (HR: 1.31; 95%

262 rombotic therapies in TE or MI risk, whereas bleeding risk was significantly increased for VKA with a

263 Stroke and bleeding risk were calculated using congestive heart fai

264 Four categories for bleeding risk were defined for the modified Mehran risk

265 among weight, pharmacodynamic response, and bleeding risk were observed between reduced-dose prasugr

266 Empirical stroke and bleeding risks were assessed by using the congestive hea

267 empirical and physician-estimated stroke and bleeding risks were low (weighted Kappa 0.1 and 0.11, re

268 botic and profibrinolytic actions with a low bleeding risk when administered orally, but its benefit

269 uld weigh the trade-off between ischemic and bleeding risk when choosing the shorter or longer durati

270 ents with severe kidney disease may increase bleeding risk, whereas dose reductions without a firm in

271 icantly affects OAC use among those with low bleeding risk, whereas those with high bleeding risk dem

272 2) ischemic/thrombotic cardiac risk, and (3) bleeding risk, which are pivotal for discerning the choi

273 dures can be separated into those with a low bleeding risk, which generally do not require complete r

274 ctivity, engineered to reduce APC-associated bleeding risk while retaining normal cell-signaling acti

275 use of such APC variants may reduce serious bleeding risks while providing the beneficial effects of

276 Bleeding risk with antiplatelet therapy is an increasing

277 Several studies reported lower bleeding risk with continued oral anticoagulation rather

278 Bleeding risk with continued thienopyridine was similar

279 After 90 days, the reduction in bleeding risk with edoxaban versus warfarin was similarl

280 c systemic anticoagulation does not increase bleeding risk with intrapleural tPA, but therapeutic ant

281 For nonrandomized studies we compared bleeding risk with other HCC single-arm studies that did

282 The mean absolute increase in the bleeding risk with prasugrel versus clopidogrel was 1.3+

283 y (within 90 days) and delayed (90-360 days) bleeding risk with TT exposure in relation to VKA+antipl

284 Bleeding risk with vitamin K antagonists (VKAs) is close

285 Women and men had lower absolute bleeding risks with BAS; however, these absolute risk di

286 Significantly higher gastrointestinal bleeding risks with dabigatran 150 mg (1.78, 1.35-2.35)

287 evation myocardial infarction have increased bleeding risks with fibrinolysis relative to whites, yet

288 Important steps in minimizing bleeding risks with NOACs include dose adjustment of the

289 aortic bioprosthesis significantly increases bleeding risk without a favorable effect on thromboembol

290 a substantial reduction in gastrointestinal bleeding risk without apparent increase in cardiovascula

291 A substantial reduction in gastrointestinal bleeding risk without increase in cardiovascular events