ライフサイエンスコーパス: bleeding risk

1 in cardiovascular disease, but it increases bleeding risk.

2 able link between antithrombotic therapy and bleeding risk.

3 d tomographic angiography, respectively) and bleeding risk.

4 alization, without a significant increase in bleeding risk.

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

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

7 nts with hemodynamic decompensation and high bleeding risk.

8 ardiac events irrespective of the underlying bleeding risk.

9 lder without known CVD and without increased bleeding risk.

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

11 e creatinine clearance and procedure-related bleeding risk.

12 and little is known about their intraocular bleeding risk.

13 hromboembolism, with no apparent increase of bleeding risk.

14 concentrations, which significantly increase bleeding risk.

15 vascular disease relative risk reduction and bleeding risk.

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

17 ilter placement because of known significant bleeding risk.

18 y in procedures below the 90th percentile of bleeding risk.

19 tricular assist device support and increased bleeding risk.

20 ion is controversial because of an increased bleeding risk.

21 observed benefits are influenced by baseline bleeding risk.

22 t eliminate thrombosis, and have substantial bleeding risk.

23 NSAID exposure was associated with increased bleeding risk.

24 nd thromboembolic stroke, without increasing bleeding risk.

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

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

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

28 tithrombotic strategy with a potentially low bleeding risk.

29 h clopidogrel but are associated with higher bleeding risk.

30 edicaid, and features associated with higher bleeding risk.

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

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

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

34 urrent mainstream use cannot reliably assess bleeding risk.

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

36 ce in optimizing management while mitigating bleeding risk.

37 bocytopenia was not linked with an excessive bleeding risk.

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

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

40 hose associated with an intermediate or high bleeding risk.

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

42 ation conjunctively used for MI with reduced bleeding risk.

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

44 vitamin K antagonists is closely related to bleeding risk.

45 reatment categories did platelet dose affect bleeding risk.

46 resent an important contributor to increased bleeding risk.

47 ance strategies (BAS) for PCIs stratified by bleeding risk.

48 tting in rabbits, all without increasing the bleeding risk.

49 h potential benefits limited by an increased bleeding risk.

50 sts are often perceived to have an increased bleeding risk.

51 according to varying levels of ischemic and bleeding risk.

52 ntial future clinical implications to reduce bleeding risk.

53 t therapy, have high ischaemic risk, and low bleeding risk.

54 thy control patients and individuals at high bleeding risk.

55 ring both antiplatelet therapy and traumatic bleeding risk.

56 py groups according to level of ischemic and bleeding risk.

57 -6 months) treatment in relation to baseline bleeding risk.

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

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

60 e metabolic pathways that may increase major bleeding risk.

61 hrombotic therapeutic potential with reduced bleeding risk.

62 sights into the balance between ischemic and bleeding risks.

63 cantly than empirical models when estimating bleeding risks.

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

65 intravascular coagulation without increasing bleeding risks.

66 ention of ischemic events, despite increased bleeding risks.

67 ely), but a more modest absolute increase in bleeding risk (1.5% [95% CI: 0.9% to 2.1%], 1.8% [95% CI

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 study evaluated the balance of ischemic and bleeding risks according to the presence of >=1 enrichme

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

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

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

79 ent benefits for stroke prevention with less bleeding risk and less tedious monitoring requirements c

80 reater absolute increase in ischemic than in bleeding risk and may be good candidates for low-dose ri

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

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

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

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

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

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

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

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

89 iplatelet therapy, which increases costs and bleeding risk, and which may delay elective surgeries.

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

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

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

93 chemic events, and it did not decrease major bleeding risk as compared with conventional treatment.

94 f physical functioning despite mortality and bleeding risks as high as 10%.

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

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

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

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

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

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

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

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

103 14-3-3zeta-deficient mice does not increase bleeding risk, but results in decreased thrombin generat

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

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

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

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

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

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

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

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

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

113 re across the world, including in China, but bleeding-risk concerns and organisational challenges ham

114 nts (p < 0.001), with a stepwise increase in bleeding risk corresponding to the number of times the A

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

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

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

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

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

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

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

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

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

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

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

126 to obtain kidney samples from patients with bleeding risk factors (e.g., antiplatelet therapy and an

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

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

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

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

131 l patients, even in the presence of multiple bleeding risk factors.

132 postdischarge between groups, adjusting for bleeding risk factors.

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

134 Bleeding risk for NOACs may be increased in persons olde

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

136 rs (P<0.0001) in high, intermediate, and low bleeding risk groups, respectively.

137 k of major adverse cardiac events across all bleeding risk groups.

138 modes of DAPT cessation and outcomes across bleeding risk groups.

139 n factor VIII (FVIII) replacement levels and bleeding risk, guiding the current practice in hemophili

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

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

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

143 antiplatelet therapy (DAPT) duration in high bleeding risk (HBR) patients after drug-eluting stents,

144 High bleeding risk (HBR) patients undergoing percutaneous cor

145 High bleeding risk (HBR) patients were older and had greater

146 clinical criteria to define patients at high bleeding risk (HBR).

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

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

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

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

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

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

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

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

155 k scores may be used to predict longitudinal bleeding risk in patients with ACS treated with DAPT wit

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

157 e state-of-the-art of assessing and managing bleeding risk in patients with acute VTE and highlight a

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

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

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

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

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

163 lus aspirin, but at the expense of increased bleeding risk in patients with stable vascular disease.

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

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

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

167 onth DAPT can favorably balance ischemic and bleeding risks in patients with multivessel PCI.

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

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

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

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

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

173 Balancing ischemic and bleeding risk is an evolving framework.

174 Inhibiting thrombosis without generating bleeding risks is a major challenge in medicine.

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

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

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

183 stimate aspirin's absolute benefits, but few bleeding risk models are available to estimate its likel

184 Stroke and bleeding risk models have been created and validated.

185 Prognostic bleeding risk models were developed that can be used to

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

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

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

189 The main models predicted a median 5-year bleeding risk of 1.0% (interquartile range, 0.8% to 1.5%

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

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

192 On the other hand, the high bleeding risk of this population and the current lack of

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

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

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

196 features of this disorder include a lack of bleeding risk, only mildly low platelet counts, elevated

197 sments should be studied, because changes in bleeding risk over time likely constitute the best predi

198 re x proportional effect of aspirin on major bleeding risk) over 5 years.

199 zards models were developed to predict major bleeding risk; participants were censored at the earlies

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

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

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

203 728), intermediate (n=634), and high (n=135) bleeding risk patients.

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

205 anticoagulation prescribing does not reflect bleeding risk per se.

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

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

208 rombotic therapy with an improved benefit to bleeding risk profile over existing antithrombotic agent

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

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

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

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

213 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;

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

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

216 be performed to enhance our understanding of bleeding risk related to revascularization and amputatio

217 evaluation of the individual thrombotic and bleeding risks related to both clinical and procedural f

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

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

220 Bleeding risk represents a major concern in anticoagulat

221 to LMWH, DOACs showed no difference in major bleeding risk (RR 1.31; 95% CI 0.78-2.18; p = 0.31), tho

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

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

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

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

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

227 ng to their risk of bleeding using the PARIS bleeding risk score.

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

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

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

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

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

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

234 Longitudinal bleeding risk scores have been validated in patients tre

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

236 E-DAPT, PARIS, and DAPT (bleeding component) bleeding risk scores in the medically managed patients w

237 biomarker, clinical history)-stroke and ABC-bleeding risk scores incorporate clinical variables and

238 Bleeding risk scores may be used to predict longitudinal

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

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

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

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

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

244 There was no interaction between bleeding risk status and clinical outcomes for any cessa

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

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

247 12 months had lower ischemic risk but higher bleeding risk than those treated with placebo and aspiri

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

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

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

251 In patients with increased bleeding risk, the biolimus A9-coated BioFreedom stent,

252 have antiplatelet effects without associated bleeding risks, the NOX1-selective inhibitor 2-acetylphe

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

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

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

256 s' tolerance for 30-day mortality or serious bleeding risks to achieve improvements in physical funct

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

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

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

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

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

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

263 Bleeding risk was assessed per the National Cardiovascul

264 Baseline bleeding risk was calculated by using modified Mehran bl

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

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

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

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

269 0.98; p = 0.039), whereas an increased major bleeding risk was observed among patients with persisten

270 The bleeding risk was significantly higher for dual-therapy

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

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

273 Stroke and bleeding risk were calculated using congestive heart fai

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

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

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

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

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

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

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

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

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

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

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

285 Bleeding risk with antiplatelet therapy is an increasing

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

287 Bleeding risk with continued thienopyridine was similar

288 Lower bleeding risk with edoxaban compared with warfarin was s

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

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

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

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

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

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

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

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

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

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

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

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