ライフサイエンスコーパス: VTE

1 VTE is among most common causes of death after bariatric

2 ciation study for a genetic risk score of 10 VTE-associated variants.

3 METHODS AND We identified 3290 VTE cases and 116 868 controls through billing code-base

4 d for 3 years in both studies there were 343 VTE events in 301 patients (Kaplan-Meier rate at 3 years

5 dies included 244 865 participants with 4910 VTE events occurring during a mean follow-up of 4.7 to 1

6 We screened plasma samples from 88 VTE cases and 85 matched controls, collected as part of

7 ery), and the points total is converted to a VTE risk score.

8 The absolute VTE risk in the antepartum period is not above a thresho

9 Postpartum, the absolute VTE risk is above a threshold where postpartum LMWH prop

10 e 12-month period prevalence of cancer after VTE diagnosis was 5.2% (95% CI, 4.1% to 6.5%).

11 SWR rates were diminished immediately after VTE behaviors and an increase in the rate of SWR events

12 e CTP are equally safe in protecting against VTE.

13 ), and the expression of THBD is lower among VTE cases compared with controls (P= 9.87 x 10(-6)).

14 ationship between atherosclerosis burden and VTE risk, and they support inclusion of VTE as a prospec

15 eased incidence of cardiovascular events and VTE.

16 cancer, an association between TF(+) MVs and VTE has been observed only in pancreatic cancer.

17 the association between genetic variants and VTE risk.

18 Rates of prophylaxis for VTE and VTE events.

19 Women had an annual VTE incidence of 6% while receiving chemotherapy which w

20 The average annual VTE attack rates related and unrelated to hospitalizatio

21 9.4% of patients were prescribed appropriate VTE prophylaxis and only 45% of residents prescribed app

22 For common diseases such as VTE, biobanks provide potential to perform genetic disco

23 ata on the epidemiology of cancer-associated VTE beyond the initial 6 months, it is not possible for

24 in-hospital and outpatient cancer-associated VTE in specific subgroups of patients with cancer.

25 undamental questions about cancer-associated VTE, or Trousseau syndrome, remain unanswered.

26 onsequences of living with cancer-associated VTE.

27 nd translational issues in cancer-associated VTE.

28 t therapy in patients with cancer-associated VTE.

29 idents in Denmark for at least 1 year before VTE diagnosis, patients with outpatient VTE diagnosis on

30 identified significant associations between VTE occurrence and plasma levels of human immunodeficien

31 understanding about the relationship between VTE and height.

32 l in patients with cancer by preventing both VTE and the progression of metastases.

33 rivaroxaban or enoxaparin/VKA for confirmed VTE.

34 ear follow-up, 29 (13.6%) patients developed VTE.

35 Overall, 40.6% of patients developed VTE.

36 ients are at an increased risk of developing VTE and are more likely to have a recurrence of VTE and

37 nical tool to predict the risk of developing VTE in pediatric trauma patients.

38 ated with the highest risk of post-discharge VTE.

39 es of stroke, venous thromboembolic disease (VTE), and heart failure were lower than expected (absolu

40 in expression by the endothelium may enhance VTE by increasing the recruitment of leukocytes.

41 the prevalence of vicarious trial and error (VTE) behaviors, thought to be involved in deliberation p

42 at choice points (vicarious trial and error [VTE]), during which hippocampal representations alternat

43 ing in the presence of 1 or more established VTE risk factors), and unprovoked VTE, pulmonary embolis

44 We estimated VTE attack (incident plus recurrent VTE) rates and the t

45 0.37] for stroke, -2.43 [-1.35 to -3.70] for VTE, and -0.77 [-0.28 to -1.27] for heart failure), alth

46 Outcomes were hospital admissions for VTE/IS.

47 risk" during established anticoagulation for VTE.

48 studies, 11 (n = 14,776) contained data for VTE events and 8 (n = 7590) contained data for clinicall

49 ssess whether obesity is a causal factor for VTE, we performed Mendelian randomization analysis using

50 ing trauma, the independent risk factors for VTE are different based on mechanism of injury.

51 Identified risk factors for VTE included older age (61.0 years vs 46.0 years; P = .0

52 Differences in risk factors for VTE with blunt vs penetrating trauma.

53 While national evidence-based guidelines for VTE screening and prevention are in place for adults, no

54 had little precision in estimating IRRs for VTE/IS among warfarin-treated persons discontinuing indi

55 e of appropriate ordering of prophylaxis for VTE (odds ratio, 2.35; 95% CI, 1.78-3.10; P < .001) and

56 who were prescribed adequate prophylaxis for VTE and correlates with a reduction in VTE events.

57 Rates of prophylaxis for VTE and VTE events.

58 ssist clinicians and improve prophylaxis for VTE.

59 is could decrease the threshold required for VTE.

60 ication of medical patients at high risk for VTE.

61 85 surgical and trauma patients screened for VTE at 3 level I trauma centers in the United States.

62 The genome-wide association study for VTE replicated previous findings at the F5, F2, ABO, F11

63 erformed a genome-wide association study for VTE with approximately 9 000 000 imputed single-nucleoti

64 that LMWH may be more effective than UH for VTE prophylaxis in trauma patients.

65 An important finding from VTE subtype analyses was that cigarette smoking was asso

66 evaluated the individual risk of gestational VTE associated with heritable thrombophilia, and current

67 l probability (absolute risk) of gestational VTE associated with thrombophilia and to see whether the

68 hilias have an increased risk of gestational VTE independent of a positive family history of VTE.

69 hest quartile of TF experienced the greatest VTE recurrence (> 64.6 pg/mL; 38 [19%] of 203 patients v

70 risk were significantly more likely to have VTE.

71 le-blind, double-dummy, multicentre, Hokusai-VTE trial done between Jan 28, 2010, and Oct 31, 2012.

72 The Hokusai-VTE trial (NCT00986154) was a randomised, double-blind,

73 The Hokusai-VTE trial was a randomised, double-blind, event-driven n

74 patients with cancer enrolled in the Hokusai-VTE trial.

75 justed hospitalization-related (in-hospital) VTE attack rates from 2005 to 2010 ranged from 251 to 30

76 variables included ESA use and hospitalized VTE.

77 The trends in hospitalized VTE were relatively stable.

78 sociated with the likelihood of hospitalized VTE.

79 However, VTE remains an important source of morbidity and mortali

80 an be considered for high-risk patients (ie, VTE risk >0.4%).

81 obtained for overall VTE, provoked VTE (ie, VTE occurring in the presence of 1 or more established V

82 older pediatric trauma patients and improved VTE rates with institutional interventions.

83 g the optimal duration of anticoagulation in VTE patients, for diagnosing and monitoring disseminated

84 1 polymorphism rs3176891 was more common in VTE vs. controls (odds ratio 1.26-1.9); it did not affec

85 the messenger RNA expression differences in VTE cases and controls.

86 nce interval, 1.05-1.10 per unit increase in VTE odds; P=1.08x10(-9)).

87 s for VTE and correlates with a reduction in VTE events.

88 A significant reduction in VTE is associated with an increase in clinically relevan

89 A 14-fold variation in VTE risk (from 0.7% to 10.7%) was identified among surgi

90 we identified 29 963 patients with incident VTE.

91 Outcomes included VTE complications, mortality, and unplanned return to th

92 Neutrophils could increase VTE in cancer patients by releasing neutrophil extracell

93 understanding of the pathways that increase VTE in cancer patients may lead to the development of ne

94 Furthermore, SWR disruptions increased VTE behaviors.

95 sk factors are not associated with increased VTE risk.

96 Studies have demonstrated increasing VTE risk in older pediatric trauma patients and improved

97 SUMMARY OF BACKGROUND DATA: Individualized VTE risk stratification may identify high risk surgical

98 Precision medicine using individualized VTE risk stratification helps ensure that chemoprophylax

99 r biomarkers measured at the time of initial VTE with recurrent VTE in a prespecified analysis of the

100 Low VTE incidence may be due to an early time to enoxaparin

101 Most VTEs occur after hospital stay; still a few patients rec

102 he chosen path from the unchosen path on non-VTE laps to appear before reaching the choice point.

103 A total of 75% of VTE events occurred after hospital discharge, with a 19.

104 , established to reduce the global burden of VTE in patients with cancer, published international gui

105 ients is increasing, and the consequences of VTE in children are significant.

106 for rivaroxaban or warfarin within 7 days of VTE, and patients who redeemed prescriptions for both ri

107 Diagnosis of VTE during hospital admission.

108 ctors are independent of a family history of VTE in first-degree relatives.

109 independent of a positive family history of VTE.

110 (FVL) depend on a positive family history of VTE.

111 independent of a positive family history of VTE.

112 Baseline incidence of VTE of 1:483 pregnancies in women >/=35 years and 1:741

113 The incidence of VTE was lower in those with factor XI deficiency (activi

114 Incidence of VTE was significantly lower in the adjustment group than

115 Main Outcomes and Measures: The incidence of VTE, bleeding complications, anti-Factor Xa deficiency,

116 and VTE risk, and they support inclusion of VTE as a prospective end point in long-term secondary pr

117 Management of VTE in patients with cancer is a major therapeutic chall

118 direct oral anticoagulants for management of VTE in patients with cancer is an emerging treatment tre

119 ct of implementing CCDSSs on the ordering of VTE prophylaxis and the rates of VTE.

120 cate novel insights into the pathogenesis of VTE in primary brain tumors.

121 for the understanding of the pathogenesis of VTE.

122 common and cancer type-specific pathways of VTE in cancer patients.

123 Height is an independent predictor of VTE.

124 nalyses identified independent predictors of VTE.

125 s of biomarkers can be used as predictors of VTE.

126 delines for the treatment and prophylaxis of VTE and central venous catheter-associated thrombosis.

127 The rate of VTE in patients with atherosclerosis is approximately 0.

128 (mean [SD] age, 35 [15] years), the rate of VTE was 9.1% overall (104 of 1137) and similar between g

129 age adjustment may lead to a reduced rate of VTE without an increased risk of bleeding.

130 ith a graded increase in the 3-year rates of VTE (0.76% for 1, 1.53% for 2, and 2.45% for 3 territori

131 Rates of VTE (6 [6.7%] vs 6 [6.3%]; P > .99) were similar, but th

132 Primary outcomes included rates of VTE and clinically relevant bleeding after surgical proc

133 Although rates of VTE are the same in patients who experienced blunt and p

134 ordering of VTE prophylaxis and the rates of VTE.

135 and are more likely to have a recurrence of VTE and bleeding while taking anticoagulants.

136 ion was associated with an increased risk of VTE (hazard ratio for high vs no podoplanin expression:

137 ease) was associated with 57% higher risk of VTE (odds ratio, 1.57; 95% confidence interval, 1.08-1.9

138 ether the mechanism of injury alters risk of VTE after trauma.

139 rlying population differences in the risk of VTE are poorly understood.

140 rategies to target those at greatest risk of VTE are warranted.

141 A clinical tool to predict the risk of VTE based on individual patient clinical characteristics

142 67617, and rs1998081) that increased risk of VTE by 2.3-fold (P< 6 x 10(-7)).

143 or pooled) significantly reduced the risk of VTE by 29% compared with background antiplatelet therapy

144 1) and a significant decrease in the risk of VTE events (risk ratio, 0.78; 95% CI, 0.72-0.85; P < .00

145 There was a reduction in the risk of VTE from 9.7% to 5.5% (HR, 0.57; 95% CI, 0.42 to 0.79; P

146 nt risk of VTE, whereas an increased risk of VTE immediately after endocrine therapy is restricted to

147 n genetic variants that increase the risk of VTE in AAs, a population disproportionately affected by

148 ymorphisms associated with increased risk of VTE in AAs.

149 cin-like glycoprotein, increases the risk of VTE in primary brain tumors via its ability to induce pl

150 The predicted risk of VTE ranged from 0.0% to 14.4%.

151 The risk of VTE was independently associated with age, body mass ind

152 Risk of VTE was noticeably higher in the 3 months after initiati

153 t cancer have a clinically important risk of VTE, whereas an increased risk of VTE immediately after

154 ase aimed at identifying patients at risk of VTE.

155 ive antiplatelet therapy reduces the risk of VTE.

156 ty, and is associated with increased risk of VTE.

157 SA boxed warnings on utilization and risk of VTE.

158 atment on the absolute and relative risks of VTE by using several recently linked data sources from E

159 nt, is a landmark change in the treatment of VTE.

160 of the unchosen path at the choice point on VTE laps and hastened the differentiation of spatial rep

161 The benefit of peri-operative VTE chemoprophylaxis was only found among surgical patie

162 agulant proteins synergistically orchestrate VTE remain incompletely understood.

163 fore VTE diagnosis, patients with outpatient VTE diagnosis only, patients with other indications for

164 ass index-adjusted hazard ratios for overall VTE were 0.98 (95% confidence interval [CI]: 0.89-1.07)

165 Estimates were obtained for overall VTE, provoked VTE (ie, VTE occurring in the presence of

166 1 as novel susceptibility loci for pediatric VTE and warrant future functional studies to unravel the

167 Management of pediatric VTE is a complex undertaking, considering that the vast

168 GWAS in 212 nuclear families with pediatric VTE followed by targeted next-generation sequencing (NGS

169 and rs2748331 are associated with pediatric VTE with unpermuted/permuted values of P = 1.42 x 10(-6)

170 SUMMARY BACKGROUND DATA: Pharmacological VTE prophylaxis with LMWH or UH is the current standard

171 n study, a 10 single-nucleotide polymorphism VTE genetic risk score was associated with coronary arte

172 In those experiencing a postdischarge VTE, mortality increased about 28-fold (2.60% vs 0.09%;

173 he overall 30-day incidence of postdischarge VTE was 0.29% (N = 269).

174 ssment tool to predict risk of postdischarge VTE.

175 5% of patients had a predicted postdischarge VTE risk >1%.

176 ible studies contained data on postoperative VTE and/or bleeding events with and without chemoprophyl

177 ears (OR, 2.69; 95% CI, 1.19-6.08) predicted VTE, with an area under the receiver operator curve of 0

178 ture (OR, 2.09; 95% CI, 1.23-3.55) predicted VTE, with an area under the receiver operator curve of 0

179 Patients with previous VTE, chronic kidney disease, liver disease, cancer, and

180 Patients with previous VTE, chronic kidney disease, liver disease, cancer, and

181 870), born in 1951 to 1992 without previous VTE, was followed from enlistment (1969-2010) until 2012

182 the medical birth register, without previous VTE, was followed from first pregnancy (1982-2012) until

183 ation between cigarette smoking and provoked VTE, which is potentially mediated through comorbid cond

184 % CI, 1.41-6.89; P= .005), previous provoked VTE (HR, 3.20; 95% CI, 1.19-8.62; P= .022), and current

185 ates were obtained for overall VTE, provoked VTE (ie, VTE occurring in the presence of 1 or more esta

186 o 2010, the proportion of patients receiving VTE prophylaxis or with an indication that prophylaxis w

187 ient at high risk for incident and recurrent VTE and target (longer duration) primary and secondary p

188 strated a significant reduction in recurrent VTE with aspirin monotherapy.

189 We compared the incidences of recurrent VTE and abnormal uterine bleeding with and without conco

190 use, the risks and risk factors of recurrent VTE and bleeding, and patient preference and values rega

191 The rate of recurrent VTE at 6 months' follow-up was 9.9 incidents per 100 per

192 as associated with reduced risk of recurrent VTE compared with standard treatment, without compromisi

193 ibe TF as a potential biomarker of recurrent VTE in patients with cancer who are on anticoagulation t

194 temporary estimates on the risk of recurrent VTE off anticoagulation, risk of bleeding on anticoagula

195 zard ratio (HR) for the effects on recurrent VTE and abnormal uterine bleeding.

196 nesota, residents with incident or recurrent VTE over the 6-year period 2005-2010.

197 population comprised 900 patients (recurrent VTE, n = 76; 8.4%).

198 stimated VTE attack (incident plus recurrent VTE) rates and the total annual number of US VTE events

199 isk regression analysis of time to recurrent VTE was conducted, accounting for multiple variables.

200 isk regression analysis of time to recurrent VTE, TF remained strongly associated with recurrent VTE

201 Primary effectiveness outcome was recurrent VTE and primary safety outcome was major bleeding.

202 remained strongly associated with recurrent VTE (subdistribution hazard ratio [SHR], 3.3; 95% CI, 1.

203 ed at the time of initial VTE with recurrent VTE in a prespecified analysis of the CATCH (Comparison

204 more intensive antiplatelet therapy reduces VTE risk beyond aspirin monotherapy is unknown.

205 olecular insight into a mechanism regulating VTE susceptibility and identify common genetic variants

206 e unchosen path when the animal did not show VTE at the choice point.

207 nd these patients did not have a significant VTE risk reduction with chemoprophylaxis.

208 (OR 0.41, 95% CI 0.26-0.65) had significant VTE risk reduction after surgery with chemoprophylaxis.

209 step toward the development of the specific VTE protocols for pediatric trauma patients.

210 ents and may reflect improvements in stroke, VTE, and heart failure.

211 ward site predicted a decrease in subsequent VTE behaviors at the choice point.

212 More than 80% of post-bariatric surgery VTE events occurred post-discharge.

213 early markers associated with post-surgical VTE.

214 outcomes included metastasis-free survival, VTE-free survival, toxicity, and quality of life.

215 patients with cancer and acute, symptomatic VTE.

216 Outcomes and Measures: Rates of symptomatic VTE (deep vein thrombosis and pulmonary embolism, confir

217 The VTE rate when enoxaparin sodium is dosed by anti-factor

218 30-day postdischarge venous thromboembolism (VTE) after bariatric surgery and to identify potential i

219 vide prophylaxis for venous thromboembolism (VTE) among surgical patients.

220 n risk mutations for venous thromboembolism (VTE) and identified a number of novel susceptibility loc

221 for the diagnosis of venous thromboembolism (VTE) and is used routinely for this indication.

222 antified the risk of venous thromboembolism (VTE) and ischemic stroke (IS) due to statin and fibrate

223 ce the occurrence of venous thromboembolism (VTE) and may impact Medicare reimbursement because of pe

224 provoked symptomatic venous thromboembolism (VTE) are unknown.

225 ncreased the risk of venous thromboembolism (VTE) by about 2.3-fold in African Americans (AAs) in the

226 iated with recurrent venous thromboembolism (VTE) during anticoagulation.

227 annual number of US venous thromboembolism (VTE) events, the number of potentially preventable event

228 cidence of pediatric venous thromboembolism (VTE) has been increasing significantly over the past dec

229 , but not recurrent, venous thromboembolism (VTE) in cancer, a setting in which predictors are incomp

230 re, the incidence of venous thromboembolism (VTE) in pediatric trauma patients is increasing, and the

231 evaluate the risk of venous thromboembolism (VTE) in pregnant women with essential thrombocythemia.

232 Venous thromboembolism (VTE) is a leading cause of maternal mortality.

233 Venous thromboembolism (VTE) is common in cancer patients.

234 Venous thromboembolism (VTE) is common in patients with brain tumors, and underl

235 The risk for venous thromboembolism (VTE) is increased in cancer and particularly with chemot

236 Venous thromboembolism (VTE) is the second leading cause of death in patients wi

237 Venous thromboembolism (VTE) is the third most common life-threatening cardiovas

238 th cancer-associated venous thromboembolism (VTE) is unknown.

239 ted previously known venous thromboembolism (VTE) loci near the F5, FGA-FGG, F11, F2, PROCR and ABO g

240 oagulant therapy for venous thromboembolism (VTE) may use estrogen or progestin hormonal therapy to c

241 ents with unprovoked venous thromboembolism (VTE) often is considered, but clinicians need precise da

242 ted heparin (UH) for venous thromboembolism (VTE) prophylaxis in patients with severe traumatic brain

243 risk stratified for venous thromboembolism (VTE) using Caprini scores.

244 whether the risk of venous thromboembolism (VTE) varies with blunt or penetrating trauma.

245 inherited basis for venous thromboembolism (VTE), a leading cause of cardiovascular mortality.

246 an increased risk of venous thromboembolism (VTE), but the association can be confounded with shared

247 Venous thromboembolism (VTE), caused by altered hemostasis, remains the third mo

248 at increased risk of venous thromboembolism (VTE), particularly in the peridiagnosis period.

249 ollectively known as venous thromboembolism (VTE), which is a common vascular disease and a major cau

250 an increased risk of venous thromboembolism (VTE).

251 erse events, such as venous thromboembolism (VTE).

252 KA) in patients with venous thromboembolism (VTE).

253 as key mediators of venous thromboembolism (VTE).

254 risk for developing venous thromboembolism (VTE).

255 ociated with risk of venous thromboembolism (VTE).

256 se risk factors with venous thromboembolism (VTE).

257 ischemic attack) and venous thromboembolism (VTE).

258 isms associated with venous thromboembolism (VTE).

259 t elevated levels of PAI-1 may contribute to VTE.

260 predispose otherwise healthy individuals to VTE.

261 e underlying molecular mechanisms leading to VTE.

262 al discharge, with a 19.5-day median time to VTE.

263 (AIS >/= 3), those that received LMWH or UH VTE prophylaxis.

264 current smoking with provoked and unprovoked VTE were 1.36 (95% CI: 1.22-1.52) and 1.08 (95% CI: 0.90

265 stablished VTE risk factors), and unprovoked VTE, pulmonary embolism, and deep-vein thrombosis.

266 utine care patients with incident unprovoked VTE.

267 associated with provoked but not unprovoked VTE.

268 ith a first hospital diagnosis of unprovoked VTE who were new users of rivaroxaban or warfarin.

269 year of receiving a diagnosis of unprovoked VTE.

270 reening strategies in adults with unprovoked VTE that began enrolling patients after 1 January 2000 a

271 ing, rivaroxaban in patients with unprovoked VTE was associated with reduced risk of recurrent VTE co

272 of occult cancer in patients with unprovoked VTE, including in subgroups of different ages or those t

273 VTE) rates and the total annual number of US VTE events related and unrelated to hospitalization usin

274 The estimated average number of US VTE events was 495 669 per year (48% unrelated to hospit

275 ovascular disease risk factors and validated VTE events.

276 Whether VTE risk is associated with more severe symptomatic athe

277 aromatase inhibitors was not associated with VTE (HR, 0.8; 95% CI, 0.5-1.4; AR, 28.3).

278 ic procoagulant factors were associated with VTE in 32 older orthopedic surgery patients.

279 Podoplanin expression is associated with VTE in patients with brain cancer and may activate plate

280 her, they were independently associated with VTE risk in a joint model in FARIVE (VWF P < .001; PDGFB

281 fy candidate protein markers associated with VTE risk.

282 evels, and d-dimers were not associated with VTE.

283 pressure showed an inverse association with VTE.

284 test was used to screen for association with VTE; competing risk regression analysis of time to recur

285 mong surgical patients comparing CCDSSs with VTE risk stratification and assistance in ordering proph

286 ovel association of PDGFB plasma levels with VTE.

287 stolic blood pressure or lipid measures with VTE.

288 es (43.8% vs 21.4%; P < .001); patients with VTE also had higher mean (SD) Greenfield Risk Assessment

289 ars (41.9% vs 23.2%; P = .02); patients with VTE also had higher mean (SD) Greenfield Risk Assessment

290 Patients with VTE had a significant increase in circulating PMAs and C

291 n the blunt trauma group, more patients with VTE than without VTE had abnormal coagulation results (4

292 penetrating trauma group, more patients with VTE than without VTE had abnormal coagulation results (6

293 2016, 12%, 70%, 16%, and 2% of patients with VTE were initiated on VKA, rivaroxaban, apixaban, and da

294 erplay between PMAs and CRP in patients with VTE.

295 arameters were prevalent among patients with VTE.

296 care for the full spectrum of patients with VTE.

297 ing significantly over time in patients with VTE.

298 a group, more patients with VTE than without VTE had abnormal coagulation results (49.3% vs 35.7%; P

299 a group, more patients with VTE than without VTE had abnormal coagulation results (64.5% vs 44.4%; P

300 post-operatively, compared to those without VTE.