ライフサイエンスコーパス: VTE

1 VTE developed despite extensive AT supplementation, whic

2 VTE during follow-up was associated with long-term morta

3 VTE in patients with HF is associated with long-term mor

4 VTE outcome measures are invalidated for interhospital c

5 VTE process measures (e.g., SCIP-VTE-2) do not comprehen

6 VTE provoked by a persistent or progressive risk factor

7 VTE provoked by a reversible risk factor, or a first unp

8 uartile of LDL-C(corrected) (P(trend)=0.06); VTE tended to associate with baseline quartile of lipopr

9 nalyzed GWAS data from 18 studies for 30 234 VTE cases and 172 122 controls and assessed the associat

10 sed nested case-control study comprising 416 VTE patients and 848 age- and sex-matched controls deriv

11 A VTE risk assessment survey was distributed to providers.

12 .3 months, 152 patients (20.79%) developed a VTE.

13 e analyzed with 4426 patients experiencing a VTE (1.9%).

14 performed in FOURIER to determine whether a VTE polygenic risk score could identify high-risk patien

15 Operations with a VTE rate >3% were designated high risk.

16 relative (P(interaction)=0.04) and absolute VTE reduction (P(heterogeneity)=0.009) in comparison wit

17 nt option for patients with cancer and acute VTE, although caution is needed in patients at high risk

18 evel (ie, D-dimer <500 ng/mL) excludes acute VTE when combined with a low pretest probability (ie, We

19 agents of choice for the treatment of acute VTE in the majority of patients.

20 anaging bleeding risk in patients with acute VTE and highlight a practical approach for daily practic

21 ere compared using risk-reliability adjusted VTE prophylaxis and postoperative VTE event rates.

22 of dabigatran were similar to those in adult VTE patients.

23 This retrospective cohort study analyzed VTE incidence, morbidity and mortality amongst post-surg

24 210G>A carriers nor between asymptomatic and VTE+ carriers of these mutations.

25 VTF) activity levels associates with DIC and VTE (grouped as intravascular coagulation) in HFRS patie

26 VTF) activity levels associates with DIC and VTE (grouped as intravascular coagulation) in HFRS patie

27 PAD events and VTE occurred in 246 and 92 patients, respectively.

28 etween HF or echocardiographic exposures and VTE.

29 ularization, or amputation for ischemia) and VTE (deep vein thrombosis or pulmonary embolism) were as

30 between the chorismate-tyrosine pathway and VTE, we engineered tomato plants to bypass the pathway a

31 tion between 12 923 718 genetic variants and VTE.

32 The management of cancer-associated VTE is challenging.

33 For cancer-associated VTE, we now prefer full-dose oral Xa inhibitors over low

34 ted for many patients with cancer-associated VTE.

35 g root-cause analysis of hospital-associated VTE (HA-VTE).

36 , their contribution to pregnancy-associated VTE has received little attention.

37 Overall, pregnancy-associated VTE is complex, and management decisions should be indiv

38 s of these plants reveal a trade-off between VTE and natural variation in chorismate metabolism expla

39 ng as a plausible mechanism for breakthrough VTE in surgical patients, and identifies anticoagulant d

40 rgical patients often develop "breakthrough" VTE events-those which occur despite receiving chemical

41 When stratified further by VTE risk scoring, even the highest risk patients did not

42 In modern day post-surgical care, VTE remains a significant occurrence, despite wide adopt

43 Atherosclerosis Risk In Communities) cohort, VTE risk associated with incident HF, HF subtypes, and a

44 This measure assessed comprehensive VTE chemoprophylaxis during each patient's entire hospit

45 e critically ill, radiographically confirmed VTE and major bleeding rates were 7.6% (95% CI, 3.9-13.3

46 The radiographically confirmed VTE rate was 4.8% (95% confidence interval [CI], 2.9-7.3

47 In cell culture, VTE-associated variants of STAB2 had a reduced surface e

48 Current VTE quality measures are inadequate.

49 ere significantly more likely to have 90-day VTE than patients with adequate or high aFXa (4.2% vs. 1

50 tients, 2.3% (n = 23) had symptomatic 90-day VTE, 4.2% (n = 41) had 90-day clinically relevant bleedi

51 levels will be more likely to develop 90-day VTE, and those with high aFXa will be more likely to ble

52 emoprophylaxis was associated with decreased VTE events.

53 ophylaxis would be associated with decreased VTE incidence and mortality.

54 However, currently described VTE variants account for an insufficient portion of risk

55 Patients who developed VTE during follow-up had shorter times of PFS (HR, 1.74;

56 ks and benefits of chemoprophylaxis, discuss VTE risk stratification, and recommend which patients sh

57 edian of 19 months), inflammatory disorders (VTE risk is 4.7% in patients with rheumatoid arthritis a

58 Extended duration VTE prophylaxis should be considered in all patients und

59 constitute the different forms of vitamin E (VTE), essential components of the human diet, and displa

60 0.89]; P=0.004), with nonsignificantly fewer VTE events (HR, 0.67 [95% CI, 0.44-1.01]; P=0.06).

61 For VTE, moderate-certainty evidence showed a probable assoc

62 identified potential prognostic factors for VTE and bleeding in hospitalized adult medical patients.

63 ic review to identify prognostic factors for VTE and bleeding in hospitalized medical patients and se

64 ever, little is known about risk factors for VTE or its outcomes in patients with PDAC.

65 ntion to transient acquired risk factors for VTE remains paramount, as they have generally been shown

66 and bleeding; it also informs guidelines for VTE prevention and future research.

67 In FOURIER, the hazard ratio (HR) for VTE with evolocumab was 0.71 (95% CI, 0.50-1.00; P=0.05)

68 identified 16 novel susceptibility loci for VTE; for some loci, the association signals are likely m

69 y of heparin compared with other methods for VTE prevention.

70 and edoxaban have been added as options for VTE treatment; patients with brain metastases are now ad

71 highest quartile (>=358 pg/mL) had an OR for VTE of 2.05 (95% confidence interval, 1.37-3.08) compare

72 We found that the ORs for VTE increased across GDF-15 quartiles (Ptrend = .002).

73 was used to calculate odds ratios (ORs) for VTE across GDF-15 quartiles.

74 agement of hospitalized medical patients for VTE and bleeding; it also informs guidelines for VTE pre

75 Recommendations for VTE prevention in surgical patients include chemoprophyl

76 associated with increased long-term risk for VTE (adjusted hazard ratio: 3.13; 95% confidence interva

77 ele had a 15% reduction in relative risk for VTE (odds ratio, 0.85; 95% confidence interval, 0.77-0.9

78 ients who were at >2-fold increased risk for VTE and who derived greater relative (P(interaction)=0.0

79 Long-term risk for VTE associated with incident HF, HF subtypes, or structu

80 Medical inpatients are at high risk for VTE because of immobility as well as acute and chronic i

81 ollowed for a mean of 10 years, the risk for VTE was similar for HF with preserved ejection fraction

82 e associated with greatly increased risk for VTE, which persisted through long-term follow-up.

83 more convenient and safer than warfarin for VTE treatment, bleeding remains the major side effect, p

84 besity is a well-established risk factor for VTEs, such as pulmonary embolism and deep vein thrombosi

85 of practitioners reported performing formal VTE risk assessment.

86 y reasons for failure to provide defect-free VTE chemoprophylaxis, and (3) examine patient- and hospi

87 -risk patients who would derive the greatest VTE reduction from evolocumab.

88 s associated with COVID-19, 9 episodes of HA-VTE were diagnosed within 42 days, giving a postdischarg

89 ical admission; there were 56 episodes of HA-VTE within 42 days (3.1 per 1000 discharges).

90 The odds ratio for postdischarge HA-VTE associated with COVID-19 compared with 2019 was 1.6

91 ear to increase the risk of postdischarge HA-VTE compared with hospitalization with other acute medic

92 ause analysis of hospital-associated VTE (HA-VTE).

93 the same operations had significantly higher VTE rates.

94 r up to 12 months, or less if the identified VTE clinical risk factor resolved.

95 ensity score matched cohorts to determine if VTE chemoprophylaxis was associated with decreased VTE e

96 d a previously unrecognized role for PAR4 in VTE.

97 r adjusting for confounders, no reduction in VTE was observed in at risk surgical patients.

98 ntial mechanisms explaining the reduction in VTE with evolocumab.

99 emonstrated a 31% relative risk reduction in VTE with PCSK9 inhibition (HR, 0.69 [95% CI, 0.53-0.90];

100 ter (P=0.015) in asymptomatic (n=13) than in VTE+ (n=12) heterozygous FVL carriers, with an increase

101 ligible patients, there was no difference in VTEs between attenuated CRD (CRDa) and CTDa (10.4% [n =

102 Physicians adjudicated incident VTE using hospital records.

103 ma GDF-15 levels and future risk of incident VTE and explored the potential of a causal association u

104 reatment period and in those with incidental VTE.

105 Primary end points included VTE recurrence, bleeding events, and mortality at 6 and

106 aploinsufficiency of stabilin-2 may increase VTE risk through elevated levels of these procoagulants.

107 mbosis in homozygotes and markedly increased VTE risk in heterozygotes.

108 sk patients did not have an associated lower VTE rate (3.68 vs 4.22% p = .092).

109 elevated heart rate are not included in most VTE risk assessment models.

110 We examined adherence to a novel VTE chemoprophylaxis process measure in patients who und

111 ights into the opportunities for these novel VTE therapies.

112 At STAB2, 7.8% of VTE cases and 2.4% of controls had a qualifying rare var

113 ificant occurrence, despite wide adoption of VTE risk assessment.

114 ppropriations to improve public awareness of VTE, tracking VTE nationwide with the use of standardize

115 To reduce the complications of VTE, attenuation of thrombin activatable fibrinolysis in

116 ed with the risk of VTE and the composite of VTE and PAD events.

117 nticoagulation therapy is the cornerstone of VTE treatment.

118 ants conferring increased varying degrees of VTE risk have been identified by genome-wide association

119 oven to be the most important determinant of VTE recurrence risk.

120 3) had an objectively confirmed diagnosis of VTE treated with standard of care (SOC) for >=3 months,

121 level quality measure identified failures of VTE chemoprophylaxis in 0% to 3% of patients.

122 ed a genome-wide association study (GWAS) of VTE and a transcriptome-wide association study (TWAS) ba

123 as found in patients with a prior history of VTE (HR = 23; 95% CI, 4-127; P < .001), multilumen CVC (

124 deliveries to women with no prior history of VTE or thrombophilia.

125 is indicated in most women with a history of VTE.

126 re; immobility; paresis; previous history of VTE; thrombophilia; malignancy; critical illness; and in

127 The incidence of VTE recurrence after negative MRDTI was low, and MRDTI p

128 ew HF diagnosis, the cumulative incidence of VTE was 1.4%, 2.5%, and 10.5% at 30 days, 1 year, and 5

129 We evaluated the incidence of VTE, central line-associated bloodstream infections (CLA

130 E risk assessment and reporting the level of VTE risk in all hospitalized patients, integrating preve

131 aseline Lp(a) concentration and magnitude of VTE risk reduction (P(interaction)=0.04).

132 oprotein cholesterol levels and magnitude of VTE risk reduction.

133 al approach to anticoagulation management of VTE and AF in cancer.

134 nor UC was associated with increased odds of VTE after any operation.

135 The odds of VTE were greatest immediately after new-onset HF and ste

136 The primary endpoint was the onset of VTE during follow-up.

137 ian time from PDAC diagnosis to the onset of VTE was 4.49 months.

138 re independent risk factors for the onset of VTE.

139 , we found that frequent and early onsets of VTE after diagnoses of PDAC are associated with signific

140 The rate of the primary composite outcome of VTE or death was 5.1% (41 of 804) in the low-intensity-w

141 riority for risk of the composite outcome of VTE or death.

142 ed the incidence, predictors and outcomes of VTE in HF.

143 fficacy that may underlie the persistence of VTE over the past several decades.

144 all thickness were independent predictors of VTE.

145 thesized that a high rate of prescription of VTE chemoprophylaxis would be associated with decreased

146 implementation, tracking, and prevention of VTE events.

147 nsensus for the treatment and prophylaxis of VTE in patients with cancer.

148 to determine whether primary prophylaxis of VTE in patients with PDAC will improve morbidity and mor

149 The overall rate of VTE ranged widely based on the operation performed from

150 The rate of VTE recurrence after L-ASP reintroduction was 3% (1 of 3

151 The incidence rate of VTE was 16%, with 69% of cases occurring during inductio

152 hylaxis (80.5% vs 22.3%) with lower rates of VTE for identical regimens (CTD, 13.2% vs 16.1%; CTDa, 1

153 nsity matched cohort, we found that rates of VTE were similar in those receiving UFH or LMWH compared

154 Greater recognition of VTE risk factors and advances in anticoagulation have fa

155 olicy statement provides a focused review of VTE, risk scoring systems, prophylaxis, and tracking met

156 eloma XI, there was no difference in risk of VTE (12.2% [n = 124 of 1014] vs 13.2% [n = 133 of 1008];

157 d its isoform, gamma' fibrinogen, on risk of VTE and ischemic stroke subtypes using summary statistic

158 (corrected), was associated with the risk of VTE and the composite of VTE and PAD events.

159 cumab reduced Lp(a) by 33 nmol/L and risk of VTE by 48% (HR, 0.52 [95% CI, 0.30-0.89]; P=0.017), wher

160 ethasone (CVAD) induction had higher risk of VTE compared with patients treated with cyclophosphamide

161 ed CTD (CTDa) induction had a higher risk of VTE compared with those treated with melphalan and predn

162 , which is increasing the underlying risk of VTE detection.

163 sting whether evolocumab reduces the risk of VTE events (deep venous thrombosis or pulmonary embolism

164 study is required to confirm whether risk of VTE is related to lipoprotein(a) level and its reduction

165 These patients are at a high risk of VTE recurrence and bleeding during anticoagulant therapy

166 levels are associated with increased risk of VTE, but MR suggests that this association is not causal

167 isin/kexin type 9) inhibition on the risk of VTE, explore potential mechanisms, and examine the effic

168 tes was associated with an increased risk of VTE, whereas transfusion of fresh frozen plasma had no e

169 ry patients with cancer at increased risk of VTE.

170 ss effect of PCSK9 inhibition on the risk of VTE.

171 f 10.9%), are associated with higher risk of VTE.

172 inhibition significantly reduces the risk of VTE.

173 xis was associated with an increased risk of VTE.

174 its may contribute to the underlying risk of VTE.

175 iority margin of 3% for the absolute risk of VTE.

176 symptoms of normal pregnancy mimic those of VTE and algorithmic tools used in the nonpregnant popula

177 Treatment of VTE consists of 3 phases: the initial treatment (first 5

178 anticoagulants (DOACs) for the treatment of VTE in patients with cancer reported that edoxaban and r

179 l alternatives to DOACs for the treatment of VTE in specific patient categories such as those with se

180 iatric clinical trials to guide treatment of VTE is lacking so treatment is often extrapolated from a

181 Cumulative incidence values of VTE were 8.07% (95% confidence interval [CI], 6.31-10.29

182 The primary endpoint was the occurrence of VTEs; secondary endpoints were the occurrence of deep ve

183 ct of bariatric surgery on long-term risk of VTEs in a large cohort of patients with obesity.

184 Lp(a) by only 7 nmol/L and had no effect on VTE risk (P(interaction) 0.087 for HR; P(heterogeneity)

185 genetically determined gamma' fibrinogen on VTE and ischemic stroke risk.

186 a' fibrinogen and higher total fibrinogen on VTE risk.

187 ntation did not have a significant impact on VTE.

188 ystematic review included 35 publications on VTE prophylaxis and treatment and 18 publications on VTE

189 hylaxis and treatment and 18 publications on VTE risk assessment.

190 studies in our analysis: 14 that reported on VTE, and 3 that reported on bleeding.

191 entralized data steward for data tracking on VTE risk assessment, prophylaxis, and rates.

192 inhibition reduces the risk of PAD events or VTE after acute coronary syndrome, and if such effects a

193 EDT reduced symptomatic VTE or VTE-related death compared with standard of care (0.8% v

194 warfarin (absolute rate of recurrent VTE or VTE-related death, 2.0% vs 2.2%).

195 Pediatric VTE encompasses a highly heterogenous population, with v

196 s of direct oral anticoagulants in pediatric VTE are ongoing, with results anticipated soon.

197 tudy outcomes of rare subgroups of pediatric VTE (eg, renal vein thrombosis), and will be important t

198 They include performing VTE risk assessment and reporting the level of VTE risk

199 from >3 months to <18 years with persistent VTE risk factor(s).

200 We report postdischarge VTE data from an ongoing quality improvement program inc

201 Postoperative VTE risk varies widely by the operation performed, and a

202 ations, there were 480 (1.46%) postoperative VTE, and an overall mortality of 609 (1.85%) patients.

203 ospital specific risk adjusted postoperative VTE rates.

204 y adjusted VTE prophylaxis and postoperative VTE event rates.

205 correlation was found between postoperative VTE chemoprophylaxis application and hospital specific r

206 ease have an increased risk of postoperative VTE, but prior studies have not accounted for the operat

207 For each operation, postoperative VTE rates were similar regardless of diagnostic indicati

208 While postoperative VTE chemoprophylaxis was broadly applied, after adjustin

209 ave higher risk of antepartum and postpartum VTE, with odds ratios between 1.4 and 1.8.

210 spitalized patients, integrating preventable VTE as a benchmark for hospital comparison and pay-for-p

211 laxis, or low-dose anticoagulation, prevents VTE in selected medical inpatients.

212 nd FII 20210G>A mutation carriers with prior VTE (VTE+).

213 To identify new rare VTE risk variants, we performed a whole-exome study of 3

214 ovement efforts on ensuring patients receive VTE prophylaxis throughout their entire hospitalization.

215 central-line thrombosis as their most recent VTE.

216 Prophylaxis for recurrent VTE prevention in subsequent pregnancies is indicated in

217 outcomes included the composite of recurrent VTE and major bleeding, clinically relevant nonmajor ble

218 The incidence of recurrent VTE in all patients with MRDTI negative for DVT was 1.1%

219 The risk of the composite of recurrent VTE or major bleeding was nonsignificantly lower with DO

220 rior to warfarin (absolute rate of recurrent VTE or VTE-related death, 2.0% vs 2.2%).

221 Rates of recurrent VTE range from 20% to 36% during the 10 years after an i

222 prising 2607 patients, the risk of recurrent VTE was nonsignificantly lower with DOACs than with LMWH

223 importance to decrease the risk of recurrent VTE while minimizing the risk of bleeding.

224 ective than LMWH for prevention of recurrent VTE with CAT though carry an increased risk for non-majo

225 eated with DOACs had lower risk of recurrent VTE, overall (RR 0.63; 95% CI 0.51-0.79; p < 0.0001), co

226 ration in patients at high risk of recurrent VTE.

227 The primary outcome (efficacy) was recurrent VTE and the secondary outcomes (safety outcomes) include

228 efficacy and safety outcomes were recurrent VTE and major bleeding, respectively.

229 ignificantly higher risk of catheter-related VTE than subjects with TLs (hazard ratio [HR] = 8.5; 95%

230 icantly higher incidence of catheter-related VTE, CLABSI, and CVC malfunction over TLs.

231 The incidence of CVC-related VTE was 5.9% +/- 0.63%.

232 Increased risk of CVC-related VTE was found in patients with a prior history of VTE (H

233 CCs and TLs, and risk factors of CVC-related VTE.

234 ver, the evidence base for pregnancy-related VTE management remains weak.

235 VTE process measures (e.g., SCIP-VTE-2) do not comprehensively capture failures throughou

236 The SCIP-VTE-2 hospital-level quality measure identified failures

237 In contrast to SCIP-VTE-2, our novel quality measure unmasked VTE chemoproph

238 wed a favorable safety profile for secondary VTE prevention in children aged from >3 months to <18 ye

239 (20%) developed incident HF, 729 subsequent VTE events were identified.

240 n aFXa level category and 90-day symptomatic VTE & bleeding.

241 ied composite efficacy endpoint (symptomatic VTE, myocardial infarction, nonhemorrhagic stroke, and c

242 EDT reduced symptomatic VTE or VTE-related death compared with standard of care

243 are used to treat children with symptomatic VTE.

244 idence-based strategies to prevent long-term VTE in patients with HF, beyond time of hospitalization,

245 The VTE risk appears highest in those with critical care adm

246 th brain metastases are now addressed in the VTE treatment section; and the recommendation regarding

247 3-month incidence of venous thromboembolism (VTE) after a MRDTI negative for DVT.

248 risk of arterial and venous thromboembolism (VTE) and bleeding events.

249 e many predictors of venous thromboembolism (VTE) and bleeding in hospitalized medical patients, but

250 eports describe high venous thromboembolism (VTE) and disseminated intravascular coagulation (DIC) ra

251 ic diseases, such as venous thromboembolism (VTE) and ischemic stroke.

252 suggested to prevent venous thromboembolism (VTE) and thus may increase exposure to ASP.

253 t-free postoperative venous thromboembolism (VTE) chemoprophylaxis, (2) identify reasons for failure

254 1000 will experience venous thromboembolism (VTE) during pregnancy or postpartum.

255 an increased risk of venous thromboembolism (VTE) has resulted in specific guidelines for its prevent

256 tio (INR) to prevent venous thromboembolism (VTE) in warfarin-treated patients with recent arthroplas

257 Venous thromboembolism (VTE) incidence in children has sharply increased with th

258 Venous thromboembolism (VTE) is a major preventable disease that affects hospita

259 Venous thromboembolism (VTE) is a significant contributor to morbidity and morta

260 Venous thromboembolism (VTE) is a significant public health burden.

261 Venous thromboembolism (VTE) is associated with significant mortality and morbid

262 ng-term treatment of venous thromboembolism (VTE) is how long to anticoagulate.

263 Venous thromboembolism (VTE) is rare in healthy children, but is an increasing p

264 l levels and risk of venous thromboembolism (VTE) is uncertain.

265 highest incidence of venous thromboembolism (VTE) of any cancer type.

266 xilate for secondary venous thromboembolism (VTE) prevention.

267 n between GDF-15 and venous thromboembolism (VTE) remains uncertain.

268 All patients with venous thromboembolism (VTE) should receive anticoagulant treatment in the absen

269 m at position 310 in venous thromboembolism (VTE) using the International Network Against Venous Thro

270 lectively defined as venous thromboembolism (VTE), are the third leading cause of cardiovascular deat

271 are at high risk of venous thromboembolism (VTE), but data are lacking from large prospective cohort

272 ith cancer and acute venous thromboembolism (VTE), but studies have reported inconsistent results.

273 Venous thromboembolism (VTE), composed of pulmonary embolism and deep venous thr

274 For patients with venous thromboembolism (VTE), prediction of bleeding is relevant throughout the

275 Risk factors for venous thromboembolism (VTE), such as older age, malignancy (cumulative incidenc

276 ber of patients with venous thromboembolism (VTE), the initial hope that their presence would inform

277 Venous thromboembolism (VTE), which includes both deep venous thrombosis and pul

278 Venous thromboembolism (VTE), which includes deep vein thrombosis (DVT) and pulm

279 short-term risk for venous thromboembolism (VTE).

280 nal risk factors for venous thromboembolism (VTE).

281 an increased risk of venous thromboembolism (VTE).

282 without a history of venous thromboembolism (VTE).

283 oagulation (DIC) and venous thromboembolism (VTE).

284 ase (PAD) events and venous thromboembolism (VTE).

285 understanding of the biology contributing to VTE, we conducted a genome-wide association study (GWAS)

286 l improve morbidity and mortality related to VTE.

287 ith genome-wide significance were related to VTE.

288 to improve public awareness of VTE, tracking VTE nationwide with the use of standardized definitions,

289 203 children (1.0%) experienced on-treatment VTE recurrence, and 3 of 203 (1.5%) experienced major bl

290 IP-VTE-2, our novel quality measure unmasked VTE chemoprophylaxis failures in 18% of colectomies.

291 ome study of 393 individuals with unprovoked VTE and 6114 controls.

292 I 20210G>A mutation carriers with prior VTE (VTE+).

293 When VTE is diagnosed, anticoagulation is the backbone of tre

294 dicted by the SNPs, were not associated with VTE in MR.

295 transfusion are known to be associated with VTE risk, their contribution to pregnancy-associated VTE

296 issue and assessed them for association with VTE.

297 election of anticoagulants for patients with VTE.

298 ement of high-quality care for patients with VTE.

299 r of rare damaging variants in patients with VTE: PROS1, STAB2, PROC, and SERPINC1.

300 y of first- and second-degree relatives with VTE.

301 ngst post-surgical patients with and without VTE chemoprophylaxis between April 2013 - September 2017