ライフサイエンスコーパス: venous thrombosis

1 ves, and had no history to suggest past deep venous thrombosis).

2 important players in the pathophysiology of venous thrombosis.

3 medical illnesses are at prolonged risk for venous thrombosis.

4 ation of PGE2, contributes to cancer-induced venous thrombosis.

5 s by the investigators; the patient had deep venous thrombosis.

6 alignancy after initiating treatment of deep venous thrombosis.

7 lity (adjOR = 5.2, 95%CI = 2.6-10.5) but not venous thrombosis.

8 itamin supplementation decreases the risk of venous thrombosis.

9 ality (adjOR = 2.0,95%CI = 1.3-3.0), but not venous thrombosis.

10 and femoral sites, and for diagnosis of deep venous thrombosis.

11 a potential therapeutic target for limiting venous thrombosis.

12 ultrasonography of both legs showed no deep venous thrombosis.

13 phism (SNP) analysis would predict recurrent venous thrombosis.

14 mutation, is the most common risk factor for venous thrombosis.

15 In addition, 2 patients had venous thrombosis.

16 his aging-related enhanced susceptibility to venous thrombosis.

17 ients with cancer have an increased risk for venous thrombosis.

18 al protein S levels were not associated with venous thrombosis.

19 tein S deficiency is clearly associated with venous thrombosis.

20 ovel, controlled mouse model for spontaneous venous thrombosis.

21 ce interval [CI], 4.4-6.8) increased risk of venous thrombosis.

22 factors may explain the risk of developing a venous thrombosis.

23 ot be considered in unselected patients with venous thrombosis.

24 ately predict a person's risk for developing venous thrombosis.

25 for conditions associated with arterial and venous thrombosis.

26 n, whereas TF on circulating MPs may trigger venous thrombosis.

27 tream infections, and the prevalence of deep venous thrombosis.

28 the computed tomography scan to detect deep venous thrombosis.

29 olisms, 11 (33.3%) were associated with deep venous thrombosis.

30 lotting system and are at increased risk for venous thrombosis.

31 l biomarker to identify patients at risk for venous thrombosis.

32 k of cardiovascular disease and arterial and venous thrombosis.

33 g the TL PICC was performed to detect occult venous thrombosis.

34 us access, lower extremity itching, and deep venous thrombosis.

35 elet interaction in flow disturbance-induced venous thrombosis.

36 t of the SLC44A2 rs2288904-A polymorphism in venous thrombosis.

37 associated with a slightly increased risk of venous thrombosis.

38 nolysis, and the development of experimental venous thrombosis.

39 ys, and is a critical vascular checkpoint in venous thrombosis.

40 1 in vivo, and efficacy in a murine model of venous thrombosis.

41 r approach to the management of arterial and venous thrombosis.

42 ing alpha2AP may prove useful for preventing venous thrombosis.

43 rinolytic system to block the development of venous thrombosis.

44 ants for primary and secondary prevention of venous thrombosis.

45 ssary for grade 1 and 2 arterial and grade 1 venous thrombosis.

46 45 patients (42.2%) were found to have deep venous thrombosis.

47 iciency is associated with increased risk of venous thrombosis.

48 roteinase inactivation, increase the risk of venous thrombosis.

49 , arrhythmias, arteriosclerosis, stroke, and venous thrombosis.

50 inferior vena cava (IVC) ligation to induce venous thrombosis.

51 ilter, whether in the presence or absence of venous thrombosis.

52 etical data sets on the effect of OC use and venous thrombosis.

53 of PCSK9 is associated with protection from venous thrombosis.

54 a in individuals with clinically established venous thrombosis.

55 anemias, and malaria, with both arterial and venous thrombosis.

56 is pathway in patients with altitude-induced venous thrombosis.

57 ease in the rate of lower limb proximal deep venous thrombosis.

58 efault drugs for anticoagulant management in venous thrombosis.

59 te ischemic infarct (23.3%), one with a deep venous thrombosis (1.4%), eight with multiple microhemor

60 stroke (9 more per 10 000 woman-years), deep venous thrombosis (12 more per 10 000 woman-years), pulm

61 mbosis, 7 obstetrical complications, and 151 venous thrombosis (122 VTE and 29 superficial vein throm

62 arterial thromboses, 2 combined arterial and venous thrombosis, 2 thromboses secondary to allograft p

63 Of 13 PNF cases, 2 were due to early venous thrombosis, 2 to arterial thrombosis, and 2 to fa

64 -Barr virus+ tumors 4%), vascular/lymphatic (venous thrombosis 25%, lymphedema 11%), sensorineural he

65 with ischemic stroke, and 1 (0.1%) with deep venous thrombosis; 28 patients (2.4%) died for cardiovas

66 based case-control study on risk factors for venous thrombosis, 2915 patients with a first venous thr

67 tologic toxicities were proteinuria (2%; 0), venous thrombosis (4%; 2%), arterial thrombosis (2%; 0),

68 troke (11 more per 10 000 woman-years), deep venous thrombosis (7 more per 10 000 woman-years), gallb

69 traction) and the incidence of postoperative venous thrombosis, 78 patients with brain tumors that we

70 omplications were hemorrhage (9%) and portal venous thrombosis (9.9%).

71 1% of patients (145/284) had associated deep venous thrombosis, 91% (279/306) had cardiovascular risk

72 nt in patients with pulmonary embolism, deep venous thrombosis, a body weight >/=100 kg, moderate ren

73 ractices and their association with arterial/venous thrombosis, acute myocardial infarction (AMI), st

74 As most individuals with SVT do not develop venous thrombosis, additional risk factors may explain t

75 TEM orchestrate the inflammatory response in venous thrombosis affecting thrombus resolution.

76 onavirus disease 2019 were screened for deep venous thrombosis after ICU admission with 102 duplex ul

77 e also exhibited increased susceptibility to venous thrombosis after inferior vena cava ligation at 1

78 The incidence of cannula-related venous thrombosis after venovenous extracorporeal membra

79 Secondary outcomes included symptomatic deep venous thrombosis; all pulmonary embolisms; fatal pulmon

80 There was no difference in incidence of deep venous thrombosis among different pharmacologic prophyla

81 ll-established for suspected lower limb deep venous thrombosis, an algorithm combining a clinical dec

82 .8%) developed an asymptomatic proximal deep venous thrombosis and 7 patients (5.9%) developed distal

83 ascular complications, including arterial or venous thrombosis and bleeding.

84 troversial because of its potential risks on venous thrombosis and breast cancer.

85 l effects of plasma FVIII activity levels on venous thrombosis and coronary artery disease risk and p

86 iator of the sterile inflammatory process in venous thrombosis and could be an attractive target for

87 p disturbance, head drop, prevention of deep venous thrombosis and end-of-life issues.

88 s a useful imaging tool for the detection of venous thrombosis and for the estimation of a complete b

89 n reduced the composite outcome of recurrent venous thrombosis and major bleeding compared with place

90 e in line with previous studies on recurrent venous thrombosis and may have implications for future t

91 (APS) is characterized by recurrent arterial/venous thrombosis and miscarriages in the persistent pre

92 nts, infections in 4 of 8 patients, and deep venous thrombosis and neutropenia in one patient each.

93 n the neutrophil is crucial for pathological venous thrombosis and present neutrophil activation and

94 omboembolism (VTE), which includes both deep venous thrombosis and pulmonary embolism, is a common an

95 enectomy; venous thromboembolism (VTE) (deep venous thrombosis and pulmonary embolus) after splenecto

96 Using the stasis model of venous thrombosis and resolution in mice, we found that

97 enous thrombosis, 2915 patients with a first venous thrombosis and their partners as control subjects

98 Superficial venous thrombosis and UEDVT were diagnosed in 54 (13%) a

99 WF) are associated with risk of arterial and venous thrombosis and with hemorrhagic disorders.

100 Additionally, biopsies detected vascular (venous thrombosis) and overimmunosuppression (cytomegalo

101 lates the expression of tissue factor during venous thrombosis, and (2) cancer promotes a procoagulan

102 cluding coronary heart disease, arterial and venous thrombosis, and chronic fibrotic diseases.

103 cal site infection, pulmonary embolism, deep venous thrombosis, and death.

104 nocarcinoma, no uncontrolled hypertension or venous thrombosis, and Eastern Cooperative Oncology Grou

105 applications for hemorrhagic transformation, venous thrombosis, and microvascular disorders are consi

106 k, ischemic and hemorrhagic stroke, cerebral venous thrombosis, and nonspecified PAS.

107 e of hydrocephalus, vasogenic edema, central venous thrombosis, and/or mass lesion.

108 show that individuals with prior superficial venous thrombosis are at increased risk of developing ve

109 Changes in the course of cerebral venous thrombosis are less common causes of acute cerebr

110 and the evidence for the valvular origin of venous thrombosis are reviewed.

111 play increased susceptibility to arterial or venous thrombosis as measured by photochemical injury in

112 by counting risk-increasing alleles from 31 venous thrombosis-associated SNPs for subjects of a larg

113 iable for screening for lower extremity deep venous thrombosis at or above a concentration of 3,000 n

114 e typical of the commonest manifestations of venous thrombosis at the lower extremities.

115 Two kidneys were lost from venous thrombosis before function returned and two devel

116 eventing mortality, pulmonary embolism, deep venous thrombosis, bleeding outcomes, or thrombocytopeni

117 s were markedly higher in patients with deep venous thrombosis, both for maximum value and value on d

118 Risk for symptomatic deep venous thrombosis, but not risk for death or nonfatal pu

119 tion is a mainstay of therapy for those with venous thrombosis, but practice patterns remain heteroge

120 Of the 176 patients, 35 (19.9%) had deep venous thrombosis by compression ultrasonography, includ

121 ciation between impaired kidney function and venous thrombosis can be explained by the concurrent pre

122 t failure, atrial fibrillation, stroke, deep venous thrombosis, cardiovascular death, and total morta

123 er imaging diagnosis of the first three deep venous thrombosis cases was confirmed; therapeutic antic

124 tory of cancer, past medical history of deep venous thrombosis, coma, and high platelet count.

125 e interval, 1.9-2.4) increased risk of first venous thrombosis compared with women without reproducti

126 rom a case-control study on risk factors for venous thrombosis, conducted in the Netherlands.

127 pplied, it appeared that subjects at risk of venous thrombosis could be identified at levels < 0.10th

128 cal and clinical characteristics of cerebral venous thrombosis (CVT) based on material from 34 patien

129 er obesity is associated with adult cerebral venous thrombosis (CVT) has not been assessed.

130 d the rates of recanalisation after cerebral venous thrombosis (CVT).

131 (ICHs) are common in patients with cerebral venous thrombosis (CVT).

132 ncer is a heterogeneous disease, the risk of venous thrombosis depends on cancer types and stages, tr

133 sis, thus resulting in 38.7% with PE or deep venous thrombosis, despite 40% receiving prophylactic an

134 Adjustments for other risk factors for venous thrombosis did not affect the odds ratios.

135 In general, cancer patients with venous thrombosis do not fare well and have an increased

136 Venous thrombosis due to indwelling catheters is a frequ

137 sk reduction [ARR], 0.8%), asymptomatic deep venous thrombosis (DVT) (4 trials; relative risk [RR], 0

138 asma fibrinogen is associated with both deep venous thrombosis (DVT) and its complication, pulmonary

139 The mortality risks for patients with deep venous thrombosis (DVT) and pulmonary embolism (PE) were

140 Deep venous thrombosis (DVT) and secondary pulmonary embolism

141 pathways that have been associated with deep venous thrombosis (DVT) in the general population are ri

142 t of lipid lowering on the incidence of deep venous thrombosis (DVT) is controversial.

143 Deep venous thrombosis (DVT) is one of the most common cardio

144 Deep venous thrombosis (DVT) remains a common and serious car

145 We also determined the association of deep venous thrombosis (DVT) with the presence of an IVC filt

146 Standardised incidence ratios (SIR) of deep-venous thrombosis (DVT), pulmonary embolism, and arteria

147 ary tract infection, pneumonia, sepsis, deep venous thrombosis (DVT), pulmonary embolism, venous thro

148 a common and burdensome complication of deep venous thrombosis (DVT).

149 nsitive but not specific for diagnosing deep venous thrombosis (DVT).

150 ic PE might be different from those for deep venous thrombosis (DVT).

151 atran, anticoagulation in patients with deep venous thrombosis, estimation of warfarin dose, use of o

152 ptomatic VTEs and lower rates of superficial venous thrombosis extension and recurrence with no incre

153 vents (VTE), major bleeding, and superficial venous thrombosis extension?

154 s issue provides a clinical overview of deep venous thrombosis, focusing on prevention, diagnosis, tr

155 l and Genetic Assessment of risk factors for venous thrombosis follow-up study, 4480 patients with VT

156 Potent in vivo activity in a rat model of venous thrombosis following iv and, more importantly, po

157 d effective prophylaxis against arterial and venous thrombosis for up to 24 hours.

158 .8 was associated with a higher incidence of venous thrombosis (four of 13 vs one of 217, respectivel

159 vein thrombosis (SVT) increases the risk of venous thrombosis fourfold to sixfold.

160 protein S deficiency was not associated with venous thrombosis: free protein S < 53 U/dL, odds ratio

161 < .001) and proteinuria (5% v 1%; P = .002); venous thrombosis grade > or = 3 was equivalent in both

162 Grade 3 deep venous thrombosis, grade 3 back pain, and grade 3 vomiti

163 Patients found to have deep venous thrombosis had no difference in time to intubatio

164 no such sex difference in the risk of first venous thrombosis has been reported.

165 wever, their role in sterile inflammation in venous thrombosis has not been systematically examined.

166 rial injury and that platelets contribute to venous thrombosis has prompted trials comparing anticoag

167 lity; however, key molecular determinants in venous thrombosis have not been fully elucidated.

168 ciation between impaired kidney function and venous thrombosis have not been identified so far.

169 rial thrombosis and the role of platelets in venous thrombosis have prompted new treatment paradigms.

170 acranial vascular malformation, intracranial venous thrombosis, head trauma, or tumour; haemorrhagic

171 ith 12 cases (16.7%) of lower extremity deep venous thrombosis identified.

172 Prolonged air leak in 141, deep venous thrombosis in 64, Atrial fibrillation in 42, chyl

173 Autopsy revealed deep venous thrombosis in 7 of 12 patients (58%) in whom veno

174 re, we evaluated the contribution of CD39 to venous thrombosis in a restricted-flow model of murine i

175 se of immunosuppression in the management of venous thrombosis in Behcet's disease.

176 o deep vein thromboses, with 1 superfificial venous thrombosis in each group.

177 factor XI in the prevention of postoperative venous thrombosis in humans is unknown.

178 us thrombosis study, we assessed the risk of venous thrombosis in individuals with previous SVT and a

179 ombin III (at3) locus results in spontaneous venous thrombosis in larvae.

180 a the adenosine A(2A) receptor and mitigates venous thrombosis in mice.

181 The prevalence of deep venous thrombosis in patients with advanced cancer is un

182 e mechanisms responsible for the increase in venous thrombosis in patients with cancer are not unders

183 sed levels of TF-positive MPs correlate with venous thrombosis in patients with cancer.

184 astography may accurately reflect the age of venous thrombosis in polidocanol sclerotherapy model.

185 complimentary technique for the detection of venous thrombosis in such of cases.

186 o longer associated with a decreased risk of venous thrombosis in this study.

187 Using a mouse model of venous thrombosis induced by flow reduction in the vena

188 VTE) using the International Network Against Venous Thrombosis (INVENT) consortium multi-ancestry gen

189 used data from the International Network on Venous Thrombosis (INVENT) consortium to examine whether

190 The risk of recurrent venous thrombosis is 2-fold higher in men than in women.

191 Cancer-associated venous thrombosis is a common condition, although the re

192 Venous thrombosis is a leading cause of morbidity and mo

193 Venous thrombosis is a multicausal disease involving int

194 Cerebral venous thrombosis is a relatively uncommon neurologic di

195 In contrast, venous thrombosis is dominated by stasis or depressed fl

196 In conclusion, the risk of venous thrombosis is markedly increased in individuals w

197 Lower extremity deep venous thrombosis is prevalent in coronavirus disease 20

198 are taken into account, the risk of a first venous thrombosis is twice as high in men as in women.

199 Deep venous thrombosis is very common in critically ill patie

200 TE), composed of pulmonary embolism and deep venous thrombosis, is a significant cause of maternal mo

201 The causal relationship that deep venous thrombosis leads to impairment in lung function a

202 T include pulmonary embolism, recurrent deep venous thrombosis, loss of central venous access, and po

203 ved stem cell; and a tendency to arterial or venous thrombosis, marrow fibrosis, splenomegaly, or tra

204 knowledge on risk factors for cancer-related venous thrombosis may enhance the understanding of the p

205 Understanding the mechanisms of venous thrombosis may lead to the development of new tre

206 l and Genetic Assessment of Risk Factors for Venous Thrombosis (MEGA) study, a population-based case-

207 In a mouse stagnant flow venous thrombosis model Pecam-1(-/-) thrombi were larger

208 In a rat deep venous thrombosis model used to assess antithrombotic ef

209 uced thrombus formation in both arterial and venous thrombosis models, without an apparent effect on

210 to thrombosis in mouse models, particularly venous thrombosis models.

211 atomas (1 of them due to needing heparin for venous thrombosis, none required interventions).

212 nous stenosis, right heart failure, and deep venous thrombosis occurred in 10, 7, 4, and 4 patients,

213 nce interval 1.6-10) but not upper-limb deep venous thrombosis (odds ratio 0.6; 95% confidence interv

214 bolism risk was increased by lower-limb deep venous thrombosis (odds ratio 4.0; 95% confidence interv

215 es, laboratory values, clinical outcome, and venous thrombosis of the patients were recorded.

216 Studies on treatment of venous thrombosis or acute coronary syndrome have shown

217 locumab reduces the risk of VTE events (deep venous thrombosis or pulmonary embolism).

218 and 10 (20%) had thromboembolic events (deep venous thrombosis or pulmonary embolism).

219 e presence of hypercoagulability, prior deep venous thrombosis, or a cavopulmonary anastomosis.

220 rain MRI showing ischemic infarcts, cerebral venous thrombosis, or chronic lesions unrelated to the c

221 , other major psychiatric diagnosis, cancer, venous thrombosis, or infertility treatment.

222 Patients with metastases, portal venous thrombosis, or who had received transplants were

223 us line (P < .001), and prior PE and/or deep venous thrombosis (P < .001), were found to be significa

224 regimen was not related to presence of deep venous thrombosis (p = 0.35).

225 ge, 638-3,735 ng/mL] for no evidence of deep venous thrombosis; p < 0.0001).

226 Critical vascular information includes venous thrombosis (partial or complete), arterial occlus

227 f treatment, there was no recurrence of deep venous thrombosis, partial recanalization within affecte

228 he proposed roles of neutrophils and FXII in venous thrombosis pathophysiology.

229 filtration rate was estimated (eGFR) in 2473 venous thrombosis patients and 2936 controls from a popu

230 can prevent 4 instances of symptomatic deep venous thrombosis per 1000 treated patients (CI, 3 to 6

231 de consideration improved on the use of deep venous thrombosis prophylaxis (p < .05), stress ulcer pr

232 ty-two patients (44%) were treated with deep venous thrombosis prophylaxis on postoperative day 4 aft

233 ary tract infection, pneumonia, sepsis, deep venous thrombosis, pulmonary embolism, venous thromboemb

234 other diseases of the vascular system (deep venous thrombosis/pulmonary embolism, peripheral vascula

235 ) in liver cirrhosis complicated with portal venous thrombosis (PVT) has been mainly treated with tra

236 or the 5-SNP risk score, the odds ratios for venous thrombosis ranged from 0.37 (95% confidence inter

237 Venous thrombosis rarely occurs at unusual sites such as

238 when a scheduled interim analysis detected a venous thrombosis rate that was considered unacceptably

239 in this study resulted in unacceptably high venous thrombosis rates.

240 Using the Scripps Venous Thrombosis Registry population for a case-control

241 r loop of SLC44A2 that is protective against venous thrombosis results in severely impaired binding t

242 oncerns about sudden death, pancreatitis and venous thrombosis returned.

243 re known to have a deleterious effect on the venous thrombosis risk and a preventive action on the de

244 e concurrent presence of genetic or acquired venous thrombosis risk factors.

245 Whether vitamin supplements decrease venous thrombosis risk is controversial.

246 single nucleotide polymorphisms (SNPs) in a venous thrombosis risk model improves the risk predictio

247 Impaired kidney function affects venous thrombosis risk via concurrently raised factor VI

248 ated with plasma levels of vWF and increased venous thrombosis risk.

249 ncrease the risk of lower limb proximal deep venous thrombosis (RR 0.97, 95% CI 0.72-1.29, P = 0.78,

250 itive MPs may explain the increased rates of venous thrombosis seen in patients with cancer.

251 ophylaxis, only patients with a high risk of venous thrombosis should be considered.

252 The odds ratios for venous thrombosis similarly increased across the categor

253 mon complication was cannula-associated deep venous thrombosis (six patients, 23.1%).

254 , a substantial number of patients with deep venous thrombosis still develop PTS.

255 alternative outcome measure for future deep venous thrombosis studies.

256 l and Genetic Assessment of risk factors for venous thrombosis study, we assessed the risk of venous

257 l and Genetic Assessment of Risk Factors for Venous Thrombosis study, which was a large Dutch case-co

258 nts with a clinical diagnosis of superficial venous thrombosis (SVT) are thoroughly evaluated, the de

259 It is unknown if splanchnic venous thrombosis (SVT) is a marker of occult cancer and

260 Venous thrombosis (symptomatic or asymptomatic) was dete

261 able to improve the individual prediction of venous thrombosis, taking into account information from

262 Vitamin use yielded a 37% lower risk of venous thrombosis than no vitamin use (OR: 0.63; 95% CI:

263 Many risk factors have been identified for venous thrombosis that alter blood flow, activate the en

264 -dependent model of flow restriction-induced venous thrombosis that complement factors make distinct

265 s 0.78 (95% CI, 0.31-1.96), for treatment of venous thrombosis the OR was 1.59 (95% CI, 1.03-2.44), a

266 large population-based case-control study on venous thrombosis (the MEGA study).

267 en are at increased risk for developing deep venous thrombosis, there are few pediatric studies estab

268 that, as a result of the natural history of venous thrombosis, there are special patient populations

269 arin and mortality, pulmonary embolism, deep venous thrombosis, thrombocytopenia, and bleeding outcom

270 ed disorder that can cause fatal arterial or venous thrombosis/thromboembolism.

271 ween 2009 and 2014, the ATTRACT trial (Acute Venous Thrombosis: Thrombus Removal With Adjunctive Cath

272 The ATTRACT trial (Acute Venous Thrombosis: Thrombus Removal with Adjunctive Cath

273 ry disorders that predispose to arterial and venous thrombosis through similar prothrombotic mechanis

274 Epidural catheters may directly prevent deep venous thrombosis through sympathetic blockade, resultin

275 results at CT pulmonary angiography had deep venous thrombosis, thus resulting in 38.7% with PE or de

276 thrombus burden in the setting of acute deep venous thrombosis to prevent both short- and long-term m

277 evaluated for suspected upper extremity deep venous thrombosis (UEDVT).

278 ous thrombosis were followed for a recurrent venous thrombosis up to 2009 (MEGA follow-up study), whi

279 In patients with deep venous thrombosis, use of elastic compression stockings

280 The prediction of recurrent venous thrombosis using individual genetic risk predicto

281 3,176-30,770 ng/mL] for lower extremity deep venous thrombosis vs 2,087 ng/mL [interquartile range, 6

282 t a mathematical model for the initiation of venous thrombosis (VT) due to slow flow and the conseque

283 Patients with venous thrombosis (VT) have an increased risk of subsequ

284 oteomic data suggest they may play a role in venous thrombosis (VT).

285 associated with VWF level, a risk factor for venous thrombosis (VT).

286 ers in the pathophysiology of (experimental) venous thrombosis (VT).

287 The risk of deep venous thrombosis was assessed in the two randomized con

288 Venous thrombosis was induced by inferior vena cava liga

289 Venous thrombosis was induced in the vena cava of BALB/C

290 Using an established model of venous thrombosis, we here show that systemic hypoxia ac

291 atios and 95% confidence intervals for first venous thrombosis were assessed in men compared with wom

292 Patients with a first venous thrombosis were followed for a recurrent venous t

293 Cardiac events and venous thrombosis were not increased with bevacizumab.

294 contributions by blood cells to pathological venous thrombosis were only recently appreciated.

295 ents with the first episode of proximal deep venous thrombosis were randomized to wear either thigh-l

296 there was no difference in the risk of deep venous thrombosis when the femoral site was compared to

297 herapy constitutes a good clinical model for venous thrombosis with known age.

298 We present a total of four cases of complete venous thrombosis with preservation of function that wer

299 ce of and risk factors for cancer-associated venous thrombosis, with the aim to provide a basis for i

300 absolute risk reduction in symptomatic deep venous thrombosis without increasing bleeding.