ライフサイエンスコーパス: venous thrombosis

1 ants for primary and secondary prevention of venous thrombosis.

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

3 In addition, 2 patients had venous thrombosis.

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

5 his aging-related enhanced susceptibility to venous thrombosis.

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

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

8 tein S deficiency is clearly associated with venous thrombosis.

9 ovel, controlled mouse model for spontaneous venous thrombosis.

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

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

12 ot be considered in unselected patients with venous thrombosis.

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

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

15 for conditions associated with arterial and venous thrombosis.

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

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

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

19 the computed tomography scan to detect deep venous thrombosis.

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

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

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

23 k of cardiovascular disease and arterial and venous thrombosis.

24 of PCSK9 is associated with protection from venous thrombosis.

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

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

27 elet interaction in flow disturbance-induced venous thrombosis.

28 a in individuals with clinically established venous thrombosis.

29 ents having both pulmonary embolism and deep venous thrombosis.

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

31 including bladder neck contracture and deep venous thrombosis.

32 such as pulmonary embolism or recurrent deep venous thrombosis.

33 ation for diagnosing upper extremity or neck venous thrombosis.

34 f pulmonary embolism or lower-extremity deep venous thrombosis.

35 iated with an increased risk of arterial and venous thrombosis.

36 with a history of fetal loss or arterial or venous thrombosis.

37 microM and was efficacious in a rat model of venous thrombosis.

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

39 the placebo group, 1 patient developed deep venous thrombosis.

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

41 efault drugs for anticoagulant management in venous thrombosis.

42 important players in the pathophysiology of venous thrombosis.

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

44 medical illnesses are at prolonged risk for venous thrombosis.

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

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

47 alignancy after initiating treatment of deep venous thrombosis.

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

49 itamin supplementation decreases the risk of venous thrombosis.

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

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

52 iciency is associated with increased risk of venous thrombosis.

53 a potential therapeutic target for limiting venous thrombosis.

54 roteinase inactivation, increase the risk of venous thrombosis.

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

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

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

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

59 Toxicities included allergy (1.5%), venous thrombosis (2%), and pancreatitis (4.6%).

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

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

62 st incidence of arterial thrombosis (17.4%), venous thrombosis (25.7%), and livedo reticularis (31.4%

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

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

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

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

67 due to cerebrovascular accident (12.8%) and venous thrombosis (7.8%).

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

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

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

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

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

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

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

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

76 .8%) developed an asymptomatic proximal deep venous thrombosis and 7 patients (5.9%) developed distal

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

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

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

80 O-1 gene may increase the risk for recurrent venous thrombosis and dysfunction of hemodialysis arteri

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

82 s the induction of HO-1 in a murine model of venous thrombosis and explores the downstream consequenc

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

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

85 that factor XIa plays a significant role in venous thrombosis and may be a suitable target for the d

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

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

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

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

90 aid in the diagnosis of lower extremity deep venous thrombosis and pulmonary embolism.

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

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

93 vel disease characterized by a propensity to venous thrombosis and seizures in which deficiency of GP

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

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

96 tent of shared pathways between arterial and venous thrombosis and whether treatments of known effica

97 developed thromboembolic complications (deep venous thrombosis and/or pulmonary emboli).

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

99 here were 1 death, 1 stroke, 2 cases of deep venous thrombosis, and 1 case of thrombosis in an arteri

100 arterial Y-graft caused by a kink, complete venous thrombosis, and arteriovenous fistula with pseudo

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

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

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

104 e to medical care, respiratory failure, deep venous thrombosis, and sepsis.

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

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

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

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

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

110 Risk of venous thrombosis associated with global variation withi

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

112 It is critical to treat deep venous thrombosis at an early stage to avoid development

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

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

115 al failure or insufficiency, pneumonia, deep venous thrombosis, bleeding, deep wound infection, reope

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

117 V Leiden) are involved in the development of venous thrombosis, but studies of such variants in coron

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

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

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

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

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

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

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

125 ial ischemic stroke (AIS) and cerebral sinus venous thrombosis (CSVT).

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

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

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

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

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

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

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

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

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

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

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

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

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

139 rd anticoagulation for acute, occlusive deep venous thrombosis (DVT) of the proximal lower extremitie

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

141 Clinical assessment of suspected deep venous thrombosis (DVT) should be based on systematicall

142 The presence of pulmonary embolism or deep venous thrombosis (DVT) was recorded for all patients.

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

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

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

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

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

148 contrast agent, ferumoxytol, to depict deep venous thrombosis (DVT).

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

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

151 ents with PR3-ANCA, nine had documented deep venous thrombosis events, five of whom were positive for

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 brillation (14 of 44 patients, 32%) and deep venous thrombosis (four of 44 patients, 9%).

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

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

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

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

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 A/gamma' fibrinogen levels with arterial and venous thrombosis have been reported, indicating that th

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

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

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

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

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

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

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

175 Because the high rates of arterial and venous thrombosis in lupus cannot be explained by tradit

176 at serious and life-threatening arterial and venous thrombosis in neonates and children.

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

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

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

180 odies (aPL) are associated with arterial and venous thrombosis in systemic lupus erythematosus (SLE),

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

182 myelofibrotic transformation, but decreased venous thrombosis, in patients with ET treated with anag

183 and thereby protective against arterial and venous thrombosis, including through the activation of p

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

185 eep venous valves are frequent sites of deep venous thrombosis initiation.

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

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

188 Venous thrombosis is a common disease process leading to

189 Venous thrombosis is a leading cause of morbidity and mo

190 important in pancreas transplantation where venous thrombosis is a major problem.

191 Venous thrombosis is a multicausal disease involving int

192 Venous thrombosis is a relatively frequent and serious c

193 Cerebral venous thrombosis is a relatively uncommon neurologic di

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

195 diagnostic imaging studies to rule out deep venous thrombosis is exacerbated by increased susceptibi

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

197 icting studies published, the role of VWF in venous thrombosis is still unclear.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

212 Six patients presented with only a deep venous thrombosis or a pulmonary embolism; 1 patient had

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

214 incipal outcome measure was the incidence of venous thrombosis or pulmonary embolism occurring during

215 Documented VTE (deep venous thrombosis or pulmonary embolism) and unprovoked

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

217 ents who have been given a diagnosis of deep venous thrombosis or pulmonary embolism.

218 [95% CI, 1.41 to 3.06]); postoperative deep venous thrombosis (OR, 1.96 [95% CI, 1.18 to 3.26]); and

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

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

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

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

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

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

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

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

227 Venous thrombosis patients had significantly lower level

228 little is known about plasma lipoproteins in venous thrombosis patients.

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

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

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

232 pplied to other populations of patients with venous thrombosis, providing for more effective clinical

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

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

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

240 thromboembolic complications, including deep venous thrombosis, renal vein thrombosis, and pulmonary

241 more importantly, those patients at risk for venous thrombosis, represents a paradigm for a genomic a

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 nown for its mild deficiency associated with venous thrombosis risk and severe deficiency associated

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

246 Whether vitamin supplements decrease venous thrombosis risk is controversial.

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

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

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

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

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

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

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

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

255 e, and ProS deficiencies are associated with venous thrombosis, stroke, and autoimmunity.

256 alternative outcome measure for future deep venous thrombosis studies.

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

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

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

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

261 Venous thrombosis (symptomatic or asymptomatic) was dete

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

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

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

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

266 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

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

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

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

270 ermine the significance of HO-1 induction in venous thrombosis, this model was imposed in HO-1(+/+) a

271 t of six assessable patients resulted in one venous thrombosis; this dose level was expanded to 26 pa

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

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

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

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

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 tein C (PC) deficiency increases the risk of venous thrombosis (VT) among members of Kindred Vermont

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

283 c variation in these constituents to risk of venous thrombosis (VT) has not been fully investigated.

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

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

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

287 95.8 per 100,000), and the incidence of deep venous thrombosis was 3 times higher than that of pulmon

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

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

298 luded 3.9% pulmonary embolism and 16.3% deep venous thrombosis, with 1.5% of patients having both pul

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.