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1 <2 years of age with catheter-related venous thromboembolism).
2 ing, infection of the amniotic fluid, venous thromboembolism).
3 the pressing public health problem of venous thromboembolism.
4 ard of care in treating children with venous thromboembolism.
5 site of adjudicated major arterial or venous thromboembolism.
6 injury, myocarditis, arrhythmias, and venous thromboembolism.
7 lity; and the coagulation system, leading to thromboembolism.
8 rhythmia, acute coronary syndrome and venous thromboembolism.
9  mobility places patients at risk for venous thromboembolism.
10 ndard anticoagulants in children with venous thromboembolism.
11 ism and patients that did not develop venous thromboembolism.
12 ent (0.05%; 95% CI, 0.01 to 0.30) had venous thromboembolism.
13 ajor bleeding events in patients with venous thromboembolism.
14 ancer therapy are at varying risk for venous thromboembolism.
15  were followed for 3 months to detect venous thromboembolism.
16  coagulation and an increased risk of venous thromboembolism.
17 roved for treatment and prevention of venous thromboembolism.
18 peutic strategies to prevent the sequelae of thromboembolism.
19 ls were not associated with a higher risk of thromboembolism.
20 , asthma, chronic kidney disease, and venous thromboembolism.
21 ed to estimate hazard ratios for the outcome thromboembolism.
22 option for treatment of patients with venous thromboembolism.
23 patients with atrial fibrillation and venous thromboembolism.
24 presented elevated odds for prevalent venous thromboembolism.
25 ry disease, ischemic stroke (IS), and venous thromboembolism.
26 variables known to be associated with venous thromboembolism.
27 ns other than atrial fibrillation and venous thromboembolism.
28 troke, peripheral artery disease, and venous thromboembolism.
29 onal variant of VWF plays a role in arterial thromboembolism.
30 ce the occurrence of PTS or recurrent venous thromboembolism.
31 e strategy to reduce the incidence of venous thromboembolism.
32  HbA1c were associated with a higher risk of thromboembolism.
33  phase 3 trial in children with acute venous thromboembolism.
34  of standard of care in children with venous thromboembolism.
35 tentially modifiable risk factors for venous thromboembolism.
36 associated bloodstream infections and venous thromboembolism.
37 uctive sleep apnoea, osteoporosis and venous thromboembolism.
38 r suspected pulmonary arterial thrombosis or thromboembolism.
39 entify patients at increased risk for venous thromboembolism.
40 patients (1.4%) developed symptomatic venous thromboembolism.
41 aged birth to less than 18 years with venous thromboembolism.
42 ining ICs may also reduce the risk of venous thromboembolism.
43 ch dominated the overall reduction in venous thromboembolism.
44             The secondary outcome was venous thromboembolisms.
45 e deterioration 1.59%/y (95% CI, 1.21-2.10), thromboembolism 0.53%/y (95% CI, 0.42-0.67), bleeding 0.
46 ed RR was 0.58 (95% CI 0.47-0.71) for venous thromboembolism, 1.27 (0.92-1.74) for major bleeding, an
47 on the MV 4.6%, infective endocarditis 1.1%, thromboembolism 10.3%, and bleeding 6.4%.
48     All of these patients experienced venous thromboembolism: 10 patients (76.9%) had isolated cannul
49 ke (11 more cases [95% CI, 2 to 23]), venous thromboembolism (11 more cases [95% CI, 3 to 22]), and u
50  of 78%, structural valve deterioration 71%, thromboembolism 12%, bleeding 5%, and endocarditis 9%.
51 ore cases [95% CI, 606 to 1168]), and venous thromboembolism (21 more cases [95% CI, 12 to 33]).
52 equence variants for association with venous thromboembolism (26,066 cases and 624,053 controls) and
53 thrombosis but also for prevention of venous thromboembolism, (3) the finding that dual pathway inhib
54 o 4 days (4 points), prior history of venous thromboembolism (4 points), mechanical ventilation (2 po
55 ntrations (thromboembolism, 78.3 ng/mL vs no thromboembolism, 59.5 ng/mL; p = 0.031; area under the r
56 parable to plasma P-selectin concentrations (thromboembolism, 78.3 ng/mL vs no thromboembolism, 59.5
57  events (25%), arrhythmias (22%), and venous thromboembolism (9%).
58 7 resulted from sepsis and 31 from pulmonary thromboembolism, accounted for 51.6%.
59 0.8-7.6); the cumulative incidence of venous thromboembolism alone at day 30 postdischarge was 0.6% (
60 ted by hemoglobin A1c (HbA1c) on the risk of thromboembolism among patients with atrial fibrillation
61  <=48 mmol/mol, we observed a higher risk of thromboembolism among patients with HbA1c=49-58 mmol/mol
62                 Patients who had both venous thromboembolism and atrial fibrillation were excluded, a
63 h multiple health problems, including venous thromboembolism and atrial fibrillation, both of which a
64 rates and low, though not absent, hazards of thromboembolism and bleeding.
65 s synergistic mechanisms involved, including thromboembolism and cerebral vasculitis, promoted by a s
66  patients are also at higher risk for venous thromboembolism and dialysis.
67 al and environmental underpinnings of venous thromboembolism and its complications.
68  Differences in the risk of recurrent venous thromboembolism and major bleeding events between the tw
69 ivaroxaban in prevention of recurrent venous thromboembolism and major bleeding events in patients wi
70 eventing the development of recurrent venous thromboembolism and major bleeding events.
71  oral anticoagulants in patients with venous thromboembolism and non-valvular atrial fibrillation hav
72 with vitamin K antagonist therapy for venous thromboembolism and nonvalvular atrial fibrillation, maj
73 pared between patients that developed venous thromboembolism and patients that did not develop venous
74 entified in asthma, cystic fibrosis, chronic thromboembolism and primary carcinomas.
75 mechanisms, and provides an update on venous thromboembolism and pulmonary hypertension associated wi
76 ghts into the genetic epidemiology of venous thromboembolism and suggest a greater overlap among veno
77 relation between the uni- or bilateralism of thromboembolism and the D-dimer levels, we also found a
78 udy was to determine the frequency of venous thromboembolism and the degree of inflammatory and coagu
79 utcome was the incidence of recurrent venous thromboembolism and the primary safety outcome was the i
80 r the 50% of patients with unprovoked venous thromboembolism and to better understand mechanisms that
81 key terms relating to the population (venous thromboembolism and total knee replacement) and the inte
82 esolution, and freedom from recurrent venous thromboembolism and venous thromboembolism-related death
83                                 The risks of thromboembolism and ventricular arrhythmias in LVNC pati
84 bosis in a lower limb, and death from venous thromboembolism and was assessed up to day 180.
85 patients who were at elevated risk of venous thromboembolism and were randomly assigned to either ant
86 which might mitigate the lethality of venous thromboembolism) and those for which mortality data were
87 phy was associated with an increased risk of thromboembolism, and a reduced risk of requiring transfu
88 es the effect of heparin on survival, venous thromboembolism, and bleeding in patients with cancer in
89 nancies, major cardiovascular events, venous thromboembolism, and mortality.
90 ly a minority of COVID(pos) patients develop thromboembolism, and rarely, disseminated intravascular
91 risk of all outcomes in patients with venous thromboembolism, and stroke and composite bleeding in pa
92                      Respiratory failure and thromboembolism are frequent in SARS-CoV-2-infected pati
93 ficacy outcome, symptomatic recurrent venous thromboembolism (assessed by intention-to-treat), and th
94         Apixaban for the treatment of venous thromboembolism associated with cancer.
95 wn loci, bringing the total number of venous thromboembolism-associated loci to 33, and subsequently
96 y outcomes were symptomatic recurrent venous thromboembolism, asymptomatic deterioration on repeat im
97 r the primary outcome of incidence of venous thromboembolism at 10 to 13 days postoperatively.
98  primary outcome was the incidence of venous thromboembolism at 3 months.
99  statistics outlined the frequency of venous thromboembolism at any time during severe coronavirus di
100 including two patients diagnosed with venous thromboembolism at presentation to the hospital.
101    This study evaluated the risk of arterial thromboembolism before cancer diagnosis.
102    These findings are consistent with venous thromboembolism being a manifestation of advanced diseas
103 atients with an incident diagnosis of venous thromboembolism between January 2010 and December 2016 u
104 impact of LVT regression on the incidence of thromboembolism, bleeding, and mortality.
105 ted with dialysis initiation and with venous thromboembolism but not with major adverse cardiac event
106 tive strategy to prevent arterial and venous thromboembolism, but treating older individuals is chall
107 lammation and hypercoagulability rather than thromboembolism.(C) RSNA, 2020.
108 pendent replication with up to 17,672 venous thromboembolism cases and 167,295 controls.
109 sm seemed to have a risk of recurrent venous thromboembolism comparable to that of patients with more
110                                              Thromboembolism complicates disorders caused by immunogl
111 r adult patients with newly diagnosed venous thromboembolism (deep vein thrombosis or pulmonary embol
112  with lower use of DOACs for incident venous thromboembolism despite controlling for other clinical a
113 hlights future research priorities in venous thromboembolism, developed by experts and a crowdsourcin
114 and peak D-dimer were associated with venous thromboembolism development (p < 0.05).
115 tion marker elevation associated with venous thromboembolism development.
116 e of inflammatory marker elevation to venous thromboembolism development.
117 r milliliter, respectively), none had venous thromboembolism during follow-up (95% confidence interva
118 e was objectively confirmed recurrent venous thromboembolism during the trial period.
119  significant effects of prevention on venous thromboembolism endpoints.
120 he secondary objective was to compare venous thromboembolism events and coagulation variables in pati
121 dy was to determine the prevalence of venous thromboembolism events in patients infected with severe
122 erence in baseline characteristics or venous thromboembolism events.
123  in children who had catheter-related venous thromboembolism for at least 6 weeks.
124 parin reduces the risk of symptomatic venous thromboembolism for patients with cancer; however, wheth
125                         Historically, venous thromboembolism has received the greatest attention but,
126 er scores indicating a higher risk of venous thromboembolism) has been validated to identify patients
127 15-18 (2%) had a high (17.7%) risk of venous thromboembolism (hazard ratio, 28.1; 95% CI, 21.7-36.5).
128 %) had an intermediate (3.6%) risk of venous thromboembolism (hazard ratio, 6.7; 95% CI, 5.3-8.4); an
129  patients face an increased risk of arterial thromboembolism; however, it is uncertain when this exce
130 ated with decreased risk of recurrent venous thromboembolism (HR 0.37 [95% CI 0.24-0.55]; p<0.0001) a
131 t (HR, 6.0; 95% CI, 2.6 to 14.1), and venous thromboembolism (HR, 24.7; 95% CI, 14.0 to 43.6).
132       High-grade HAT/DRT was associated with thromboembolism in 2 cases, whereas low-grade HAT was no
133 wn to be efficacious for treatment of venous thromboembolism in adults, and has a reduced risk of ble
134     We found no symptomatic recurrent venous thromboembolism in any patients (0%, 0.0-3.9).
135 cular-weight heparin for treatment of venous thromboembolism in cancer patients: an updated meta-anal
136 roxaban regimens for the treatment of venous thromboembolism in children and adolescents.
137                          Treatment of venous thromboembolism in children is based on data obtained in
138 udy was to determine the frequency of venous thromboembolism in critically ill coronavirus disease 20
139 y aimed to describe the prevalence of venous thromboembolism in critically ill patients receiving dif
140        We report a 100% occurrence of venous thromboembolism in critically ill patients supported by
141 ed to reduce the risk of venous and arterial thromboembolism in large randomized clinical trials of p
142  measured by thromboelastography, to predict thromboembolism in patients with abnormal coagulation pr
143 a, and 30-day risks of bleeding and arterial thromboembolism in patients with atrial fibrillation (AF
144 n or rivaroxaban for the treatment of venous thromboembolism in patients with cancer.
145 laxis may be inadequate in preventing venous thromboembolism in severe coronavirus disease 2019.
146 enous thromboembolism or death due to venous thromboembolism in the 180-day trial period.
147 ith regard to the prevention of major venous thromboembolism in these patients.
148               The primary outcome was venous thromboembolism incidence between 10 and 13 days postope
149 dren younger than 18 years with acute venous thromboembolism initially treated (5-21 days) with paren
150 cations (acute kidney injury, sepsis, venous thromboembolism, intensive care unit admission >48 hours
151                   The perception that venous thromboembolism is a common cause of mortality should be
152                                       Venous thromboembolism is a major cause of morbidity and mortal
153                   Hospital-associated venous thromboembolism is a major patient safety concern.
154                                       Venous thromboembolism is a significant cause of mortality(1),
155                                       Venous thromboembolism is associated with increased mortality r
156 pulmonary embolism, risk of recurrent venous thromboembolism is significant despite anticoagulant tre
157 cation that often leads to limb ischemia and thromboembolism, is proposed.
158 were at intermediate-to-high risk for venous thromboembolism (Khorana score, >=2) and were initiating
159                     Major arterial or venous thromboembolism, major adverse cardiovascular events, an
160               Outcomes were recurrent venous thromboembolism, major bleeding, and all-cause mortality
161                     The occurrence of stroke/thromboembolism, major bleeding, myocardial infarction,
162      Frequencies of major arterial or venous thromboembolism, major cardiovascular adverse events, an
163 ternational registry of patients with venous thromboembolism (March 2001-January 2019), we explored t
164                           In-hospital death, thromboembolism, mechanical ventilation, or hemodynamic
165 PN7-null mice than in WT mice in a pulmonary thromboembolism model.
166 teonecrosis [n = 29]; pancreatitis [n = 24]; thromboembolism [n = 17]) was 9.3% in the experimental a
167 consistent with the increased rate of venous thromboembolism observed in patients with sickle cell di
168 ots may explain the increased risk of venous thromboembolism observed in SCD.
169      Clinically diagnosed symptomatic venous thromboembolism occurred in 1.4% of this large populatio
170                                       Venous thromboembolism occurred in 12 of 288 patients (4.2%) in
171                             Recurrent venous thromboembolism occurred in 32 of 576 patients (5.6%) in
172                                 Major venous thromboembolism occurred in 4 of 1661 patients (0.2%) in
173                             Recurrent venous thromboembolism occurred in 41 patients (12-month cumula
174 1 month (n=37), symptomatic recurrent venous thromboembolism occurred in four (1%) of 335 children re
175 ardiovascular events, and symptomatic venous thromboembolism occurred with high frequency in patients
176     Prespecified subgroup analysis of venous thromboembolism occurrence by cancer type identified the
177 dministration on all-cause mortality, venous thromboembolism occurrence, and bleeding related outcome
178 ; 95% CI, 0.336-0.759; p = 0.001) and venous thromboembolism (odds ratio, 0.569; 95% CI, 0.330-0.982;
179 who were considered to be at risk for venous thromboembolism on the basis of the investigator's judgm
180  a pro-thrombotic state (four with pulmonary thromboembolism), one of whom died; (iv) peripheral neur
181 , rivaroxaban, or warfarin for either venous thromboembolism or atrial fibrillation between March 1,
182 at examined significant predictors of venous thromboembolism or central-line associated bloodstream i
183 in a significantly lower incidence of venous thromboembolism or death due to venous thromboembolism i
184 1.27]), but inversely associated with venous thromboembolism (OR, 0.79 [95% CI, 0.67-0.93]) and hemor
185 , 1.00 [95% CI, 0.68-1.47]; P=0.996), venous thromboembolism (OR, 1.04 [95% CI, 0.77-1.39]; P=0.810),
186  versus 0.5% ( P=0.32), and recurrent venous thromboembolism over 24 months was observed in 13% versu
187 cy outcome was objectively documented venous thromboembolism over a follow-up period of 180 days.
188 tly associated with increased risk of stroke/thromboembolism (P(trend)=0.06), myocardial infarction (
189                              Previous venous thromboembolism (p=0.014), being bedbound in the past 12
190 h DOAC use among commercially insured venous thromboembolism patients.
191                  An increased rate of venous thromboembolism (peripherally inserted central catheter:
192 uded, 34 patients (16%) developed subsequent thromboembolism-predominantly among those with a normal
193 established that the causal effect of venous thromboembolism prevention on mortality was null (contro
194 evised considering the null effect of venous thromboembolism prevention on mortality.
195                     We used data from venous thromboembolism prevention trials to evaluate the causal
196 d controlled trials (RCTs) evaluating venous thromboembolism prevention.
197 ion the use of composite endpoints in venous thromboembolism-prevention trials and provide rationale
198 d children with objectively confirmed venous thromboembolism previously treated with low-molecular we
199                      Routine chemical venous thromboembolism prophylaxis may be inadequate in prevent
200 s the relative efficacy and safety of venous thromboembolism prophylaxis strategies and to populate a
201 eceived routine subcutaneous chemical venous thromboembolism prophylaxis.
202 l asthma (BA) enhances the risk of pulmonary thromboembolism (PTE).
203                                       Venous thromboembolism (pulmonary embolism or any lower-limb de
204 ials to evaluate the causal effect of venous thromboembolism reduction on mortality.
205 in thrombosis, pulmonary embolism, or venous thromboembolism-related death during the treatment perio
206  recurrent venous thromboembolism and venous thromboembolism-related death.
207 ositive, with significantly increased venous thromboembolism risk in patients in control groups versu
208  population at an equivalent incident venous thromboembolism risk to carriers of the established fact
209                                       Venous thromboembolism risk was elevated in survivors of 18 of
210                               The ICU-Venous Thromboembolism score can identify patients at increased
211                               The ICU-Venous Thromboembolism score consists of six independent predic
212           A prediction score (the ICU-Venous Thromboembolism score) was derived from independent risk
213 ndomisation was stratified by age and venous thromboembolism site.
214                 Outcomes of recurrent venous thromboembolism, stroke, and bleeding were measured from
215                    Increased risks of venous thromboembolism [summary estimate (SE), 95% confidence i
216  associated bloodstream infection and venous thromboembolism than central venous catheters in childre
217 lted in a significantly lower rate of venous thromboembolism than did placebo among intermediate-to-h
218  genome-wide polygenic risk score for venous thromboembolism that identifies 5% of the population at
219 ients prescribed an anticoagulant for venous thromboembolism, the incidence of recurrent venous throm
220  the sample) had a low (0.3%) risk of venous thromboembolism; those with a score of 9-14 (22%) had an
221 lts indicate that platelet APP limits venous thromboembolism through a negative regulation of both fi
222 k for stroke, pulmonary embolism, and venous thromboembolism through its effect on thrombin-induced p
223 study, we assigned 3396 patients with venous thromboembolism to receive either once-daily rivaroxaban
224                In children with acute venous thromboembolism, treatment with rivaroxaban resulted in
225 ting Health & Prevention, Rhythm Disorders & Thromboembolism, Valvular Heart Disease, and Vascular Me
226 of stent occlusion (patency loss) and venous thromboembolism varies substantially across indications,
227  outcome was the 3-month incidence of venous thromboembolism (VTE) after a MRDTI negative for DVT.
228 risk factors for 30-day postdischarge venous thromboembolism (VTE) after bariatric surgery and to ide
229 atify risk or provide prophylaxis for venous thromboembolism (VTE) among surgical patients.
230  at an increased risk of arterial and venous thromboembolism (VTE) and bleeding events.
231       There may be many predictors of venous thromboembolism (VTE) and bleeding in hospitalized medic
232           Early reports describe high venous thromboembolism (VTE) and disseminated intravascular coa
233 ibute to thrombotic diseases, such as venous thromboembolism (VTE) and ischemic stroke.
234 acement has been suggested to prevent venous thromboembolism (VTE) and thus may increase exposure to
235            Genetic predispositions to venous thromboembolism (VTE) are relatively frequent in the gen
236                 The increased risk of venous thromboembolism (VTE) associated with pregnancy is well-
237  to provide defect-free postoperative venous thromboembolism (VTE) chemoprophylaxis, (2) identify rea
238 regnant women in 1000 will experience venous thromboembolism (VTE) during pregnancy or postpartum.
239  (COVID-19) with an increased risk of venous thromboembolism (VTE) has resulted in specific guideline
240 boprophylaxis (EDT) for prevention of venous thromboembolism (VTE) in medical patients remain unclear
241 nal normalized ratio (INR) to prevent venous thromboembolism (VTE) in warfarin-treated patients with
242                                       Venous thromboembolism (VTE) incidence in children has sharply
243                                       Venous thromboembolism (VTE) is a major preventable disease tha
244                                       Venous thromboembolism (VTE) is a significant contributor to mo
245                                       Venous thromboembolism (VTE) is a significant public health bur
246                                       Venous thromboembolism (VTE) is associated with significant mor
247 ecision in the long-term treatment of venous thromboembolism (VTE) is how long to anticoagulate.
248                                       Venous thromboembolism (VTE) is rare in healthy children, but i
249 etween cholesterol levels and risk of venous thromboembolism (VTE) is uncertain.
250 ociated with the highest incidence of venous thromboembolism (VTE) of any cancer type.
251 th dabigatran etexilate for secondary venous thromboembolism (VTE) prevention.
252            Heparin administration for venous thromboembolism (VTE) prophylaxis in patients with ICH a
253 or to unfractionated heparin (UH) for venous thromboembolism (VTE) prophylaxis in patients with sever
254 r, the association between GDF-15 and venous thromboembolism (VTE) remains uncertain.
255                     All patients with venous thromboembolism (VTE) should receive anticoagulant treat
256 f the polymorphism at position 310 in venous thromboembolism (VTE) using the International Network Ag
257 cy are at 4- to 7-fold higher risk of venous thromboembolism (VTE), a potentially fatal, yet preventa
258 ary embolism, collectively defined as venous thromboembolism (VTE), are the third leading cause of ca
259 omodulatory drugs are at high risk of venous thromboembolism (VTE), but data are lacking from large p
260 on for patients with cancer and acute venous thromboembolism (VTE), but studies have reported inconsi
261                                       Venous thromboembolism (VTE), caused by altered hemostasis, rem
262                                       Venous thromboembolism (VTE), composed of pulmonary embolism an
263                     For patients with venous thromboembolism (VTE), prediction of bleeding is relevan
264                      Risk factors for venous thromboembolism (VTE), such as older age, malignancy (cu
265 a substantial number of patients with venous thromboembolism (VTE), the initial hope that their prese
266                                       Venous thromboembolism (VTE), which includes both deep venous t
267                                       Venous thromboembolism (VTE), which includes deep vein thrombos
268                                       Venous thromboembolism (VTE), which includes deep vein thrombos
269 ents at increased short-term risk for venous thromboembolism (VTE).
270 ents with additional risk factors for venous thromboembolism (VTE).
271 xtent HF confers an increased risk of venous thromboembolism (VTE).
272 tion in carriers without a history of venous thromboembolism (VTE).
273 d intravascular coagulation (DIC) and venous thromboembolism (VTE).
274 d intravascular coagulation (DIC) and venous thromboembolism (VTE).
275 heral artery disease (PAD) events and venous thromboembolism (VTE).
276   The 12-month incidence of recurrent venous thromboembolism was 6.4% in those with subsegmental pulm
277 The primary efficacy outcome of major venous thromboembolism was a composite of symptomatic distal or
278  ability of the maximum amplitude to predict thromboembolism was comparable to plasma P-selectin conc
279                           Symptomatic venous thromboembolism was defined as deep vein thrombosis, pul
280                                       Venous thromboembolism was diagnosed in 31 patients (28%) 8 +/-
281 erebrovascular accident (4% each) and venous thromboembolism was low (0% vs 13%, P = 0.23).
282 d prophylactic anticoagulant therapy; venous thromboembolism was not clinically suspected antemortem
283 sis in 7 of 12 patients (58%) in whom venous thromboembolism was not suspected before death; pulmonar
284 oembolism, the incidence of recurrent venous thromboembolism was similar between the apixaban, rivaro
285      The crude incidence of recurrent venous thromboembolism was three per 100 person-years in the ap
286 er scores indicating a higher risk of venous thromboembolism), we randomly assigned patients without
287 nnualized rates of stent occlusion or venous thromboembolism were 7.8 (acute thrombotic), 15.0 (postt
288 r heart failure or cardiomyopathy and venous thromboembolism were greater in patients without previou
289 cular adverse events, and symptomatic venous thromboembolism were highest in the intensive care cohor
290  associated bloodstream infection and venous thromboembolism were included.
291 ensitivity, pancreatitis, osteonecrosis, and thromboembolism were prospectively registered.
292              All complications except venous thromboembolism were significantly reduced in the ERP po
293 tients with cancer have an increased risk of thromboembolism, which is the second leading cause of de
294 tive cancer have an increased risk of venous thromboembolism, which results in substantial morbidity,
295 in 28 countries with documented acute venous thromboembolism who had started heparinisation were assi
296  diagnosing, treating, and preventing venous thromboembolism will allow tailoring of diagnostic and t
297 er greater than 2,600 ng/mL predicted venous thromboembolism with an area under the receiver operatin
298 egative rate (defined as diagnosis of venous thromboembolism within 90 d).
299 or the treatment of cancer-associated venous thromboembolism without an increased risk of major bleed
300 ecular-weight heparin reduces risk of venous thromboembolism without increasing risk of major bleedin

 
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