ライフサイエンスコーパス: thrombotic

1 thrombotic, and 79% and 94% for chronic post-thrombotic.

2 of pro-inflammatory, pro-atherogenic and pro-thrombotic adipokines.

3 Compared with patients who were unexposed to thrombotic agents, the rates of hematuria-related compli

4 templates for the development of novel anti-thrombotic agents.

5 models to predict risks for out-of-hospital thrombotic and bleeding events after percutaneous corona

6 e optimal INR based on weighted mortality of thrombotic and bleeding events was 2.6.

7 We evaluated thrombotic and bleeding outcomes in patients with contin

8 There are limited data about the risk of thrombotic and embolic complication (TEC) in adults with

9 eutic perspectives in cTTP and in general in thrombotic and inflammatory disorders associated with en

10 et for acute therapeutic intervention in the thrombotic and inflammatory post-MI environment.

11 ctive, and activating FcgammaRs also enhance thrombotic and nonthrombotic vascular occlusion.

12 99% for nonthrombotic, 87% and 89% for acute thrombotic, and 79% and 94% for chronic post-thrombotic.

13 .0 mm Hg), presence of thickened leaflets or thrombotic apposition of leaflets in 20 (77%) and a thro

14 These complications are caused by thrombotic arterial occlusion localized at the site of h

15 ews on (1) embolic/stroke risk, (2) ischemic/thrombotic cardiac risk, and (3) bleeding risk, which ar

16 atients is associated with increased risk of thrombotic cardiovascular events.

17 non-valvular AF were recruited and rates of thrombotic/cardiovascular events, major bleeding and mor

18 In response to thrombotic challenge with factor Xa/phospholipids, EPCR(

19 ents a patient with ulcerative colitis, with thrombotic complication of the left common iliac vein th

20 ls (22.6% vs. 14.9%; p = 0.03), particularly thrombotic complications (12.4% vs. 5.8%; p = 0.01).

21 primary outcome was a composite of death and thrombotic complications (nonfatal myocardial infarction

22 primary outcome was a composite of death and thrombotic complications (nonfatal myocardial infarction

23 ellitus (DM2) is associated with accelerated thrombotic complications and is characterized by high le

24 Premature atherosclerosis and thrombotic complications are major causes of morbidity a

25 folds (BVS) are associated with an excess of thrombotic complications compared with metallic everolim

26 resulted in neither a lower risk of death or thrombotic complications nor a higher risk of bleeding t

27 et activation and potentially contributes to thrombotic complications occurring in cirrhosis.

28 rget for thrombotic diseases, especially for thrombotic complications of diabetes mellitus.

29 provide a therapeutic opportunity to prevent thrombotic complications of HIT, while sparing systemic

30 tervention are critical to the management of thrombotic complications of transplant.

31 onstrate that this species can cause serious thrombotic complications of trichinellosis in humans.

32 s a therapeutic approach to treat or prevent thrombotic complications of VEGF inhibition.

33 r in the future, particularly in view of the thrombotic complications that have been reported when em

34 Prasugrel and ticagrelor reduce thrombotic complications to a greater extent than clopid

35 controversial owing to concern for increased thrombotic complications with its use.

36 not detect evidence of an increased risk of thrombotic complications with TXA exposure.

37 s placebo, without a higher risk of death or thrombotic complications within 30 days after surgery.

38 n the risk of bleeding outweighs the risk of thrombotic complications.

39 should be carefully considered when managing thrombotic complications.

40 ry intervention is associated with increased thrombotic complications.

41 in this mechanical device that can result in thrombotic complications.

42 with an ACT</=300 s are at increased risk of thrombotic complications.

43 ditions are divided into arterial and venous thrombotic conditions.

44 f CLEC-2 KO models, but not their hemostatic/thrombotic defect.

45 Small arterial, venous thrombi, thrombotic depositions on damaged endothelial surface, a

46 t, which recapitulates the key components of thrombotic development and of thrombolytic therapy of rt

47 with nephrotic syndrome at highest risk for thrombotic disease and potentially target them for antic

48 f coagulation, may better help manage venous thrombotic disease than a single DNA variant with a smal

49 Thrombotic disease, a major life-threatening complicatio

50 , we review atherothrombotic disease, venous thrombotic disease, and atrial fibrillation in patients

51 Although trichinellosis is known to cause thrombotic disease, serious thrombotic events are rare a

52 add insights into the genetic regulation of thrombotic disease, we conducted a genome-wide associati

53 hemostasis but simultaneously contributes to thrombotic disease.

54 g promising new targets for the treatment of thrombotic disease.

55 thms with proven safety for excluding venous thrombotic disease.

56 Thrombotic diseases are among the leading causes of morb

57 de a proof-of-concept approach for combating thrombotic diseases without increased bleeding risk, ind

58 h will enable elucidation of the genetics of thrombotic diseases, and serves as an example for the ge

59 herapeutic strategy and molecular target for thrombotic diseases, especially for thrombotic complicat

60 e circulation is essential for prevention of thrombotic diseases.

61 ping microbes, they promote inflammatory and thrombotic diseases.

62 processes are critical to the progression of thrombotic diseases.

63 se of cardiovascular mortality, is a complex thrombotic disorder with environmental and genetic deter

64 rd a therapeutic for patients suffering from thrombotic disorders and a diagnostic tool for monitorin

65 t activation may contribute to various human thrombotic disorders involving both the micro- and macro

66 n, the clinical utility of targeting them in thrombotic disorders is already being explored in clinic

67 thrombi and restore vessel patency in acute thrombotic disorders such as ischemic stroke, acute coro

68 be explored as a novel treatment of arterial thrombotic disorders, including hereditary and acquired

69 fened clots are associated with bleeding and thrombotic disorders.

70 ortant role in prevention of bleeding and in thrombotic disorders.

71 and might suggest novel approaches to these thrombotic disorders.

72 ociation would be a new approach to treating thrombotic disorders.

73 in acquired TTP and potentially other immune thrombotic disorders.

74 as therapeutic targets for inflammatory and thrombotic disorders.

75 poxic, ischemic/hypertensive, infectious and thrombotic etiologies were diagnosed, blinded to exposur

76 ved with anticoagulant therapy, suggesting a thrombotic etiology.

77 % of BMS patients (p = 0.95), and a coronary thrombotic event (myocardial infarction and/or stent thr

78 ng thrombus formation and growth following a thrombotic event in normal or pathological conditions.

79 We conclude that occurrence of a thrombotic event is associated with higher mortality in

80 s and the best drugs to prevent each type of thrombotic event.

81 was 27.1% for a major bleed and 26.3% for a thrombotic event.

82 e potential consequences of not treating the thrombotic event.

83 mity and that blood was drawn 3 mo after the thrombotic event.

84 splenomegaly or symptoms in the absence of a thrombotic event.

85 l events (15 cohorts; n>2543 fistulas), 0.24 thrombotic events (26 cohorts; n=4232 fistulas), and 0.0

86 Most thrombotic events (66%) occurred before the start of the

87 y intervention reduces the risk for coronary thrombotic events (CTEs) at the expense of increasing ri

88 INR was inversely associated with thrombotic events (hazard ratio, 0.40; 95% confidence in

89 IgA isotype (IgA-aB2GP1) have been linked to thrombotic events and mortality in hemodialysis patients

90 anticoagulation, such as arterial and venous thrombotic events and prevention of stroke in atrial fib

91 I-1 are correlated with an increased risk of thrombotic events and several other pathologies.

92 s known to cause thrombotic disease, serious thrombotic events are rare and have not been previously

93 haracterize the incidence of hemorrhagic and thrombotic events as well as complications of pregnancy

94 rker potential of procoagulant platelets for thrombotic events as well as on the possible clinical be

95 warfarin, significantly reduced the risk of thrombotic events at the cost of increased bleeding in p

96 Factor Xa inhibitors and aspirin each reduce thrombotic events but have not yet been tested in combin

97 mellitus (DM) are at high risk of recurrent thrombotic events despite standard therapy and may deriv

98 10-year cumulative incidence of ischemic and thrombotic events differed by arm; 24% for continuous an

99 asome complex, is a key determinant of acute thrombotic events during hypoxic conditions.

100 The incidence of major venous-thrombotic events during the study was 1.22 per 100 pers

101 let therapies is their inability to separate thrombotic events from bleeding occurrences.

102 At 90 days, thrombotic events had occurred in 6.3% of the patients i

103 plant surgery, a well-known trigger of acute thrombotic events in aPL carriers.

104 n independent and predictive risk factor for thrombotic events in humans.

105 predictive value for the appearance of acute thrombotic events in patients who are going to undergo t

106 novel therapeutic target to prevent adverse thrombotic events in patients with diabetes mellitus.

107 association of sildenafil administration and thrombotic events in patients with LLH during Heart Mate

108 in on human platelets, and reduces recurrent thrombotic events in stable patients with a previous myo

109 Neither hemolysis nor thrombotic events increased the risk of mortality.

110 ity worldwide, and is a consequence of acute thrombotic events involving activation of platelets and

111 underlying the increased incidence of acute thrombotic events observed in patients with CKD and may

112 Thrombotic events occurred in 12 of 67 patients (18%) du

113 ring a mean follow-up of 17.6+/-13.6 months, thrombotic events occurred in 46 outpatients.

114 INR is inversely related to thrombotic events occurring outside of the hospital amon

115 INR values <2.0 increase the rate of thrombotic events occurring outside of the hospital amon

116 No thrombotic events or malignancies occurred.

117 There were no thrombotic events or severe allergic reactions.

118 The highest event rate (0.40 thrombotic events per patient-year) was in the INR range

119 ues of 1.5 to 1.99 also had high rates (0.16 thrombotic events per patient-year).

120 Thrombotic events rates were not different between group

121 risk of subsequent deep venous and arterial thrombotic events remains unknown.

122 Treatments to prevent acute thrombotic events should focus on B2A-CIC-positive patie

123 agnosis, the incidence of major bleeding and thrombotic events was 2.5 and 18.7 per 1000 patient-year

124 Rates of major bleeding and coronary thrombotic events were no different and were associated

125 Rates of bleeding and thrombotic events were not significantly different accor

126 No serious adverse or thrombotic events were reported.

127 for patients who continue to display adverse thrombotic events with current antiplatelet therapies.

128 of how to provide optimal protection against thrombotic events without excessive increases in bleedin

129 of illness, circuitry components, bleeding, thrombotic events, and outcome were recorded.

130 any of the following diagnoses: ischemic and thrombotic events, endocrine events, sexual dysfunction,

131 At US of the 15 postoperative thrombotic events, the incidence of thrombosis was great

132 Seventeen patients (23 kidneys) experienced thrombotic events.

133 o patients who have or are at risk of having thrombotic events.

134 etabolic diseases and enhanced potential for thrombotic events.

135 presence of B2A-CIC is a predictor of acute thrombotic events.

136 s and an increased incidence of ischemic and thrombotic events.

137 eased hazard of bleeding but does not reduce thrombotic events.

138 mechanism by which hemolysis is connected to thrombotic events.

139 ver, rhC1INH therapy was not associated with thrombotic events.

140 y in LA-positive patients, mainly due to new thrombotic events.

141 gest an extended period of vulnerability for thrombotic events.

142 with broad potential for treatment of acute thrombotic events.

143 has been associated with occurrence of acute thrombotic events.

144 Hemolysis was predictive of subsequent thrombotic events.

145 Cirrhosis is associated with hemorrhagic and thrombotic extrahepatic complications.

146 dogenous polyP function in human blood under thrombotic flow conditions.

147 arget mRNAs important for the hemostatic and thrombotic function of platelets.

148 cally engineered mice affects hemostatic and thrombotic functions of platelets.

149 inflammatory genes and down-regulating anti-thrombotic genes.

150 s re-establishment following inflammatory or thrombotic insult.

151 927 INRs to determine INR-specific rates of thrombotic (ischemic stroke and suspected pump thrombosi

152 evention and treatment of cardiovascular and thrombotic issues associated with novel MM therapies hav

153 ad significant CAD, 35 (64%) of 55 had acute thrombotic lesions, and 46 (84%) of 55 had percutaneous

154 neutrophils were abundant in siRNA-triggered thrombotic lesions, antibody-mediated depletion of circu

155 enotype; mice were affected with more severe thrombotic lesions.

156 nt (LA)-positive individuals with or without thrombotic manifestations or pregnancy complications are

157 tic apposition of leaflets in 20 (77%) and a thrombotic mass on the leaflets in the remaining 6 (23%)

158 role in VT, likely via IL-6 and PMN-mediated thrombotic mechanisms, and may be a potential biomarker

159 ular focus will be made on the prototypes of thrombotic microangiopathic disorders, resulting from co

160 The thrombotic microangiopathies (TMAs) and C3 glomerulopath

161 ndrome during pregnancy, and implications of thrombotic microangiopathies for subsequent pregnancies

162 Novel aspects of the pathophysiology of the thrombotic microangiopathies will be discussed.

163 of necroinflammation to AKI is discussed in thrombotic microangiopathies, necrotizing and crescentic

164 the development of T3SS-dependent intestinal thrombotic microangiopathy (iTMA) and ischemic enteritis

165 Transplant-associated thrombotic microangiopathy (TA-TMA) is a common and poor

166 Transplant-associated thrombotic microangiopathy (TA-TMA) occurs frequently af

167 emonstration of impaired C regulation in the thrombotic microangiopathy (TMA) atypical hemolytic urem

168 ypical hemolytic uremic syndrome (aHUS) is a thrombotic microangiopathy (TMA) characterized by excess

169 ase reports have described the occurrence of thrombotic microangiopathy (TMA) following IV abuse of e

170 Thrombotic microangiopathy (TMA) is a life-threatening c

171 typical hemolytic uremic syndrome, a type of thrombotic microangiopathy (TMA) that causes renal failu

172 l hemolytic uremic syndrome (aHUS) develop a thrombotic microangiopathy (TMA) that in most cases is a

173 Complement activation has a major role in thrombotic microangiopathy (TMA), a disorder that can oc

174 Many patients with syndromes of thrombotic microangiopathy (TMA), including thrombotic t

175 s developed hemolytic uremic syndrome (HUS), thrombotic microangiopathy (TMA), or HUS-like events, ex

176 Many drugs have been reported to cause thrombotic microangiopathy (TMA), yet evidence supportin

177 horiocapillaris degeneration, and glomerular thrombotic microangiopathy (TMA).

178 tion after transplant, along with widespread thrombotic microangiopathy (TMA).

179 tion of innate immunity, as characterized by thrombotic microangiopathy (TMA).

180 a clinical picture consistent with an acute thrombotic microangiopathy (TMA).

181 -the PLASMIC score-to stratify patients with thrombotic microangiopathy according to their risk of ha

182 Thrombotic microangiopathy after allogeneic HSCT shares

183 icient animals developed severe C5-dependent thrombotic microangiopathy after induction of complement

184 mic medical centres in Boston, MA, USA, with thrombotic microangiopathy and a possible diagnosis of t

185 lytic uremic syndrome (aHUS), a rare form of thrombotic microangiopathy caused by complement pathogen

186 Hemolytic uremic syndrome (HUS) is a thrombotic microangiopathy characterized by intravascula

187 purpura (TTP) is a rare and life-threatening thrombotic microangiopathy characterized by microangiopa

188 tcomes in 14 women with aHUS from the Vienna Thrombotic Microangiopathy Cohort.

189 ring system also more consistently diagnosed thrombotic microangiopathy due to severe ADAMTS13 defici

190 AMR was associated with subclinical thrombotic microangiopathy in 2 patients.

191 nitoring of such pregnancies for episodes of thrombotic microangiopathy is essential but, the best st

192 ggest that in DGKE-associated aHUS patients, thrombotic microangiopathy results from impaired EC prol

193 Hemolytic-uremic syndrome (HUS) is a thrombotic microangiopathy that is characterized by micr

194 Endothelial dysfunction links thrombotic microangiopathy to steroid-refractory graft-v

195 atient demonstrated biological recurrence of thrombotic microangiopathy under treatment.

196 Thrombotic microangiopathy was an adverse event unique t

197 214 patients with thrombotic microangiopathy were included in the derivati

198 ypical hemolytic uremic syndrome (aHUS) is a thrombotic microangiopathy with severe renal injury seco

199 ation (atypical hemolytic uremic syndrome as thrombotic microangiopathy), biopsy appearance (dense de

200 In a mouse model of thrombotic microangiopathy, HDL also largely prevented t

201 elated complication, including preeclampsia, thrombotic microangiopathy, heart failure, sepsis, or po

202 lthough there was no evidence of spontaneous thrombotic microangiopathy, the hepatocyte-specific FH-d

203 Among the syndromes characterised by thrombotic microangiopathy, thrombotic thrombocytopenic

204 endothelial growth factor (VEGF) results in thrombotic microangiopathy, we addressed the possibility

205 ypertension, proteinuria, renal failure, and thrombotic microangiopathy.

206 luminal deposits, which are classic signs of thrombotic microangiopathy.

207 essing the diagnostic challenge presented by thrombotic microangiopathy.

208 ation of coagulation, potentially leading to thrombotic obstruction of small and midsize vessels, the

209 ng cause of synthetic graft failure includes thrombotic occlusion and intimal hyperplasia at the site

210 -catalyzed oxidative reaction for preventing thrombotic occlusion and neointimal formation of synthet

211 A thrombotic occlusion at the injection side was found, wh

212 In mice with thrombotic occlusion of the middle cerebral artery, tPA

213 However, thrombotic occlusion of the placental vascular bed is ra

214 allergy (p=0.36), pancreatitis (p=0.55), or thrombotic or bleeding complications (p=0.26).

215 ities (defined as allergy, pancreatitis, and thrombotic or bleeding complications).

216 linear correlation was found between ACT and thrombotic or bleeding events.

217 apy, published in any language and reporting thrombotic or hemorrhagic events.

218 No thrombotic or thromboembolic events, systemic allergic r

219 Hemorrhagic and thrombotic outcomes were retrieved </= 365 days after im

220 ding complications, without increasing major thrombotic outcomes, including stroke, myocardial infarc

221 ze, in this study, onset and severity of the thrombotic phenotype are dependent on the presence of pl

222 This thrombotic phenotype is fatal but can be fully rescued b

223 argeting Serpinc1 and Proc also results in a thrombotic phenotype, which is spontaneous (no additiona

224 If the thrombotic process can be controlled, these patients can

225 ny cardiovascular complications, including a thrombotic propensity.

226 Myxomavirus Serp-1 inhibits thrombolytic and thrombotic proteases, whereas mammalian neuroserpin (NSP

227 Addition of myosin to blood augmented the thrombotic responses of human blood flowing over collage

228 residual serum TXB2 associated with elevated thrombotic risk (<99.0% inhibition or TXB2 >3.1 ng/ml) w

229 Our data suggest the increased thrombotic risk associated with splenectomy, and patient

230 y threshold, but as there was no increase in thrombotic risk compared with standard-intensity warfari

231 Identification of hereditary thrombotic risk factors before transplantation may be a

232 therapy, adverse effect profile, and ongoing thrombotic risk factors.

233 the development of cardiovascular disease or thrombotic risk need to be further investigated.

234 sociated with both lower efficacy and higher thrombotic risk over time.

235 wledge about risk of bleeding and short-term thrombotic risk resides in many specialties, further com

236 In patients whose coronary thrombotic risk was defined by a prior MI rather than by

237 l practice, demonstrated large reductions in thrombotic risk when aspirin was compared with placebo,

238 ly elevated risk of thrombosis, although the thrombotic risk with IBD appears to wax and wane with di

239 ate and molecular mechanisms of clot growth, thrombotic risk, pharmacological response, and utility o

240 e available to improve management and reduce thrombotic risk.

241 ntly prolong prophylactic hemostasis without thrombotic risk.

242 P levels have been associated with increased thrombotic risk.

243 o account for confounders of transfusion and thrombotic risk.

244 d at least equal efficacy to VKA in managing thrombotic risks in the elderly, but bleeding patterns w

245 ell membranes could ameliorate microvascular thrombotic sequelae posttransplantation.

246 ell membranes could ameliorate microvascular thrombotic sequelae posttransplantation.

247 tly within grafts and decrease microvascular thrombotic sequelae, while avoiding systemic anticoagula

248 tly within grafts and decrease microvascular thrombotic sequelae, while avoiding systemic anticoagula

249 ulation occur with progression of ALI: a pro-thrombotic state progresses to hypocoagulability.

250 Experimental models of thrombotic stroke induced by either intra-arterial throm

251 ole of PKal on cerebral outcomes in a murine thrombotic stroke model treated with tPA.

252 in the percentage of patients with the post-thrombotic syndrome (47% in the pharmacomechanical-throm

253 primary outcome was development of the post-thrombotic syndrome between 6 and 24 months of follow-up

254 n did not result in a lower risk of the post-thrombotic syndrome but did result in a higher risk of m

255 s was not associated with prevention of post thrombotic syndrome compared with controls (OR 0.56 [95%

256 were not associated with prevention of post thrombotic syndrome despite trying to account for hetero

257 The post-thrombotic syndrome frequently develops in patients with

258 ings are effective in the prevention of post thrombotic syndrome in patients with deep vein thrombosi

259 tic compression stockings on preventing post thrombotic syndrome in patients with deep vein thrombosi

260 Moderate-to-severe post-thrombotic syndrome occurred in 18% of patients in the p

261 Severity scores for the post-thrombotic syndrome were lower in the pharmacomechanical

262 significantly reduce the development of post thrombotic syndrome, however the current body of evidenc

263 is with primary outcome as incidence of post thrombotic syndrome.

264 hypothesized to reduce the risk of the post-thrombotic syndrome.

265 Catastrophic thrombotic syndromes are characterized by rapid onset of

266 confirming this receptor as a promising anti-thrombotic target for myocardial infarction.

267 est that targeting this interaction has anti-thrombotic therapeutic potential with reduced bleeding r

268 By studying 20 patients with congenital thrombotic thrombocytopenic purpura (cTTP) who cannot cl

269 Acquired thrombotic thrombocytopenic purpura (TTP) and hemolytic

270 Immune-mediated thrombotic thrombocytopenic purpura (TTP) is a life-thre

271 Acquired thrombotic thrombocytopenic purpura (TTP) is a life-thre

272 Thrombotic thrombocytopenic purpura (TTP) is a microangi

273 Thrombotic thrombocytopenic purpura (TTP) is a rare and

274 Acquired thrombotic thrombocytopenic purpura (TTP) is caused by a

275 Acquired thrombotic thrombocytopenic purpura (TTP) is characteriz

276 ascular thrombosis in patients with acquired thrombotic thrombocytopenic purpura (TTP).

277 ivity leads to a potentially fatal syndrome, thrombotic thrombocytopenic purpura (TTP).

278 13 (ADAMTS13) revolutionized our approach to thrombotic thrombocytopenic purpura (TTP).

279 thrombotic microangiopathy (TMA), including thrombotic thrombocytopenic purpura and hemolytic-uremic

280 I in microvascular occlusion associated with thrombotic thrombocytopenic purpura and sepsis was revea

281 microangiopathy and a possible diagnosis of thrombotic thrombocytopenic purpura between Jan 8, 2004,

282 Patients suffering from acquired thrombotic thrombocytopenic purpura develop autoantibodi

283 characterised by thrombotic microangiopathy, thrombotic thrombocytopenic purpura is distinguished by

284 such as atypical hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, C3GN, and dense dep

285 13 to make management decisions in suspected thrombotic thrombocytopenic purpura, new evidence suppor

286 erturbation associated with diseases such as thrombotic thrombocytopenic purpura, sepsis, and diabete

287 mage: atypical hemolytic uremic syndrome and thrombotic thrombocytopenic purpura.

288 to distinguish aHUS from other TMAs, such as thrombotic thrombocytopenic purpura; however, novel bioa

289 , grade 3 nausea, grade 3 infection, grade 3 thrombotic thrombocytopenic purpurea, grade 2 nausea, gr

290 Thrombotic/thromboembolic events (TEE) have been reporte

291 ses and a long-term follow-up, especially on thrombotic total occlusion of main portal vein (MPV).

292 ients diagnosed with liver cirrhosis related thrombotic total occlusion of MPV and treated with TIPS

293 l outcome of TIPS on liver cirrhosis-related thrombotic total occlusion of MPV, 98 patients diagnosed

294 ffective in treating liver cirrhosis-related thrombotic total occlusion of MPV.

295 sions were 5.8% versus 11.4% (P < .001), and thrombotic vascular events were 2.8% versus 1.4% (P = .0

296 overall response rate, RBC transfusions, and thrombotic vascular events.

297 ear rates were significantly diminished, and thrombotic vascular occlusion in vivo was significantly

298 crease in exposure on the ln-scale) of fetal thrombotic vasculopathy (FTV) both with increasing PM2.5

299 Mapping inflammatory conditions in the thrombotic vein, we identify a set of deep vein thrombos

300 This is the first report of an acute thrombotic vessel occlusion leading to a compartment syn