ライフサイエンスコーパス: thrombolytic

1 use of the limited effectiveness of existing thrombolytics.

2 ing vessel recanalization with intraarterial thrombolytics.

3 tracerebral haemorrhage after treatment with thrombolytics (2 [7%] telemedicine vs 2 [8%] telephone,

4 from baseline to the fifth year: intravenous thrombolytics (42.09% versus 72.84%), early antithrombot

5 the systemic circulation but regenerate its thrombolytic action upon contact with thrombin present o

6 Our objective was to assess endogenous thrombolytic activity in acute coronary syndrome (ACS) p

7 These data show for the first time a potent thrombolytic activity of ADAMTS13 in the setting of stro

8 hen evaluated in a rat thrombosis model, the thrombolytic activity of camouflaged tPA was similar to

9 ether ultrasonography can safely enhance the thrombolytic activity of t-PA.

10 ntration-dependent fashion the catalytic and thrombolytic activity of tissue plasminogen activator in

11 reactivity, allows assessment of endogenous thrombolytic activity to identify ACS patients who remai

12 besides the unquestionable benefit from its thrombolytic activity, tPA also has a deleterious effect

13 y patients at risk for thrombosis and inform thrombolytic administration for treating acute thrombosi

14 ystolic flow reversal (pulsatile flow) after thrombolytic administration on coronary angiography is a

15 would be related to long-term outcomes after thrombolytic administration.

16 ctive treatment option in conjunction with a thrombolytic agent for stroke patients.

17 uture directions for a safer use of tPA as a thrombolytic agent in the setting of acute ischemic stro

18 The effect of a thrombolytic agent on biochemical bond degradation was m

19 VWF) that blocks VWF binding to GPIb, of the thrombolytic agent recombinant tissue plasminogen activa

20 Finally, we show that the thrombolytic agent streptokinase has therapeutic value f

21 f important virulence factors, including the thrombolytic agent streptokinase, the protease inhibitor

22 ich regulates the expression of pili and the thrombolytic agent streptokinase.

23 urokinase-type plasminogen activator or the thrombolytic agent streptokinase.

24 lacing of the thrombus with a fibrin-binding thrombolytic agent such as alteplase is an alternative t

25 oup analyses to assess the effect of type of thrombolytic agent used and the strategy of emergent hos

26 up, and were independent of both the type of thrombolytic agent used, and whether or not the patient

27 minogen activator (TPA) with a direct-acting thrombolytic agent, plasmin, in an animal model of fibri

28 sue plasminogen activator, is an alternative thrombolytic agent.

29 ffinity obviates continuous infusion of this thrombolytic agent.

30 therapy and it is also used clinically as a thrombolytic agent.

31 , including intra-arterial administration of thrombolytic agents and mechanical interventions, show p

32 outcomes of patients with OTPHV treated with thrombolytic agents and with surgery since 1996.

33 TAFIa could enhance the efficacy of existing thrombolytic agents for the treatment of acute myocardia

34 All thrombolytic agents in current clinical usage are plasmi

35 as well as local intra-arterial delivery of thrombolytic agents in patients with acute stroke, are t

36 py may be a non-invasive safe alternative to thrombolytic agents in treating thrombotic CVC occlusion

37 Newer thrombolytic agents may have advantages, but are less we

38 Our findings indicate that thrombolytic agents may have therapeutic value in the tr

39 New devices, new thrombolytic agents, and new antithrombotic agents are c

40 learest indication for the administration of thrombolytic agents, but patients with acute pulmonary e

41 swered questions remain regarding the use of thrombolytic agents.

42 inogen activator are the currently available thrombolytic agents.

43 nimizes the duration of systemic exposure to thrombolytic agents.

44 tra-arterial thrombolysis, and trials of new thrombolytic agents.

45 tion, and the concomitant use of intravenous thrombolytics, among others.

46 a, a condition shown by itself to reduce the thrombolytic and proteolytic properties of tissue plasmi

47 Myxomavirus Serp-1 inhibits thrombolytic and thrombotic proteases, whereas mammalian

48 ilities, patients who received intracoronary thrombolytics, and those who received no medications wit

49 therefore also help in designing new, safer thrombolytic approaches.

50 ral arterial access site, >6-Fr sheath size, thrombolytics, arterial dissection, fluoroscopy time >30

51 lready arrested, the difficulty of obtaining thrombolytics at the bedside rapidly enough to administe

52 Furthermore, facilitated interventions with thrombolytic-based regimens should be avoided.

53 elevation myocardial infarction who receive thrombolytics, clopidogrel therapy confers broad benefit

54 bition in myocardial infarction treated with thromboLYtics (COMPLY) and COMplement inhibition in Myoc

55 ment elevation were eligible for IMR but had thrombolytic contraindications after excluding patients

56 inutes, from emergency department arrival to thrombolytic delivery.

57 as shortening ischemic times with the use of thrombolytic donor flush, may prevent IC after DCD LT.

58 Plasmin at 4-fold, 6-fold, and 8-fold the thrombolytic dose (1 mg/kg) induced a dose-dependent eff

59 a dose-dependent manner, even at 25% of the thrombolytic dose (1 mg/kg), manifest as rebleeding from

60 Bleeding occurred only at 8-fold the thrombolytic dose, on complete depletion of fibrinogen a

61 inogen activator (t-PA) is the only approved thrombolytic drug for ischemic stroke.

62 The newer thrombolytic drug tenecteplase has been investigated in

63 clots using a significantly lower amount of thrombolytic drug than is required when administered in

64 er, whether or not helium interacts with the thrombolytic drug tissue plasminogen activator, the only

65 ed alternative anticoagulants (11 patients), thrombolytic drugs (3 patients), inferior vena cava filt

66 The administration of thrombolytic drugs outside hospital by emergency physici

67 formed with a variety of neuroprotective and thrombolytic drugs provide many lessons that will help t

68 selection are investigating alteplase, other thrombolytic drugs, and novel endovascular devices, for

69 Despite the common use of thrombolytic drugs, especially in stroke treatment, ther

70 ally improve both the efficacy and safety of thrombolytic drugs, particularly in patients who are at

71 nt mass loss/min in vitro without any use of thrombolytic drugs.

72 ate and thus minimizing the required dose of thrombolytic drugs.

73 d diagnosis of pulmonary embolism and use of thrombolytics during cardiopulmonary resuscitation may n

74 the lack of good data supporting the use of thrombolytics during resuscitation, the belief that thro

75 We hypothesized that ADAMTS13 can exert a thrombolytic effect in VWF-containing thrombi in the set

76 After stroke, the thrombolytic effect of tissue-type plasminogen activator

77 oelastography and was able to potentiate the thrombolytic effect of tPA in vivo in a murine model.

78 d widening of the therapeutic window for the thrombolytic effect of tPA.

79 erformed to study the molecular bases of NAC thrombolytic effect, including platelet aggregometry, pl

80 nce that the molecular target underlying the thrombolytic effects of NAC is principally the VWF that

81 Although thrombolytic effects of tissue plasminogen activator (tP

82 ic stroke outcome, suggesting that it exerts thrombolytic effects without significantly impairing nor

83 ic GpIIb/IIIa inhibitor further improved its thrombolytic efficacy, essentially by accelerating throm

84 developed systems, and (iv) testing of their thrombolytic efficacy.

85 Thrombolytics (eg, tissue-type plasminogen activator [tP

86 rials, which together randomly assigned 7739 thrombolytic-eligible patients with ST-segment elevation

87 in blood, where its primary function is as a thrombolytic enzyme, and in the central nervous system w

88 Plasmin, the pivotal thrombolytic enzyme, is generated on the surface of many

89 n of plasminogen, the zymogen of the primary thrombolytic enzyme, plasmin, is markedly promoted when

90 sue-type plasminogen activator (tPA) is as a thrombolytic enzyme.

91 r inhibitor-1 (PAI-1) are causal factors for thrombolytic failure.

92 ient warm ischemia time (WIT) and the use of thrombolytic flush at the time of procurement to minimiz

93 Prophylaxis with thrombolytic flushes might prevent CVC infections and ca

94 To increase the effective use of thrombolytics for acute stroke, the expertise of vascula

95 the fulfillment of the dual, hemostatic and thrombolytic, functions of thrombin.

96 ng stroke recovery long after the window for thrombolytics has passed.

97 Clinically approved thrombolytics have significant drawbacks, including blee

98 m outcomes prediction on original Killip and thrombolytic in myocardial infarction scores.

99 rdiopulmonary arrest and discuss the role of thrombolytics in cardiopulmonary resuscitation.

100 ted heparin was administered in 33 (87%) and thrombolytics in four (11%).

101 hermore, combination treatment compared with thrombolytic monotherapy increased cerebral blood flow a

102 , the practicality of using alteplase as the thrombolytic of choice for this indication remained conj

103 assess their suitability for treatment with thrombolytics, on the basis of standard criteria.

104 enzyme elevation, some argue for the use of thrombolytics or catheter thrombectomy even for hemodyna

105 .7, 95% CI 1.3 to 5.5; p = 0.0092) with more thrombolytic (OR 4.7, 95% CI 2.3 to 9.7; p < 0.0001) and

106 as mammalian neuroserpin (NSP) inhibits only thrombolytic proteases.

107 diated sonothrombolysis device for improving thrombolytic rate and thus minimizing the required dose

108 Nine children who underwent the thrombolytic regimen and 13 who received standard antico

109 analyze our institutional experience with a thrombolytic regimen versus standard anticoagulation for

110 The thrombolytic regimen was associated with a markedly decr

111 UFH as adjunctive therapy in fibrin-specific thrombolytic regimens and improve coronary reperfusion r

112 ase is an alternative to continuous-infusion thrombolytic regimens and minimizes the duration of syst

113 sed the importance of presenting the risk of thrombolytic-related intracranial hemorrhage.

114 vere cerebral WMLs were associated with post-thrombolytic rPH but not with iPH within the ischemic ar

115 gment elevation AMI and contraindications to thrombolytics should be strongly considered.

116 ntial solution of this problem by developing thrombolytic sol-gel coatings which potentially could le

117 Assessment of endogenous thrombolytic status based on the lysis of platelet-rich

118 rombosis test (GTT) to assess thrombotic and thrombolytic status in 300 ACS patients receiving dual-a

119 Recent thrombolytic studies have suggested that simple measures

120 ed is an effective therapy with an excellent thrombolytic success rate for the treatment of prostheti

121 able by contact pathway inhibition, although thrombolytic susceptibility may benefit from polyP antag

122 rfusion induced by the administration of the thrombolytic Tenecteplase (TNK, 1.5 mg/kg, IV bolus) in

123 Thrombolytic therapies were permitted.

124 t from anticoagulation, and less frequently, thrombolytic therapies.

125 However, this model is not amenable to thrombolytic therapies.

126 nalyzed for standard ST-segment criteria for thrombolytic therapy (>1 mm in two or more contiguous le

127 sease (1.33); treatment approaches including thrombolytic therapy (1.39) and non-stent devices (1.64)

128 th HF, P<0.0001), and more likely to receive thrombolytic therapy (14% versus 11%; P=0.0001).

129 -3.6% to -1.4%; P < .001) and greater use of thrombolytic therapy (4.8% vs 1.7%; adjusted difference,

130 Most patients who received thrombolytic therapy (76%, n=2939) received a fibrin-spe

131 nt elevation AMI to primary PTCA (n=3872) or thrombolytic therapy (n=3867).

132 erfusion therapy, mainly owing to "patented" thrombolytic therapy (odds ratio 1.15; p = 0.016).

133 that have impeded the more widespread use of thrombolytic therapy (tPA, tissue plasminogen activator)

134 t the bleeding complications associated with thrombolytic therapy after ischemic stroke might be coun

135 ies comprising 756 patients who had received thrombolytic therapy and 13 studies comprising 662 patie

136 With the advent of thrombolytic therapy and angioplasty, it has become poss

137 I, resulting in failure to meet criteria for thrombolytic therapy and as a consequence leading to ina

138 It is widely used as a fibrinolytic agent in thrombolytic therapy and it is also used clinically as a

139 The equivalency of thrombolytic therapy and surgery for the treatment of su

140 y group did not meet ST-segment criteria for thrombolytic therapy as compared with the control group

141 ly reperfusion has led to the development of thrombolytic therapy as the cornerstone of current manag

142 Primary PTCA was better than thrombolytic therapy at reducing overall short-term deat

143 rials is greatly needed to establish whether thrombolytic therapy can be considered standard of care

144 there is a low haemorrhagic threshold after thrombolytic therapy compared with that in wild-type mic

145 ry PTCA remained better than those seen with thrombolytic therapy during long-term follow-up, and wer

146 a patient who was successfully treated with thrombolytic therapy during pulmonary embolism-induced c

147 ity of Food and Drug Administration-approved thrombolytic therapy for acute ischemic stroke since 199

148 ave been introduced are discussed, including thrombolytic therapy for acute ischemic stroke, induced

149 erfusion success and clinical outcomes after thrombolytic therapy for acute myocardial infarction (AM

150 tracerebral haemorrhage is a complication of thrombolytic therapy for acute myocardial infarction, pu

151 ransluminal coronary angioplasty (PTCA) with thrombolytic therapy for acute ST-segment elevation myoc

152 th a poor prognosis in patients treated with thrombolytic therapy for AMI.

153 w is to provide an update on the progress of thrombolytic therapy for CRAO.

154 size and improve mortality in the setting of thrombolytic therapy for ST-elevation myocardial infarct

155 and safety and increase the time window for thrombolytic therapy for stroke with full- and half-dose

156 resent findings suggest that APC may improve thrombolytic therapy for stroke, in part, by reducing tP

157 unable to apply stockings, or they received thrombolytic therapy for the initial treatment of acute

158 Primary PTCA is more effective than thrombolytic therapy for the treatment of ST-segment ele

159 percutaneous coronary intervention (PCI) and thrombolytic therapy for treatment of acute myocardial i

160 These data suggest that thrombolytic therapy for treatment of CNS ischemic disor

161 Recently, thrombolytic therapy has been suggested as a viable ther

162 Thrombolytic therapy has rarely been used in these patie

163 Thrombolytic therapy has yet to be validated as an effec

164 tly increasing the time window for effective thrombolytic therapy in acute ischemic stroke.

165 review is to offer an overview of the use of thrombolytic therapy in acute pulmonary embolism.

166 Registry, we examined the outcomes of use of thrombolytic therapy in patients with ischemic stroke wh

167 The use of thrombolytic therapy in pediatrics has increased over th

168 inical trials suggests a survival benefit of thrombolytic therapy in the elderly with STEMI, whereas

169 quate statistical power to determine whether thrombolytic therapy is associated with improved surviva

170 lytics during resuscitation, the belief that thrombolytic therapy is ineffective once a patient has a

171 However, administration of conventional thrombolytic therapy is limited by a low efficacy of pre

172 When this occurs, thrombolytic therapy is not routinely administered.

173 Current treatment of ischaemic stroke with thrombolytic therapy is restricted to 3-4.5 h after symp

174 Thrombolytic therapy is the cornerstone of treatment of

175 Case reports and case series suggest that thrombolytic therapy may be associated with lower risks

176 Thrombolytic therapy may be beneficial in the treatment

177 en for CRAO, emerging evidence suggests that thrombolytic therapy may be effective if administered pr

178 Intracoronary infusion of fibrin-specific thrombolytic therapy may provide a valuable and safe opt

179 Thrombolytic therapy may reduce the frequency of high in

180 the latest prospective study has shown that thrombolytic therapy not only has no beneficial effect b

181 Thrombolytic therapy of PVT has an unpredictable risk of

182 components of thrombotic development and of thrombolytic therapy of rtPA observed from human ischemi

183 re hemodynamically stable and do not require thrombolytic therapy or other interventions.

184 rin, beta-blockers, and reperfusion therapy (thrombolytic therapy or percutaneous coronary interventi

185 our of initial ECG, and overall reperfusion (thrombolytic therapy or PTCA).

186 morbidity and mortality, and the efficacy of thrombolytic therapy propelled the development and matur

187 best subsequent management of patients after thrombolytic therapy remains unclear.

188 Thrombolytic therapy results in the accelerated lysis of

189 Thrombolytic therapy sessions were performed under trans

190 Thrombolytic therapy should be considered first-line the

191 Thrombolytic therapy use increased from 0.7% to 1.0% (p

192 Thrombolytic therapy using tissue plasminogen activator

193 es were randomized clinical trials comparing thrombolytic therapy vs anticoagulant therapy in pulmona

194 echocardiogram suggesting pulmonary embolus, thrombolytic therapy was administered during cardiopulmo

195 y stable with right ventricular dysfunction, thrombolytic therapy was associated with lower rates of

196 ystolic BP <100 mm Hg) who were eligible for thrombolytic therapy were randomized to either transfer

197 of ST-segment elevation and the frequency of thrombolytic therapy were significantly lower in the sul

198 Thrombolytic therapy with rtPA increases the risk of hem

199 mboembolism at baseline conditions and after thrombolytic therapy with streptokinase or alteplase.

200 on is, however, essential to improve current thrombolytic therapy with tissue plasminogen activator (

201 controls and 53.3% of TPI patients received thrombolytic therapy within 1 hour (P > 0.2), and 67.6%

202 of patients receiving thrombolytic therapy, thrombolytic therapy within 1 hour of initial ECG, and o

203 rapy, 41.1% versus 53.6% (P = 0.04) received thrombolytic therapy within 1 hour, and 50.7% versus 66.

204 rapy, 40.5% versus 48.4% (P = 0.10) received thrombolytic therapy within 1 hour, and 55.7% versus 65.

205 erapy, 51.4% versus 45.3% (P > 0.2) received thrombolytic therapy within 1 hour, and 67.6% versus 63.

206 rapy, 53.2% versus 58.6% (P = 0.08) received thrombolytic therapy within 1 hour, and 67.7% versus 74.

207 ncreased use of thrombolytic therapy, use of thrombolytic therapy within 1 hour, and use of overall c

208 roup, 48.1% versus 58.2% (P = 0.03) received thrombolytic therapy, 40.5% versus 48.4% (P = 0.10) rece

209 roup, 47.3% versus 63.2% (P = 0.01) received thrombolytic therapy, 41.1% versus 53.6% (P = 0.04) rece

210 group, 59.5% versus 53.9% (P > 0.2) received thrombolytic therapy, 51.4% versus 45.3% (P > 0.2) recei

211 and 62.1% of TPI patients (P = 0.2) received thrombolytic therapy, 52.5% of controls and 53.3% of TPI

212 roup, 61.1% versus 67.6% (P = 0.03) received thrombolytic therapy, 53.2% versus 58.6% (P = 0.08) rece

213 d, including vascular pathologies, diabetes, thrombolytic therapy, and dysfibrinogenemia.

214 ss likely to receive aspirin, beta-blockers, thrombolytic therapy, angiography, and angioplasty durin

215 d discusses the current agents available for thrombolytic therapy, as well as indications for their u

216 there was no systematic worsening of time to thrombolytic therapy, balloon inflation, medication use

217 to reduce the complications associated with thrombolytic therapy, broaden the therapeutic window, an

218 as early enough to make it relevant to acute thrombolytic therapy, early BBB disruption as defined by

219 al data regarding the safety and efficacy of thrombolytic therapy, inferior vena cava filters, and em

220 Despite the benefit of thrombolytic therapy, on the basis of the results of cas

221 shed studies evaluating the effectiveness of thrombolytic therapy, primary percutaneous coronary inte

222 As compared with thrombolytic therapy, primary percutaneous transluminal

223 Patients with cardiac arrest, thrombolytic therapy, prior revascularization, or missin

224 4.0% for stroke (P =.28) for primary PCI vs thrombolytic therapy, respectively.

225 includes aggressive wound care, debridement, thrombolytic therapy, restoration of tissue oxygenation,

226 t elevation myocardial infarction undergoing thrombolytic therapy, the degree of ST-segment resolutio

227 tion of patients most likely to benefit from thrombolytic therapy, the eligibility criteria were a pe

228 Percentages of patients receiving thrombolytic therapy, thrombolytic therapy within 1 hour

229 enefits of primary angioplasty compared with thrombolytic therapy, transfer to an institution with an

230 Compared with thrombolytic therapy, treatment of patients with primary

231 The TPI increased use of thrombolytic therapy, use of thrombolytic therapy within

232 re 2 reperfusion strategies, primary PCI and thrombolytic therapy, which are both supported by clinic

233 ep venous system in 16 patients (80%) during thrombolytic therapy, with complete resolution of sympto

234 es resulted in complete thrombus lysis after thrombolytic therapy.

235 ours of stroke onset prior to treatment with thrombolytic therapy.

236 Only a minority of stroke patients receive thrombolytic therapy.

237 hway may have beneficial consequences during thrombolytic therapy.

238 tly lower mortality and more frequent use of thrombolytic therapy.

239 mbosis and have significant implications for thrombolytic therapy.

240 ulmonary embolism or serious bleeding during thrombolytic therapy.

241 ce of asymptomatic pulmonary embolism during thrombolytic therapy.

242 ential to optimize management and triage for thrombolytic therapy.

243 ass grafting (CABG) is frequently used after thrombolytic therapy.

244 ical stroke and to extend the time window of thrombolytic therapy.

245 ome, other than an increased use of patented thrombolytic therapy.

246 tion MI treated with primary PCI rather than thrombolytic therapy.

247 nary artery bypass graft (CABG) surgery, and thrombolytic therapy.

248 vor with a PE index higher than 60% received thrombolytic therapy.

249 usion with percutaneous coronary stenting or thrombolytic therapy.

250 arly marker of long-term clinical benefit of thrombolytic therapy.

251 yme have potential use in antithrombotic and thrombolytic therapy.

252 ment elevation who have contraindications to thrombolytic therapy.

253 ul as a marker of microvascular injury after thrombolytic therapy.

254 better outcomes with primary PTCA than with thrombolytic therapy.

255 ed cerebral artery than systemic intravenous thrombolytic therapy.

256 rculating leukocytes prior to treatment with thrombolytic therapy.

257 who are ineligible for standard intravenous thrombolytic therapy; however, its use is limited by the

258 the facilitated approach were mainly seen in thrombolytic-therapy-based regimens.

259 stroke and total stroke rates were higher in thrombolytic-therapy-containing facilitated regimens tha

260 ular and molecular level, only one drug, the thrombolytic tissue plasminogen activator (rt-PA), is ap

261 Thrombolytic tissue plasminogen activator may be a usefu

262 In combination studies with the thrombolytic, tissue plasminogen activator (tPA) using a

263 The addition of thrombolytic to extracorporeal cardiopulmonary resuscita

264 tions associated with late administration of thrombolytic tPA.

265 lar hemorrhage volume (p=.001), but not with thrombolytic treatment (p=.05) or intracerebral hemorrha

266 wever, sex disparities persist in the use of thrombolytic treatment (with alteplase) and lipid testin

267 t included patients who received intravenous thrombolytic treatment after perfusion CT were identifie

268 Thrombolytic treatment did not affect long-term mortalit

269 therefore, encourage clinicians to: consider thrombolytic treatment for a wider variety of patients (

270 apy strategies has reset a course to advance thrombolytic treatment for acute stroke and promises to

271 herapy to improve the efficacy and safety of thrombolytic treatment for ischaemic stroke.

272 e likelihood of severe disability/death with thrombolytic treatment for SPAN-100-positive (AOR, 0.46

273 orts to accelerate hospital presentation and thrombolytic treatment in patients with stroke.

274 las who were referred for pharmacomechanical thrombolytic treatment in the intervention unit of the R

275 ted with perfusion CT to receive intravenous thrombolytic treatment more than 3 hours after symptom o

276 Thrombolytic treatment of ischemic stroke with tissue pl

277 The long-term effect of thrombolytic treatment of pulmonary embolism (PE) is unk

278 with intermediate-risk PE and the effect of thrombolytic treatment on the persistence of symptoms or

279 y representing US clinical practice, earlier thrombolytic treatment was associated with reduced morta

280 ome measure was whether the decision to give thrombolytic treatment was correct, as determined by cen

281 Thrombolytic treatment with Plg activators significantly

282 Delayed thrombolytic treatment with recombinant tissue plasminog

283 of the diabody was compared to the standard thrombolytic treatment with recombinant tissue-type plas

284 s thrombotic occlusions usually resolve with thrombolytic treatment, such as alteplase.

285 atory T cell adoptive transfer may alleviate thrombolytic treatment-induced haemorrhage in stroke vic

286 w findings have significant implications for thrombolytic treatment.

287 sured the incidence of ICH following REP and thrombolytic treatment.

288 vant treatment for stroke patients receiving thrombolytic treatment.

289 ents, and (3) delay in obtaining consent for thrombolytic treatment.

290 Effectiveness of longer duration US and MB thrombolytic treatments were studied (n = 4), which sugg

291 Mild strokes have been poorly represented in thrombolytic trials and only a few series have reported

292 Secondary outcomes were the rate of thrombolytic use, 90-day functional outcomes (Barthel in

293 Use of thrombolytics was associated with lower all-cause mortal

294 Intravenous thrombolytics were used at an overall rate of 25% (31 [2

295 Thrombolytics were used at presentation in 19 (35%) pati

296 imaging and new clinical trials that combine thrombolytics with other pharmacological and interventio

297 Activation of the thrombolytic zymogens may therefore allow for both direc

298 Additionally, the thrombolytic zymogens plasminogen, urokinase, and plasma

299 Matriptase was also found to activate thrombolytic zymogens that have been shown to cleave and

300 e examined for their ability to activate the thrombolytic zymogens, and both resulted in activation o