ライフサイエンスコーパス: fibrinolytic

1 duced mortality when compared with full-dose fibrinolytics.

2 ct of insulin in STEMI patients treated with fibrinolytics.

3 cision on whether to administer intrapleural fibrinolytics.

4 f homocysteine (Hcy), is able to prevent the fibrinolytic abnormalities present in this leukemia.(1)

5 lasminogen activator inhibitor 1 (PAI-1) and fibrinolytic activities are influenced by 1) dietary fat

6 in their tissues due to reduced perivascular fibrinolytic activity and angiogenesis was impaired.

7 intracranial bleeding are separable from its fibrinolytic activity and can be neutralized.

8 cretions of these frogs show proteolytic and fibrinolytic activity and have hyaluronidase, which is n

9 The fibrinolytic activity and protein levels of tetranectin,

10 e encapsulated tPA retained 97.4 +/- 1.7% of fibrinolytic activity as compared with that of native tP

11 in(ogen) from diabetic subjects had impaired fibrinolytic activity compared with controls (723 +/- 16

12 on and reveal that impaired endothelial cell fibrinolytic activity constitutes a barrier to effective

13 ound that it exhibited good correlation with fibrinolytic activity in human donors and with thrombin

14 Fibrinolytic activity in peritoneal fluid was assayed by

15 es peritoneal adhesion formation by limiting fibrinolytic activity in the postoperative peritoneum, t

16 Decreased fibrinolytic activity is associated with an increased ri

17 Fibrinolytic activity is not lower after meals rich in p

18 hat regulation of tPA-dependent cell surface fibrinolytic activity is precisely tuned to the intracel

19 nolytic enzymes, and suggest that changes in fibrinolytic activity may influence cross-linking of blo

20 nterference effectively blocked the enhanced fibrinolytic activity observed after induction of the PM

21 rom the diabetic environment that alters the fibrinolytic activity of AdMSCs, thereby increasing the

22 ator inhibitor type 1 ratio tests, to assess fibrinolytic activity of cells before implantation.

23 The inhibition of the fibrinolytic activity of plasmin was nearly as effective

24 f A2 and two copies of S100A10/p11, promotes fibrinolytic activity on the surface of vascular endothe

25 through cross-linking of proteins with anti-fibrinolytic activity to fibrin.

26 ffect of NK-1RA administration on peritoneal fibrinolytic activity was investigated to determine a po

27 espite evidence linking impaired spontaneous fibrinolytic activity with acute coronary events.

28 ow increases in liver Plat, circulating tPA, fibrinolytic activity, bleeding time, and time to thromb

29 crease endothelial nitric oxide synthase and fibrinolytic activity, decrease leukocyte adhesion and t

30 lled trial was used to compare the effect on fibrinolytic activity, measured as dilute clot lysis tim

31 ly, by binding to plasmin and inhibiting its fibrinolytic activity, or indirectly, by cross-reacting

32 IP-133 and aPA was confirmed by SDS-PAGE and fibrinolytic activity, respectively.

33 oxic effects of tPA without compromising its fibrinolytic activity, through the use of selective anta

34 en activator inhibitor 1, both regulators of fibrinolytic activity, was assessed in peritoneal tissue

35 oss of S100A10 is concomitant with a loss in fibrinolytic activity.

36 00A10 and also caused a dramatic increase in fibrinolytic activity.

37 ules/cell at saturation), endowing them with fibrinolytic activity.

38 ent mechanism may prevail in the presence of fibrinolytic activity.

39 nt of epicardial flow both immediately after fibrinolytic administration and after rescue/adjunctive

40 dial perfusion on angiography 3.5 days after fibrinolytic administration for STEMI is associated with

41 rwent angiography a median of 3.5 days after fibrinolytic administration for STEMI; TMPG was assessed

42 Angiography was performed 60 min after fibrinolytic administration in 3,845 Thrombolysis In Myo

43 <20%) following rescue/adjunctive PCI after fibrinolytic administration in six STEMI trials.

44 aneous coronary intervention (PCI) following fibrinolytic administration in ST-segment elevation myoc

45 t-dye motion during systole) at 60 min after fibrinolytic administration was present in 11.0% of pati

46 hrombolysis and the potential novel use as a fibrinolytic agent for thromboprophylaxis without bleedi

47 e catalytic activation of plasmin, the major fibrinolytic agent in mammals.

48 It is widely used as a fibrinolytic agent in thrombolytic therapy and it is als

49 arin and was significantly attenuated by the fibrinolytic agent streptokinase.

50 Patients received a fibrinolytic agent, aspirin, and when appropriate, hepar

51 An aerosolized fibrinolytic agent, tissue-type plasminogen activator, s

52 mation, and another 3 of these 20 received a fibrinolytic agent.

53 y randomised controlled trials that compared fibrinolytic agents as a reperfusion therapy in adult pa

54 Treatment with fibrinolytic agents has shown promise but remains of unp

55 Paradoxically, fibrinolytic agents may systemically activate platelets,

56 The use of fibrinolytic agents to prevent new thrombus formation is

57 nctive antithrombotic therapy, against other fibrinolytic agents, a placebo, or no treatment.

58 eads to faster artery-opening treatment with fibrinolytic agents, either in the pre-hospital setting

59 pidogrel and LMWH, in addition to a standard fibrinolytic and aspirin, had a particularly high rate o

60 Several studies have shown that fibrinolytic and coagulation abnormalities as well as lo

61 er) was calculated for patients treated with fibrinolytic and conservative therapies and those who re

62 demia, dysglycemia, endothelial dysfunction, fibrinolytic and inflammatory abnormalities, left ventri

63 on inhibition influences heat stroke-induced fibrinolytic and inflammatory responses.

64 Combination therapy with reduced-dose fibrinolytics and glycoprotein IIb/IIIa inhibitors for S

65 erfusion and contraindications to the use of fibrinolytics and/or mechanical reperfusion methods acco

66 ned a panel of proteases in the coagulation, fibrinolytic, and inflammatory cascades to identify thos

67 Attenuated androgens, anti-fibrinolytics, and C1 inhibitor concentrates are used fo

68 regulation of natural procoagulants and anti-fibrinolytics, and down-regulation of natural anti-coagu

69 trial data suggest that the combination of a fibrinolytic, aspirin, clopidogrel, and ENOX offers an a

70 er, these data support the importance of the fibrinolytic axis in regulating renal fibrosis and point

71 repeated episodes of clamped hypoglycemia on fibrinolytic balance, proinflammatory biomarkers, proath

72 summary, acute moderate hypoglycemia impairs fibrinolytic balance; increases proinflammatory response

73 coronary intervention are expected, a modern fibrinolytic-based pharmacoinvasive strategy may need to

74 Crude 5-year survival was 88% for the fibrinolytic-based strategy, 83% for pPCI, and 59% for n

75 nstrated by screening plasmin inhibitors and fibrinolytic bioactives from mixtures of standards and s

76 o generate plasmin, which further diminishes fibrinolytic capacity in active MS lesions and possibly

77 e response by enhancing the acute endogenous fibrinolytic capacity in healthy men.

78 myocardial ischemia and inhibits endogenous fibrinolytic capacity in men with stable coronary heart

79 cute systemic inflammation on the endogenous fibrinolytic capacity in men.

80 This was associated with a rise in fibrinolytic capacity, asymptomatic myocardial ischemia,

81 e, whereas the S100A10 subunit initiates the fibrinolytic cascade by colocalizing with the urokinase

82 tor inhibitor 1 (PAI-1), a key enzyme in the fibrinolytic cascade, was assessed and related to the ex

83 ctor XIIa and plasmin of the coagulation and fibrinolytic cascades, elastase and cathepsin G released

84 he control of inflammatory, coagulation, and fibrinolytic cascades.

85 Fibrinolytic components, d-dimer, and plasminogen activa

86 Fibrinolytic cotherapy is therefore a rapidly translatab

87 or-1 (PAI-1) is largely responsible for this fibrinolytic defect.

88 ance of plasma clots that displayed impaired fibrinolytic degradation (+25% prolonged clot lysis time

89 blood coagulation regulator thrombomodulin, fibrinolytic degradation products (FDP) of fibrin induce

90 Admission fibrinolytic derangement is common in injured children a

91 ing clot formation, as well as the design of fibrinolytic drug delivery strategies.

92 We developed a novel targeted fibrinolytic drug that is directed against activated pla

93 ew of randomised controlled trials comparing fibrinolytic drugs in patients with STEMI.

94 is study, we examined the effects of various fibrinolytic drugs on clinical outcomes.

95 ombosis, including heparin, FXII inhibitors, fibrinolytic drugs, nafamostat, and dipyridamole, many o

96 therapeutic approach with antimicrobials and fibrinolytic drugs, particularly during the early stages

97 c system is controversial, as is the role of fibrinolytic dysfunction in bleeding and thrombosis in p

98 ding heparin, heparinoids, antithrombins, or fibrinolytics (e.g., tissue plasminogen activator), 3) a

99 Fibrinolytic-eligible patients with high-risk AMI prospe

100 r SkzL in S. agalactiae pathogenesis through fibrinolytic enhancement.

101 ) is the main physiological inhibitor of the fibrinolytic enzyme plasmin.

102 at this can be overcome through the use of a fibrinolytic enzyme such as tissue plasminogen activator

103 Plasminogen, the primary fibrinolytic enzyme, also modifies inflammatory processe

104 time that deficiency of plasminogen, the key fibrinolytic enzyme, delays disease onset and protects f

105 sulting from the excessive generation of the fibrinolytic enzyme, plasmin, at the cell surface of the

106 We tested the hypothesis that the fibrinolytic enzyme, plasmin, is a key regulator of macr

107 Lysines are major binding sites for fibrinolytic enzymes and are also sites of plasmin cleav

108 lytic system may affect interactions between fibrinolytic enzymes and inhibitors.

109 is a novel and complementary means by which fibrinolytic enzymes can reduce thrombus size.

110 were always susceptible to dispersal by the fibrinolytic enzymes plasmin or nattokinase.

111 inolysis by increasing the susceptibility of fibrinolytic enzymes to serpins.

112 ate that FXIIIa activity can be modulated by fibrinolytic enzymes, and suggest that changes in fibrin

113 tion factors, endogenous anticoagulants, and fibrinolytic enzymes.

114 ors (fibrinogen, prothrombin, and factor V); fibrinolytic factors (plasminogen activator inhibitor 1

115 Tertiary hemostasis assessment included fibrinolytic factors and plasmin-antiplasmin complex.

116 e relationships between the inflammatory and fibrinolytic factors and the metabolic syndrome.

117 Bilateral forearm blood flow and plasma fibrinolytic factors were assessed with venous occlusion

118 l vasodilation and the release of endogenous fibrinolytic factors.

119 t-dependent contributions of coagulation and fibrinolytic factors.

120 ed the contribution of alpha2-antiplasmin to fibrinolytic failure, and compared the effects of plasmi

121 ovides a safe and practical means to deliver fibrinolytics for thromboprophylaxis in settings charact

122 Plasma markers of fibrinolytic function are associated with incident coron

123 ttle is known about sources, regulation, and fibrinolytic function of noninjury-induced systemic plas

124 Six hours after exposure, vasomotor and fibrinolytic function were assessed by means of intraart

125 al hormone therapy (HT) may alter markers of fibrinolytic function, the relevance of this effect for

126 of PAR-1-mediated endothelial vasomotor and fibrinolytic function.

127 f air pollution on myocardial, vascular, and fibrinolytic function.

128 of thromboprophylaxis using recombinant scFv-fibrinolytic fusion proteins that target endothelium.

129 ytic vesicle formation, GAS GTPases and host fibrinolytic genes, and GAS response to interaction with

130 A fibrinolytic inhibitor prevented this healing, indicatin

131 used to assess the effects of FXIII and the fibrinolytic inhibitor, alpha(2)-antiplasmin (alpha(2)AP

132 The expression of the fibrinolytic marker tPA was significantly higher (P = 0.

133 lysis in ACS, the prognostic value of plasma fibrinolytic markers in assessing risk is limited.

134 ntrathecal administration of vasodilators or fibrinolytics may have offered advantages over systemic

135 lack of essential analytical tools has left fibrinolytic mechanisms affected by obesity poorly defin

136 olysis plasma protein analysis including the fibrinolytic mediator S100A10.

137 , chronic anticoagulation, administration of fibrinolytic medications, concurrent ischemic stroke, an

138 echanisms, we analyzed the expression of key fibrinolytic molecules in experimental pulmonary emboli,

139 Thrombus site expression of key fibrinolytic molecules was determined by immunofluoresce

140 nd no ability to predict the requirement for fibrinolytics or thoracic surgery.Objectives: To study t

141 this study, we analyzed the regulation of 2 fibrinolytic parameters, tissue plasminogen activator (t

142 Components of the fibrinolytic pathway (urokinase plasminogen activator an

143 This article reviews the fibrinolytic pathway and discusses the current agents av

144 Key components of the fibrinolytic pathway modulate cholestatic liver injury b

145 Efficient activation of the fibrinolytic pathway occurs when plasminogen and its act

146 Plasminogen activators stimulate the fibrinolytic pathway to accelerate thrombus resolution a

147 rget and cleave multiple proteins within the fibrinolytic pathway, including the plasmin inhibitor al

148 may be a central endogenous inhibitor of the fibrinolytic pathway, promoting a procoagulatory state a

149 moderate temperature ozone may activate the fibrinolytic pathway, while at elevated temperature ozon

150 r the well-known antifibrotic actions of the fibrinolytic pathway.

151 studied those found for their effects on the fibrinolytic pathway.

152 inding protein (C4BP) and plasminogen of the fibrinolytic pathway.

153 simultaneously assessing proaggregatory and fibrinolytic pathways, could play a role in risk stratif

154 istent changes in endogenous coagulation and fibrinolytic pathways.

155 Our study demonstrates a mixed fibrinolytic phenotype in acutely ill patients with cirr

156 Our finding of a previously unrecognized fibrinolytic phenotype indicates that bleeding in TM-AC

157 We assessed plasma fibrinolytic potential in a large cohort of patients wit

158 is associated with decreased CRR and reduced fibrinolytic potential resulting from alterations in clo

159 ator inhibitor (PAI-1), an antagonist of the fibrinolytic process in proportion to total body platele

160 lation of the nonlinear spatially nonuniform fibrinolytic process in thrombolysis is not currently we

161 inogen activator (uPA) plays a major role in fibrinolytic processes and also can potentiate LPS-induc

162 -fold selectivity over other coagulation and fibrinolytic protease targets, comparing favorably with

163 The primary fibrinolytic protease, plasmin, can be activated either

164 Thrombin and other clotting/fibrinolytic proteases are ineffective in cleaving CCN1.

165 Binding of the fibrinolytic proteinase plasmin (Pm) to streptokinase (S

166 site, initiating Pg proteolysis to form the fibrinolytic proteinase, plasmin (Pm).

167 concentrations/activities of key coagulation/fibrinolytic proteins and platelet counts and aggregatio

168 s suggest that the presence of tPA and other fibrinolytic proteins in human bile results in lysis of

169 n essential scaffold for the accumulation of fibrinolytic proteins that mediate fibrinolysis under fl

170 ates fibrinolysis through reduced binding of fibrinolytic proteins.

171 lained by variations in plasma levels of key fibrinolytic proteins.

172 Annexin II, a fibrinolytic receptor, binds plasminogen and tissue plas

173 ation and who receive aspirin and a standard fibrinolytic regimen, the addition of clopidogrel improv

174 Significant differences exist among various fibrinolytic regimens as reperfusion therapy in STEMI an

175 g 128 071 patients treated with 12 different fibrinolytic regimens were assessed.

176 ervention strategy for improving endothelial fibrinolytic regulation in this at-risk population.

177 cid, eicosanoid, and cholesterol metabolism; fibrinolytic regulation; cell growth and proliferation;

178 ith great potential for practical studies of fibrinolytic-related proteins.

179 s the contemporary role of an evidence-based fibrinolytic reperfusion strategy as part of a pharmacoi

180 Selection of a fibrinolytic requires consideration of several factors,

181 Activated factor XIII (FXIIIa) mediates fibrinolytic resistance and is a hallmark of newly forme

182 ibitors that in turn may locally enhance the fibrinolytic response.

183 adykinin contributes to the inflammatory and fibrinolytic responses to dialysis, we conducted a doubl

184 Tissue plasminogen activator (tPA), a fibrinolytic serine protease, is routinely given for the

185 ility to bind procoagulant and anticoagulant/fibrinolytic serine proteases.

186 0.8) with evidence of hypercoagulability and fibrinolytic "shutdown".

187 Here, we aimed to determine fibrinolytic status and its relationship with outcome in

188 those in development that favorably modulate fibrinolytic status and may offer a potential new avenue

189 was to determine how novel anticoagulant or fibrinolytic strategies may be used to protect against a

190 Fibrinolytics such as tPA are already approved for other

191 elium (plasma von Willebrand levels) and the fibrinolytic system (plasma tissue-type plasminogen acti

192 I-1) is a major physiologic regulator of the fibrinolytic system and has recently gained recognition

193 Haemodynamic forces and the fibrinolytic system are considered to be the principal m

194 tivating coagulation, yet its effects on the fibrinolytic system are not fully understood.

195 These findings define the endogenous fibrinolytic system as an important regulator of clot re

196 Although the fibrinolytic system assembles at the site of pulmonary e

197 ion system is best known as an extracellular fibrinolytic system but was previously reported to also

198 Our findings indicate that disruption of p53-fibrinolytic system cross talk may serve as a novel inte

199 allenge to develop a selective and effective fibrinolytic system for thrombolysis with minimal undesi

200 sults underscore the importance of the human fibrinolytic system in host-pathogen interactions in inv

201 tion and expression of the components of the fibrinolytic system in patients with chronic rhinosinusi

202 The status of the fibrinolytic system is controversial, as is the role of

203 Although the fibrinolytic system is strongly affected by infection, t

204 Thus, the fibrinolytic system linked by an activation cascade may

205 of disorders involving dysregulation of the fibrinolytic system may affect interactions between fibr

206 nsequently, modulation of the local cellular fibrinolytic system of catecholaminergic cells results i

207 The fibrinolytic system plays a key role in the regulation o

208 In addition, we observed altered airway fibrinolytic system protein balance consistent with prom

209 Despite abundant evidence for the fibrinolytic system regulating thrombosis, it has been o

210 hat experimental venous stasis activates the fibrinolytic system to block the development of venous t

211 gen and activity levels of components of the fibrinolytic system were measured by immunoassays, which

212 f endothelial activation, protein C pathway, fibrinolytic system, and complement.

213 coagulation and anticoagulant pathways, the fibrinolytic system, and platelets in the pathophysiolog

214 ment system, the blood clotting cascade, the fibrinolytic system, and the kallikrein-kinin system.

215 ity of uPA to induce other components of the fibrinolytic system, involves posttranscriptional regula

216 fying the activity of a key regulator of the fibrinolytic system, like alpha2-antiplasmin, may have u

217 Because of the complexity of the fibrinolytic system, mathematical models closely tied wi

218 ionally activates the central zymogen of the fibrinolytic system, plasminogen (Pg).

219 thesized that plasmin, the key enzyme of the fibrinolytic system, serves as a physiological backup en

220 However, if balanced by a healthy fibrinolytic system, thrombosis may not occur or cause l

221 ne protease plasmin, a central enzyme of the fibrinolytic system.

222 but subsequently generates inhibitors of the fibrinolytic system.

223 lts from ordered breakdown of thrombi by the fibrinolytic system.

224 n between two proteins of the complement and fibrinolytic system.

225 Additionally, the role of the coagulation/fibrinolytic systems and angiogenesis has also been exam

226 The complement, coagulation, and fibrinolytic systems are crucial for the maintenance of

227 d/or inhibition of natural anticoagulant and fibrinolytic systems by antiphospholipid antibodies.

228 The coagulation and fibrinolytic systems contribute to malignancy by increas

229 The canonical role of the hemostatic and fibrinolytic systems is to maintain vascular integrity.

230 ude components of complement and coagulation-fibrinolytic systems, as well as plasma lipoproteins.

231 door-to-needle times for patients receiving fibrinolytic therapy (19 min vs. 29 min, p = 0.003) and

232 nts experience significantly longer times to fibrinolytic therapy (door-to-drug times) and percutaneo

233 k who received acute reperfusion with either fibrinolytic therapy (n = 35,370) or primary percutaneou

234 n patients admitted with STEMI and receiving fibrinolytic therapy (n = 68,439 patients in 1,015 hospi

235 ry intervention (PPCI) is superior to onsite fibrinolytic therapy (O-FT) when administered in a timel

236 myocardial infarction is superior to onsite fibrinolytic therapy (O-FT), the generalizability of the

237 Most patients with STEMI receive fibrinolytic therapy and aspirin.

238 use of thoracentesis, chest tube placement, fibrinolytic therapy and open thoracotomy in children wi

239 ctive therapy in STEMI patients treated with fibrinolytic therapy and subsequent PCI.

240 on myocardial infarction (STEMI) who receive fibrinolytic therapy and subsequently undergo percutaneo

241 primary PCI and 14 332 patients who received fibrinolytic therapy at 444 PCI-capable hospitals.

242 patient as compared with providing immediate fibrinolytic therapy at their initial hospital; yet more

243 TEMI), or they may selectively offer PPCI or fibrinolytic therapy based on patient and hospital-level

244 al contact-to-needle) time for initiation of fibrinolytic therapy can be achieved within 30 min or do

245 re-hospital ECG was performed in 4.5% of the fibrinolytic therapy cohort and in 8.0% of the PCI cohor

246 In 1999, only 46% of the patients in the fibrinolytic therapy cohort were treated within the reco

247 ey to successful treatment, but intrapleural fibrinolytic therapy did not improve outcomes in an earl

248 The strategy of ENOX support for fibrinolytic therapy followed by PCI is superior to UFH

249 ests that a clinical trial of early systemic fibrinolytic therapy for CRAO is warranted and that cons

250 substantial proportion of patients receiving fibrinolytic therapy for myocardial infarction with ST-s

251 bridging therapies, role of aspirin, use of fibrinolytic therapy for prosthetic valve thrombosis, an

252 epicardial flow among patients treated with fibrinolytic therapy for ST-segment elevation myocardial

253 RS <0% following rescue/adjunctive PCI after fibrinolytic therapy for STEMI was independently associa

254 Among patients treated with fibrinolytic therapy for STEMI who underwent subsequent

255 Although the use of fibrinolytic therapy has progressively decreased over th

256 ry angioplasty provides outcomes superior to fibrinolytic therapy in AMI, but its use in community ho

257 ovides any propitious benefits over standard fibrinolytic therapy in diabetic patients.

258 The role of fibrinolytic therapy in patients with intermediate-risk

259 onary intervention (PCI) capability also use fibrinolytic therapy in patients with ST-segment elevati

260 on of glycoprotein IIb or IIIa inhibitors to fibrinolytic therapy increased the risk of major bleedin

261 imary PCI leads to better outcomes than when fibrinolytic therapy is administered at community hospit

262 rdial infarction (STEMI) patients undergoing fibrinolytic therapy is associated with adverse outcomes

263 ns difficult to implement in many areas, and fibrinolytic therapy is still widely used.

264 BEST PRACTICE ADVICE 8: Anti-fibrinolytic therapy may be considered in patients with

265 e and importance of the prompt, early use of fibrinolytic therapy may be underappreciated.

266 Since routine fibrinolytic therapy may decrease these complications, t

267 Fibrinolytic therapy offers an alternative to mechanical

268 s with intermediate-risk pulmonary embolism, fibrinolytic therapy prevented hemodynamic decompensatio

269 tion myocardial infarction (STEMI) receiving fibrinolytic therapy remains under study.

270 on of glycoprotein IIb or IIIa inhibitors to fibrinolytic therapy should be discouraged.

271 the advantage of this strategy over on-site fibrinolytic therapy that has been demonstrated in recen

272 ersus 86.3% with an in-hospital ECG, whereas fibrinolytic therapy was used in 4.6% versus 4.2% of pat

273 total of 20,479 STEMI patients who received fibrinolytic therapy were randomized to a strategy of EN

274 tion myocardial infarction (STEMI) receiving fibrinolytic therapy with and without clopidogrel.

275 ly assigned to undergo either primary PCI or fibrinolytic therapy with bolus tenecteplase (amended to

276 icant proportion of patients to the risks of fibrinolytic therapy without the likelihood of significa

277 visual outcomes after CRAO (with or without fibrinolytic therapy) and a series of more than 5 patien

278 pirin and other standard treatments (such as fibrinolytic therapy) safely reduces mortality and major

279 rent standard interventions (eg, aspirin and fibrinolytic therapy), and the balance of potential bene

280 rdial infarction with thrombus aspiration or fibrinolytic therapy, and postmortem pathological observ

281 ays should prompt increased consideration of fibrinolytic therapy, emergency medical services hospita

282 rvention and to promote the selective use of fibrinolytic therapy, especially prehospital fibrinolysi

283 After adjustment for age, fibrinolytic therapy, revascularization, region, and ele

284 In patients with STEMI receiving fibrinolytic therapy, the net benefit of ENOX is similar

285 for primary PCI may be superior to immediate fibrinolytic therapy, these findings are unlikely to gen

286 In patients with STEMI receiving fibrinolytic therapy, use of LMWH with other standard th

287 sk factors for intracranial hemorrhage after fibrinolytic therapy, were not associated with increased

288 dosing unfractionated heparin in support of fibrinolytic therapy.

289 >1 hour beyond door-to-needle (DN) times for fibrinolytic therapy.

290 0.64; P=0.006) but not in those treated with fibrinolytic therapy.

291 fer for direct PCI may also be preferable to fibrinolytic therapy.

292 s aged older than 70 years or in those given fibrinolytic therapy.

293 ry intervention institutions or who received fibrinolytic therapy.

294 Patients (73,032 receiving fibrinolytic therapy; 37,143 receiving primary percutane

295 y achieve greater benefit, especially if the fibrinolytic-to-PCI time delay associated with transfer

296 In fibrinolytic-treated patients with ST-segment-elevation

297 initial use of 162 versus 325 mg aspirin in fibrinolytic-treated ST-elevation myocardial infarction

298 tory factor C-reactive protein (CRP) and the fibrinolytic variables fibrinogen and plasminogen activa

299 1C]) to the levels of these inflammatory and fibrinolytic variables in recently diagnosed (<or=3 year

300 These results indicate that augmentation of fibrinolytic vascular surveillance by blockade of serine