1988
DOI: 10.1016/s0140-6736(88)90021-9
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Thrombin/Antithrombin-Iii Complex Level as Early Predictor of Reocclusion After Successful Thrombolysis

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Cited by 51 publications
(12 citation statements)
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“…19 The reason for this is activated platelets after administration of tenecteplase. 20 Several clinical studies (ie, ASSENT-4, 12 PRAGUE-2 21 and CAPTIM 22 ) have shown that the time from onset to t-PA injection is important (within 2-3 h) for effectiveness of this type of treatment. In particular, the CAPTIM study comparing long-term results of prior t-PA administration and primary PCI, recently reported that the long-term prognosis in patients with prior t-PA administration within 2 h is superior to that in those with primary PCI, and suggested that prior administration of t-PA in the super acute phase is very important.…”
Section: Prescription Before Admission (%)mentioning
confidence: 99%
“…19 The reason for this is activated platelets after administration of tenecteplase. 20 Several clinical studies (ie, ASSENT-4, 12 PRAGUE-2 21 and CAPTIM 22 ) have shown that the time from onset to t-PA injection is important (within 2-3 h) for effectiveness of this type of treatment. In particular, the CAPTIM study comparing long-term results of prior t-PA administration and primary PCI, recently reported that the long-term prognosis in patients with prior t-PA administration within 2 h is superior to that in those with primary PCI, and suggested that prior administration of t-PA in the super acute phase is very important.…”
Section: Prescription Before Admission (%)mentioning
confidence: 99%
“…12 Our results demonstrate that the TAT levels are also in- mg/L) are far greater than the TAT levels (1 to 2 jig/L).…”
Section: Discussionmentioning
confidence: 46%
“…They are not fully understood but include increased procoagulant activity induced by pharmacological activation of plasminogen, local expression of procoagulant activity when the vessel is reperfused, presence of high shear forces that promote platelet deposition, and attenuation of physiological fibrinolytic activity after pharmacological thrombolysis 7 . Thus, recurrent thrombosis after coronary thrombolysis depends on a complex interaction between procoagulant factors associated with the atherosclerotic plaque, procoagulant activity induced by the residual thrombus, and paradoxical procoagulant activity which is promoted by pharmacological thrombolysis 8,9 . The interaction between thrombus‐bound thrombin and circulating blood may not only exert a prothrombotic stimulus through the activation of factor V but also by reducing endogenous thrombolytic potential via the induction of thrombin activatable fibrinolysis inhibitor (TAFI).…”
Section: Mechanisms Of Failure Of Thrombolysismentioning
confidence: 99%