Key result
Thrombolytic therapy for acute myocardial infarction caused a significant rebound increase in PAI-1 approximately 3 hours after cessation (P<0.01), independent of the plasminogen activator used.
Why the study?
Does the type of thrombolytic agent affect the rebound increase of PAI-1 after cessation of therapy in patients with acute myocardial infarction?
Population
50 patients with acute myocardial infarction
Comparison
Intravenous thrombolytic treatment with… vs Comparison among the three thrombolytic agents
Design
Cohort
Follow-up
7 days
Authors
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May heighten post-MI reocclusion risk after thrombolysis; leaves open whether adjunctive strategies mitigate the drug-independent rebound.
Observational (n=50)
Does the type of thrombolytic agent affect the rebound increase of PAI-1 after cessation of therapy in patients with acute myocardial infarction?
p-value: p=<0.01
A marked, drug-independent rebound increase in PAI-1 occurs after cessation of thrombolytic therapy for acute myocardial infarction.
Genser et al. (1998) conducted an observational in acute myocardial infarction (n=50). Thrombolytic treatment (streptokinase, urokinase, or rt-PA) vs. Comparison among different thrombolytic agents was evaluated on Plasma concentrations of PAI-1, t-PA, and D-dimer (p=<0.01). Thrombolytic therapy for acute myocardial infarction caused a significant rebound increase in PAI-1 approximately 3 hours after cessation (P<0.01), independent of the plasminogen activator used.
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