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Updated: Aug 23, 2026

Prehospital Thrombolysis: A Manual from Berlin
Published on: November 26, 2013
Thrombolytic therapy for acute myocardial infarction. Lessons to be learned
1Department of Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania.
Trials of thrombolytic therapy have taught us that 1) lysis of hemostatic plugs, not fibrinogenolysis, is the major cause of bleeding complications; 2) as currently reported, patency rates 90 minutes after the onset of therapy are both meaningless and misleading as surrogate end-points for either myocardial salvage or reduced mortality; 3) extensive restoration of myocardial function requires much earlier administration of thrombolytic therapy than is currently the practice; 4) reduced mortality can be demonstrated well after the period in which myocardial salvage can be shown; and 5) drug development based on fibrin specificity is probably an obsolete concept, because therapy with a fibrin-specific agent such as recombinant tissue-type plasminogen activator does not enhance safety and is associated with a high degree of rethrombosis.
Trials of thrombolytic therapy have taught us that 1) lysis of hemostatic plugs, not fibrinogenolysis, is the major cause of bleeding complications; 2) as currently reported, patency rates 90 minutes after the onset of therapy are both meaningless and misleading as surrogate end-points for either myocardial salvage or reduced mortality; 3) extensive restoration of myocardial function requires much earlier administration of thrombolytic therapy than is currently the practice; 4) reduced mortality can be demonstrated well after the period in which myocardial salvage can be shown; and 5) drug development based on fibrin specificity is probably an obsolete concept, because therapy with a fibrin-specific agent such as recombinant tissue-type plasminogen activator does not enhance safety and is associated with a high degree of rethrombosis.
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