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Acylated Plasminogen‐Streptokinase Activator Complex: A New Approach to Thrombolytic Therapy
Author(s) -
Crabbe Sarah J.,
Grimm Aileen M.,
Hopkins Leigh E.
Publication year - 1990
Publication title -
pharmacotherapy: the journal of human pharmacology and drug therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.227
H-Index - 109
eISSN - 1875-9114
pISSN - 0277-0008
DOI - 10.1002/j.1875-9114.1990.tb02559.x
Subject(s) - streptokinase , medicine , anesthesia , thrombolysis , myocardial infarction , tissue plasminogen activator , venipuncture , plasminogen activator
Acylated plasminogen‐streptokinase activator complex (APSAC; anistreplase) is an inactive complex of human plasminogen and streptokinase. When it is injected, a controlled deacylation of the catalytic center occurs, activating the complex so that thrombolysis may begin. This process extends the half‐life of streptokinase, allowing for 4–6 hours of fibrinolytic activity. Anistreplase has demonstrated equivalent efficacy to intracoronary streptokinase with regard to reperfusion rates in acute myocardial infarction. In addition, patients have shown a 56% reduction in mortality at 28 days with anistreplase compared to heparin. The adverse effect profile of anistreplase includes minor bleeding and hematoma formation at the site of venipuncture, hypotensive and bradycardic episodes, arrhythmias, facial flushing, fever, and rarely, allergic reactions. Serious bleeding reactions are uncommon, with the frequency of cerebrovascular accident reported at 0.4‐0.6%. The special advantage of anistreplase is its administration as a 30‐U intravenous bolus injected over 5 minutes, eliminating the need for long infusions and increasing the ease of administration. Based on its efficacy and ease of administration, anistreplase may become the drug of choice in the emergency treatment of acute myocardial infarction.