Open AccessRecent advances using streptokinase for acute coronary thrombosis
Author(s) -
Udall J. A.
Publication year - 1984
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960070303
Subject(s) - medicine , streptokinase , creatine kinase , thrombolysis , thrombosis , chest pain , myocardial infarction , coronary thrombosis , cardiology , acute coronary syndrome , anesthesia
Most important in comparison to earlier European trials, streptokinase (STK) is administered now at the earliest time possible after acute coronary thrombosis. In this series, STK was started 2.5 (±1.5) h after onset of chest pain, with reperfusion achieved approximately 1h later in 6 (55%) of 11 patients treated. Posttreatment angiograms will not be required to identify thrombolysis if noninvasive indicators will prvoide this information correctly. Early creatine kinase enzyme peaking 8 to 15 h after chest pain appears to be the most accurate marker available. Among untreated and unsuccessfully treated patients, creatine kinase peaking usually occurs 18‐36h after chest pain. A large intravenous STK loading dose of 1,500,000 IU produces a plasma concentration of approximately 500 IU/ml, equal to that concentration employed originally by intracoronary infusions. Such large doses have been employed in 60 patients thus far, without an unusual incidence or severity of hemorrhages. High dose, ultrashort‐term treatment for only 1 h is being investigated now. Systemic STK penetrates most “blind coronary pouches” and gains access to acute thrombi, as identified by radiocontrast material washout during angiography in patients with severe coronary occlusions. Streptokinase exerts a significant anticoagulant effect, not previous considered, which may be beneficial in the prevention of new clot formation and the rapid dissolution of acute coronary thrombi.