Document Detail

Experimental reversal of acute coronary thrombotic occlusion and myocardial injury in animals utilizing streptokinase.
MedLine Citation:
PMID:  7315718     Owner:  NLM     Status:  MEDLINE    
Fresh autologous thrombus, 1.0 to 1.5 ml, was injected into the left anterior descending and/or left diagonal coronary arteries of 19 open-chest dogs to produce evolving acute myocardial infarction (AMI). Thrombotic obstruction was documented by coronary angiography. Multilead epicardial ECGs showed ST segment elevations of affected left ventricular (LV) areas within 2 minutes after thrombus injection, and LV segmental wall cyanosis with hypocontraction was observed within 10 minutes in the myocardial areas supplied by the thrombosed artery. Ten animals then received an initial dose of streptokinase (STK), 250,000 U (intravenous), followed by STK, 1000 to 3000 U/min (intracoronary), while nine control dogs untreated with STK received normal saline infusion. All but one STK-treated animal (all nine animals receiving intracoronary STK) had reestablishment of blood flow in the previously occluded vessels within 1 1/2 hours, disappearance of ventricular cyanosis, return of normal LV contractile function, and normalization of elevated ST segments within 1 hour after intracoronary STK therapy. In contrast, in the non-STK-treated control group, all animals had continued coronary obstruction, progressive ST elevations, and worsening LV cyanosis and hypocontraction until death or for more than 3 hours post thrombus; three control animals died of ventricular fibrillation (VF) within 1 hour of thrombus occlusion, three more died of VF within 2 hours post thrombus, and only three survived beyond 2 hours post thrombus. Postmortem examination of non-STK-treated animals revealed extensive residual coronary thrombus. All intracoronary STK-treated animals evidenced absence of residual coronary thrombus at postmortem examination. These data provide clinically relevant evidence that early intracoronary STK effects thrombolysis in AMI by reopening coronary vessels occluded by fresh thrombus, thereby protecting myocardium from further ischemia and necrosis, preserving LV function, and also reversing cardiac muscle injury.
G Lee; J Giddens; P Krieg; A Dajee; M Suzuki; J A Kozina; R M Ikeda; A N DeMaria; D T Mason
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  American heart journal     Volume:  102     ISSN:  0002-8703     ISO Abbreviation:  Am. Heart J.     Publication Date:  1981 Dec 
Date Detail:
Created Date:  1982-02-22     Completed Date:  1982-02-22     Revised Date:  2006-02-27    
Medline Journal Info:
Nlm Unique ID:  0370465     Medline TA:  Am Heart J     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1139-44     Citation Subset:  AIM; IM    
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MeSH Terms
Coronary Disease / drug therapy*
Heart Ventricles / drug effects
Myocardial Contraction / drug effects
Myocardial Infarction / drug therapy*
Streptokinase / therapeutic use*
Ventricular Fibrillation / mortality
Reg. No./Substance:
EC 3.4.-/Streptokinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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