Advertisement






Click here for more guidelines.
CME Topic Collections Past Issues Search Current Issue Home
     

J Am Coll Cardiol, 1989; 13:988-997
© 1989 by the American College of Cardiology Foundation
This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bassand, J.
Right arrow Articles by Ducellier, D
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bassand, J.
Right arrow Articles by Ducellier, D

Multicenter trial of intravenous anisoylated plasminogen streptokinase activator complex (APSAC) in acute myocardial infarction: effects on infarct size and left ventricular function

JP Bassand, J Machecourt, J Cassagnes, T Anguenot, R Lusson, E Borel, P Peycelon, E Wolf, and D Ducellier

Service de Cardiologie, Hopital Universitaire, Saint Jacques, Besancon, France.

Two hundred thirty-one patients with a first acute myocardial infarction were randomly allocated within 5 h after the onset of symptoms either to treatment with anisoylated plasminogen streptokinase activator complex (APSAC), 30 U over 5 min, or to conventional heparin therapy, 5,000 IU in a bolus injection. Heparin was reintroduced in both groups 4 h after initial therapy at a dosage of 500 IU/kg per day. One hundred twelve patients received APSAC and 119 received heparin within a mean period of 188 +/- 62 min after the onset of symptoms. Both groups were similar in age, location of the acute myocardial infarction, Killip functional class and time of randomization. Elective coronary arteriography was performed on an average of 4 +/- 1.2 days after initial therapy. Follow-up radionuclide angiography and thallium-201 single photon emission computed tomography were performed before hospital discharge. Infarct size was estimated from single photon emission computed tomography and expressed as a percent of total myocardial volume. The patency rate of the infarct-related artery was 77% in the APSAC group and 36% in the heparin group (p less than 0.001). Left ventricular ejection fraction determined from contrast angiography was significantly higher in the APSAC group than in the heparin group. This was true for the entire study group (0.53 +/- 0.13 versus 0.47 +/- 0.12; p = 0.002) as well as for the subgroups of patients with anterior and inferior wall infarction (0.47 +/- 0.13 versus 0.40 +/- 0.11; p = 0.04 and 0.56 +/- 0.10 versus 0.51 +/- 0.11; p = 0.02, respectively). At 3 weeks, the difference remained significant for the anterior myocardial infarction subgroup. A significant 31% reduction in infarct size was found in the APSAC group (33% for the anterior infarction subgroup [p less than 0.05] and 16% for the inferior infarction subgroup [p = NS]). A close inverse relation was found between the values of left ventricular ejection fraction and infarct size (r = -0.73, p less than 0.01). By the end of a 3 week follow-up period, seven APSAC-treated patients and six heparin-treated patients had died. In conclusion, the early infusion of APSAC in acute myocardial infarction produced a high early patency rate, significant limitation of infarct size and significant preservation of left ventricular systolic function, mainly in anterior wall infarction.


This article has been cited by other articles:


Home page
Journal of Renin-Angiotensin-Aldosterone SystemHome page
P. J de Kam, A. A Voors, F. Fici, D. J van Veldhuisen, and W. H van Gilst
Review: The revised role of ACE-inhibition after myocardial infarction in the thrombolytic/primary PCI era
Journal of Renin-Angiotensin-Aldosterone System, December 1, 2004; 5(4): 161 - 168.
[Abstract] [PDF]


Home page
ChestHome page
E. M. Ohman, R. A. Harrington, C. P. Cannon, G. Agnelli, J. A. Cairns, and J.W. Kennedy
Intravenous Thrombolysis in Acute Myocardial Infarction
Chest, January 1, 2001; 119 (2009): 253S - 277S.
[Full Text] [PDF]


Home page
CLIN APPL THROMB HEMOSTHome page
O. Iqbal, H. Messmore, D. Hoppensteadt, J. Fareed, and W. Wehrmacher
State-of-the-Art Review : Thrombolytic Drugs in Acute Myocardial Infarction
Clinical and Applied Thrombosis/Hemostasis, January 1, 2000; 6(1): 1 - 13.
[PDF]


Home page
CirculationHome page
M. H. Raitt, C. Maynard, G. S. Wagner, M. D. Cerqueira, R. H. Selvester, and W. D. Weaver
Relation Between Symptom Duration Before Thrombolytic Therapy and Final Myocardial Infarct Size
Circulation, January 1, 1996; 93(1): 48 - 53.
[Abstract] [Full Text]


Home page
ANN INTERN MEDHome page
S. Sherry and V. J. Marder
Streptokinase and Recombinant Tissue Plasminogen Activator (rt-PA) Are Equally Effective in Treating Acute Myocardial Infarction
Ann Intern Med, March 1, 1991; 114(5): 417 - 423.
[Abstract] [PDF]


Home page
Journal of Pharmacy PracticeHome page
D. W. Krichbaum and D. A. Trivedi
Thrombolytic Therapy in Acute Myocardial Infarction
Journal of Pharmacy Practice, January 1, 1990; 3(5): 332 - 348.
[PDF]



 
  CME Topic Collections Past Issues Search Current Issue Home

Advertisement