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Updated: Aug 11, 2026

Myocardial Infarction and Functional Outcome Assessment in Pigs
Published on: April 25, 2014
Heparin in acute myocardial infarction
1Division of Cardiology, Institute of Care and Research, Montescano (Pavia), Italy.
Thrombolytic therapy has become an established procedure in patients with acute myocardial infarction (AMI). However, the aftercare of such patients is still uncertain. A meta-analysis of twenty trials of intravenous or subcutaneous heparin in AMI performed during the prethrombolysis period indicated a significant reduction in mortality, reinfarction, and stroke in treated patients. More recently, a study (SCATI) aimed at investigating the clinical effects of subcutaneous heparin (12.500 U two times daily) in the setting of thrombolytic therapeutical strategy in AMI, showed a lower in-hospital mortality, a trend towards lesser transient ischemic episodes in patients given streptokinase, and no difference in recurrent infarction rate. Ventricular thrombi were markedly reduced by heparin. Anti-platelet drugs were not permitted in the SCATI. In both GISSI 2 (Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico) and International tissue plasminogen activator/streptokinase trials, aspirin was a recommended treatment, and subcutaneous heparin was randomized. No difference in mortality was noted in patients given heparin. In GISSI 2 recurrent ischemic episodes were also similar in treated and control groups, whereas embolic events were reduced by heparin. Major bleedings were rare in all trials. In conclusion, subcutaneous heparin is beneficial in AMI: however, the association with aspirin does not add consistent benefits. Heparin is effective in preventing thrombus formation and embolic complications - such effects are not shared by aspirin.
Thrombolytic therapy has become an established procedure in patients with acute myocardial infarction (AMI). However, the aftercare of such patients is still uncertain. A meta-analysis of twenty trials of intravenous or subcutaneous heparin in AMI performed during the prethrombolysis period indicated a significant reduction in mortality, reinfarction, and stroke in treated patients. More recently, a study (SCATI) aimed at investigating the clinical effects of subcutaneous heparin (12.500 U two times daily) in the setting of thrombolytic therapeutical strategy in AMI, showed a lower in-hospital mortality, a trend towards lesser transient ischemic episodes in patients given streptokinase, and no difference in recurrent infarction rate. Ventricular thrombi were markedly reduced by heparin. Anti-platelet drugs were not permitted in the SCATI. In both GISSI 2 (Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico) and International tissue plasminogen activator/streptokinase trials, aspirin was a recommended treatment, and subcutaneous heparin was randomized. No difference in mortality was noted in patients given heparin. In GISSI 2 recurrent ischemic episodes were also similar in treated and control groups, whereas embolic events were reduced by heparin. Major bleedings were rare in all trials. In conclusion, subcutaneous heparin is beneficial in AMI: however, the association with aspirin does not add consistent benefits. Heparin is effective in preventing thrombus formation and embolic complications - such effects are not shared by aspirin.
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