[Thrombolytic drugs in acute myocardial infarct]

Abstract

Thrombolytic therapy has a primary role in modifying evolving acute myocardial infarction by restoration of patency of infarct-related artery. All thrombolytic agents convert plasminogen to plasmin; 3 of them (streptokinase, urokinase and anisoylated human plasminogen streptokinase activator complex-APSAC) are not specific for fibrin and 2 (rt-PA, scu-PA) are relatively clot-specific and have limited systemic fibrinolytic activity. To date, the largest experience has been with streptokinase, which is derived from streptococci and therefore has the potential to cause allergic reactions, more frequent with repeat doses of the drug. Streptokinase is not clot-selective; despite significant systemic fibrinolysis, which is an usual consequence, major bleeding complications are uncommon. Another problem with streptokinase is hypotension, which depends on infusion rate. APSAC differs from the parent streptokinase-plasminogen complex with kinetics well suited to a sustained thrombolytic effect. Although it was expected to have clot selectivity, this feature is missed at the dose needed in the treatment of acute myocardial infarction. rt-PA is a natural occurring serum protease which presents important clot specificity with limited systemic fibrinolytic activity. However, the risk of major bleeding is not less than that observed with thrombolytic agents without clot selectivity. Of considerable interest is the potential for urokinase and prourokinase to act synergistically with other thrombolytic agents, with hypothetic improvement in efficacy and safety of thrombolytic therapy. Despite some different features among various thrombolytic agents, they are equally safe and effective in salvaging myocardium and in assuring survival benefit after acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)