Streptokinase acts indirectly by combining with plasminogen to form an activation complex which, in turn, converts plasminogen to plasmin both at the site of a thrombosis and systemically. Streptokinase is antigenic and can cause an early anaphylactic or late serum sickness-like reaction. It has a 50-60% infarct artery patency rate when used intravenously. It is the cheapest agent available and has the lowest incidence of intracerebral bleeds.
tPA directly converts plasminogen to plasmin but only in the presence of fibrin. This allows for increased, but not absolute, clot specificity. It is the most expensive agent but has the highest patency rates (75-85%). It also carries an increased risk for intracerebral bleeding.
APSAC is inactive (due to the acyl group) until exposed to fibrin, when decylation occurs and culminates in an activity similar to that of streptokinase. The patency rates and antigenic activity are similar to that of streptokinase. The acyl group only mildly improves the drug’s clot-specific activity. APSAC is very similar to streptokinase but also more expensive.
Does the use of thrombolytic agents translate into improved clinical results?
Yes. Early mortality (within the first few weeks) after Q-wave myocardial infarction has been reduced by 33%, from 10-15% to approximately 5-10%. Thrombolytic agents often lead to better recovery of left ventricular function, less ventricular dilatation or remodeling, fewer arrhythmias, and presumably improved long-term survival.