We know streptokinase is a non fibrin specific agent that results in systemic lytic state and hence more chance of bleeding.
TPA is fibrin specific and it will act only on fibrin bound to clot , hence systemic bleeding risk should be less.
However , in real world , it is well documented stroke risk with TPA is consistently more than streptokinase .(It varies between .0.3-.5% with streptokinase , 0.7-to 1% with TPA)
How do you explain this apparent paradox ?
- The fibrin selectivity pf TPA is not absolute* .
- The lytic power of TPA is more hence stroke is more likely.
- The FDP* released by TPA can trigger a systemic lytic state
- In the post TPA protocol heparin is mandatory and this contribute to stroke risk.
*What happens o fibrin degradation products (FDP) levels after TPA ?