Thrombus formation and subsequent lysis either spontaneous or pharmacological is the key events in acute vascular emergencies .We know both STEMI and acute strokes can get aborted naturally.
The thrombus which initially forms , triggers a natural lytic mechanism and this fights vigorously against the clotting process , and tries to get rid of the intravascular clot.
The early minutes are vital. (Like the T 20 cricket ) the win or loss is decided in the first few overs . The mantra is unrelented attack of the ball . . .ie thrombus ! In some patients the clot can never grow big to fill the lumen.These are lucky few .The mechanisms are common in both cerebral and coronary circulation. Here is were comes the role of antiplatelet agesnt .An aspirin or clopidogrel administered within minutes can prevent the genesis of central core of the thrombus .(This is the secret of aspirin scoring over stretokinase in STEMI in ISIS2 study done three deaceds ago !)
It should be realised, our understanding about spontaneous lysis is very little considering explosive growth of other aspects of cardiology. It is mediated by circulating TPA and antithrombin 3 . Remember every humans have it in their blood .But how much ? How to augment it ‘s power at times of thrombotic crises ?
What could be the clinical correlates of spontaneous thrombolysis ?
- In brain classically it is TIA .
- In heart do we have TIA equivalents ? .Yes it transient rest angina
Read this article to get a glimpse of natural cerebral thrombolysis and shall we extrapolate it to coronary spontaneous thrombolysis .Why not ?