coronary thrombosis

Coronary thrombosis is a blood clot forming inside one of the heart's own arteries and plugging it like a cork in a pipe. It is the direct cause of most heart attacks — the final step that turns a damaged plaque into blocked blood flow.

It usually begins where a plaque has ruptured or eroded. The exposed material activates platelets, which clump together, and switches on the clotting cascade, which lays down a mesh of fibrin. Together these build a thrombus on top of the plaque. Depending on how big and how stable the clot is, it may narrow the artery, block it intermittently, or shut it off entirely.

The size and persistence of the thrombus largely determine the clinical picture: a fully occluding, stable clot tends to cause STEMI, while a non-occluding or transient one underlies NSTEMI or unstable angina. This central role of clotting is why antiplatelet and anticoagulant drugs are cornerstones of acute treatment and why thrombolysis or mechanical removal can restore flow.

Thrombosis (a clot forming in place) is distinct from embolism (a clot that travels from elsewhere); coronary events are overwhelmingly due to local, plaque-related thrombosis rather than emboli.