It is well known that vWf (von Willebrand factor) is essential for platelet aggregation in clotting. Those individuals deficient in it are somewhat hemophiliac.
It is also known the vWf is exposed and present at sites of endothelial (inner most layer of cells of artery) injury, at which platelets are attracted like iron filings to a magnet. This begins the cascade of thrombosis which is responsible for end-stage ischemic events. This is true whether there is or isn't a large plaque.
It is best not to have a plaque, as this can be a chronic homing beacon for trouble, but it must be remembered that the biochemical cascade is not cholesterol causing a jam in the lumen of the artery (that never happens), but a blood clot.
This may happen with or without a plaque bursting, although plaque burst definitely will expose the subendothelial vWf stuck to collagen that makes platelets stick.
PGI2 inhibits this platelet adhesion extremely effectively. PGI2 is prostacyclin.
Administering supranormal levels of ascorbic acid greatly enhances the levels of prostacyclin production into the bloodstream.
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