Two molecular mechanisms of compensation after heart attack

If the heart survives after an ischemic heart attack, there are ways that it copes. The structural scaffold fibroblast cells remain, after the functional cells have died. These work much harder to maintain the akinetic region which is better than overt rupture, which would be lethal. The rest of the remaining heart undergoes stress and strain to maintain the difference in work, but at a cost.

Distinctive ERK and p38 signaling in remote and infarcted myocardium during post-MI remodeling in the mouse.

Vitamin C and Thrombosis

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.

Some work I did on Mesenchymal Stem Cell Therapy on the Infarcted Myocardium

"Myocardial survival signaling in response to stem cell transplantation."


Osiris Therapeutics had something going on in this respect. We're talking "too late," and "too far gone," not prevention.