Just in case anyone thought that it was only your myocardial cells which die as a result of hyperglycaemia, those lining your aorta are queueing up at the same time.
The people doing this research are extremely clever. The molecular mechanism looks complex and finding a drug to block the effect is certainly going to need people who are very bright to do it.
Of course you could cop out and do the simple thing, which is to avoid the hyperglycaemia in the first place. Unless you're a Kitavan that looks like LC eating to me. Where ever you live, the secret appears to be to live within the limits of carbohydrate intake dictated by your ability to maintain normoglycaemia. Of course eating less carbs than this shouldn't be a problem. More just might be.
Once the endothelial cells are dead they will leave a cell sized open wound on the lining of the aorta. This will be repaired by the endothelial cells adjoining the wound dividing or by endothelial progenitor cells from the blood stream settling down on the wound (or both). These cells need energy and cholesterol to grow or divide. Sugar caused the problem in the first place so I vote energy from lipid. Any sensible system would be set up to provide lipid and cholesterol. Perhaps the surrounding cells should up regulate their LDL receptor numbers? Note especially that a loss of glycosoaminoglycans from the endothelial surface also markedly up regulates LDL particle internalisation. These endothelial cells are not taking in LDL cholesterol particles to kill themselves. Glucose does that.