Here is the "normal". Moon would describe this, correctly, as moderately arteriosclerotic. Lots of intimal hyperplasia and you can't tell much about the degree of damage to the elastic layer from this picture. I'm loathe to believe the authors' suggestion that the elastic layer is completely normal:
Next is the "non arteriosclerotic but dysplastic" artery from a sudden death victim. Burke et al ignore 100 years of pathology by describing it as non arteriosclerotic. You might forgive them as the lesions contain no cholesterol and they are lost in the idea that LDL cholesterol is the primary driver of arteriosclerosis which means, obviously, that they are not in a position to understand what they see. Or to investigate causes. They might want to start with copper status, ascorbate status, insulin levels at the time of death and familial problems with elastin structure; these might do for a start. Maybe clotting factors too. Also, given a retrospectoscope, the post prandial sympathetic response to a PowerBar would be very interesting. But LDL cholesterol? What can that have to do with the formative lesions of arteriosclerosis which contain no cholesterol?
Notice that the intimal thickening is present but there is also marked hypertrophy of the medial muscle cells. This is a classic resonse to severe elastosis, there's another post there; elastin as a regulator of vascular smooth muscle phenotype...
Peter
Afterthought: I wonder whether location of the artery matters. The left anterior descending coronary artery, where I have my seven point calcium score, is the least supported by cardiac muscle, so experiences the greatest trans-mural pressure gradient during systole. LAD is the classic site for calcification in non smokers. It would be interesting to see if sudden death victims have more superficial arteries supplying their AV node than non sudden death people........ Haven't checked the anatomy for this, hmmmmm.
