Once again, thanks have to go to Dr Davis of Track Your Plaque for a nice introduction to an interesting subject.
Have a read through this blog post, just the comments are enough. The second comment is from a man with all of his coronary calcium score localised in to one single coronary artery. His bemused query is:
"Doesen't the same blood with the same small particle, low HDL and everything else travel through ALL the arteries? How come it only harms me in 1 artery? This doesen't make any sense to me."
Absolutely. I cannot see how the lipid hypothesis could remotely explain this phenomenon. If our liver merely makes LDL-C as a never ending supply of arterial suicide bombs, surely that evil LDL would attack ALL blood vessels? Sometimes it does, sometimes it doesn't. Often the attack is very specifically localised.
Another comment from a further anonymous poster is equally telling:
"When nurse called with results her explaination was that I must be a non smoker, which i am, because in smokers the plaque tends to spread more evenly in the coronary arteries and in non smokers they tend to show up in 1 or 2 arteries."
So another confirmation that, in non smokers at least, plaque is often localised to one or two out of four arteries. This localisation phenomenon is real. You just have to ask a lipid believer why this should occur.
Basically it was pretty well sorted out back in 1954. Well maybe not the smoking bit. My assumption for that is that smoking just damages everything, vascular linings included. Anyway, have a read here.
I really like this paper. It's solid, basic, core hydraulic physics. It could almost have been written by an anaesthetist. Page 2 of the pdf has a neat diagram, complete with algebra, explaining how the tension in the wall of a curved artery has to be highest on the inside of the curve. If you are going to get wall damage, that's where it will show first. He goes through Laplace's general law relating vessel wall tension to hydrostatic pressure (in excess of that of the surrounding tissue), the radius of curvature of the vessel along its course and the radius of the vessel itself.
He then settles down to predict where arteriosclerosis is likely and unlikely to occur under various circumstances and backs it up with histology slides. The article is over 8 pages long and does deserve careful reading, but here is his suggestion as to why some coronary arteries are more prone to arteriosclerosis than others. He suggests it may be surrounding tissue pressure that reduces wall damage in some sections of some coronary arteries. Probably also curved arteries are more prone, tortuous arteries most prone. Wide diameter arteries are more prone. Lapalce's Law predicts this.
"Geringer has pointed out that in the instances where a portion of the anterior descending coronary artery lies buried in the myocardium, the buried segment is spared from atherosclerosis. Branches of the same artery lying in the epicardial fat, and therefore not surrounded by appreciable tissue pressure, are affected by atherosclerosis."
This ref to Geringer is from 1951 and seems to have fallen off of the bottom of pubmed! It's Geringer, E.: Am. Heart J., 41: 359, 1951 for anyone with access to a well established library and a duster.
Completely independently Wexler made this observation in a detailed analysis of spontaneous arteriosclerosis in aged breeding rats, back in 1964:
"One wonders if the physical pressure of the surrounding myocardium may decrease the need for maintaining the structural rigidity of these medium sized arteries by calcification. In the case of the larger epicardial branches, however, the presence of calcium could promote increased polymerization of mucopolysaccharides. The increased polymerization would provide the turgor or rigidity required by the exposed epicardial arteries."
What would be very interesting to see is is how protected or exposed individual calcified vs non calcified arteries are on EBCT scans...
It was obvious, at least as recently as 1964, that arteriosclerosis was a repair process. Possibly a repair process gone wrong, but a repair process never the less.
In 2008, lost in the lipid hypothesis, these oddities are inexplicable.
Arteriosclerosis today is merely our liver trying to kill us with sticky Lp(a).