Tuesday, February 12, 2008

Single vessel disease

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).

Peter

5 comments:

JohnN said...

Peter,
Until a better hypothesis comes along, I incline to believe Pauling and Rath's explanation that Lp(a) is the plaster the body applies to cracked arteries at high pressure areas; Lp(a) is produced only by mammals without the ability to produce ascorbic acid. Hence the high dose Vit C - Lysine therapy where Vit C repairs the splits and Lysine to carry away Lp(a).

Peter said...

Hi johnn,

Lipoprotein (a) is very interesting. There is a lot that needs to be considered about it. I can't imagine that it was evolved to cause problems and it does appear to go up and down in situations where it can be seen as a repair process lipid. There is a third animal outside of primates and guinea pigs which produces lipoprotein (a). That's the hedgehog. If you try and imagine a worse (potential) laboratory species than the guinea pig, that's got to be it! Hedgehogs are ascorbate producers.

HH1

HH2

HH3

Particularly the later paper shows convergent independent evolution from primate lipoprotein (a), ie lipoprotein (a) has a use, independent of genetic ascorbate loss. I'm still trying to get a coherent idea about heart disease. It's a very interesting subject but there is almost no work going on at the moment outside of the lipid hypothesis. You end up trawling through some very old papers..... That doesn't make them any the less interesting, but you have to watch for the changes in standards evidence used to support conclusions. Actually, no change from today then!

Peter

Jeffrey Dach MD said...

Reversing Heart Disease

A recent publication by Detrano in the New England of Medicine confirms that "The coronary calcium score is a strong predictor of incident coronary heart disease and provides predictive information beyond that provided by standard risk factors".

The serial Heart Scan for calcium, coupled with sophisticated Lipoprotein analysis (VAP or NMR) and targeted nutritional supplements now make possible arrest and reversal of coronary artery plaque...The William Davis MD Track Your Plaque Program - in A Nut Shell

To read more, click here: Reversing Heart Disease

Jeffrey Dach MD
4700 Sheridan Suite T
Hollywood Fl 33021
954-983-1443

my web site

Peter said...

Hi Jeffery,

Nice site. If you've looked around Hyperlipid you'll see I read Dr Davis and agree with a great deal of what he says. This itself is very strange as I come from a high saturated fat, carnivore base and he does appear to have vegetarian and "healthy fats" leanings. When you get this sort of convergent evolution it makes you suspect that the basic ideas are correct.

I have been lucky enough to be sent a copy of Detrano's latest paper but haven't had time to get a comment together on it. It certainly does appear to support the coronary calcium scoring protocol. Mind you, it doesn't need much to improve on Framingham Heart Score (unless you live in Framingham, and even then it's not so hot...).

I'm very curious to get an EBCT scan on myself. Unfortunately at around $1000 a shot in the UK it's not going to happen tomorrow!

Anyway, best wishes from a total cholesterol sceptic who is being pushed towards the same supplements and diet to control insulin/glucose as yourself and Dr Davis, both of you are, I assume, lipid believers. Unimportant, provided the correct choices are made...

Peter

Peter said...

Hi Jeffery,

Nice site. If you've looked around Hyperlipid you'll see I read Dr Davis and agree with a great deal of what he says. This itself is very strange as I come from a high saturated fat, carnivore base and he does appear to have vegetarian and "healthy fats" leanings. When you get this sort of convergent evolution it makes you suspect that the basic ideas are correct.

I have been lucky enough to be sent a copy of Detrano's latest paper but haven't had time to get a comment together on it. It certainly does appear to support the coronary calcium scoring protocol. Mind you, it doesn't need much to improve on Framingham Heart Score (unless you live in Framingham, and even then it's not so hot...).

I'm very curious to get an EBCT scan on myself. Unfortunately at around $1000 a shot in the UK it's not going to happen tomorrow!

Anyway, best wishes from a total cholesterol sceptic who is being pushed towards the same supplements and diet to control insulin/glucose as yourself and Dr Davis, both of you are, I assume, lipid believers. Unimportant, provided the correct choices are made...

Peter