Fibrous cap

[Lone Dog]

When explaining plaque, and how heart attacks happen etc., books and websites refer to a "fibrous cap" that covers the plaque. How can the PT work if the plaque is covered by this cap? It sounds like the lysine & proline can't get to the plaque with that in place. Can anyone explain?

[ofonorow]

Do you have a link to what you are talking about? Dr. Levy is a board certified cardiologist who discusses atherosclerosis in great detail, in STOP AMERICA'S #1 KILLER<, and I do not believe he mentioned a "fibrous cap."

[Lone Dog]

Yes, sure. I think it's part of the standard description of this subject. Here are some instances, just search for fibrous cap on the pages... The description of a lipid core and a fibrous cap seems quite common.

http://en.wikipedia.org/wiki/Atherosclerosis

http://my.clevelandclinic.org/heart/new ... _ivus.aspx

http://www.texasheartinstitute.org/Rese ... laque1.cfm

[ofonorow]

After looking at wikipedia, they describe the contents of the atherosclerotic core, but the "fibrous cap"sule is ill defined. According to Levy, on Page 207 of STOP AMERICA'S #1 KILLER, Chapter 23, Fibrinogen and Vitamin C Deficiency

Fibrinogen is the main protein involved in the clotting mechanism in the blood plasma, and it also factors directly into how viscous ("thick") the blood is. Fibrinogen can also play a role in how readily the platelets in the blood will stick together and promote the initiation of blood clots. Fibrin, a very important component in the blood clot, results from the direct conversion of fibrinogen when the clotting mechanism in the blood as been initiated.

Dr. Levy goes on in this chapter to cite the studies that show fibrinogen is elevated when vitamin C is deficient.

According to the Pauling/Rath theory, atherosclerosis is a healing process, and specifically Lp(a), acting as a surrogate for vitamin C, is the "sticky" cholesterol that holds the patch (atherosclerotic plaques) together and attached to the artery. It makes sense then that Fibrinogen would be involved, as a clotting factor.

So what you are really asking is whether Lp(a) binding inhibitors work given the nature of the "fibrous capsule", or whether Lp(a) is involved. I believe the answer is yes, that lysine/proline can disrupt these caps and will look for references and get back to this post. There is other evidence that vitamin C all by itself can dissolve soft atheromas in a matter of days. (See. Dr. Bush's pages on Cardioretinometry.)

added

It is interesting that in the Pauling/Rath unified theory paper, they start by saying

We have recently presented ascorbate deficiency as the primary cause of human CVD. We proposed that the most frequent pathomechanism leading to the development of atherosclerotic plaques is the deposition of Lp(a) and fibrinogen/fibrin in the ascorbate-deficient vascular wall (1, 2). In the course of this work we discovered that virtually every pathomechanism for human CVD known today can be induced by ascorbate deficiency. Beside the deposition of Lp(a) this includes such seemingly unrelated processes as foam cell formation and decreased reverse-cholesterol transfer, and also peripheral angiopathies in diabetic or homocystinuric patients. We did not accept this observation as a coincidence.

http://www.drrathresearch.org/research/publications/leading-publications/97-unified-theory-of-human-cardiovascular-disease-leading-the-way-to-the-abolition-of-this-disease-as-a-cause-for-human-mortality.html

More from the paper. Note: Apo(a) is the major component of Lp(a).

In ascorbate deficiency Lp(a) is selectively retained in the vascular wall. Apo(a) counteracts increased permeability by compensating for collagens, by its binding to fibrin, as a proteinthiol and antioxidant, and as an inhibitor of plasmin-induced proteolysis (1). Moreover, as an adhesive protein apo(a) is effective in tissue-repair processes (8). Chronic ascorbate deficiency leads to a sustained accumulation of Lp(a) in the vascular wall. This leads to the development of atherosclerotic plaques and premature CVD particularly in individuals with genetically determined high plasma Lp(a) levels. Because of its association with apo(a), Lp(a) is the most specific repair particle among all lipoproteins. Lp(a) is predominantly deposited at predisposition sites and it is therefore found to be significantly correlated with coronary, cervical, and cerebral atherosclerosis but not with peripheral vascular disease.

[Lone Dog]

Thanks, Owen, I appreciate your input. I've read about the so-called 'cap' in quite a few places. Reference is often made to 'vulnerable' plaque, which is where the cap is thin and may fracture and parts of it along with material spilling out from the plaque then cause blood clotting and the artery gets blocked and a heart attack occurs.

I began wondering - if this is an accurate description, then if there is a cap in place any therapeutic agents such as the PT are not going to be able to make contact with the plaque and reverse it. To weaken or remove the cap would appear to be dangerous!

Have a look at the illustration on this page:

http://www.gcmradiology.com/ct-angiography.php

[Dolev]

From that article:

can identify the condition even before a patient experiences noticeable symptoms. This allows physicians to take steps to treat this disease in its earliest stages, before it can cause a heart attack."

Great, so now we can pay for an expensive procedure that gets more people on statins and rat poison, and even earlier.

[ofonorow]

I think the issue can be resolved by considering the "fibrous cap" part of a healing process, like a scab. So a) if the arteries are kept strong with adequate amount of collagen available, from adequate vitamin C intake, then the issue of healing is moot. And b) if the process has already started, then again, taking vitamin C to strengthen and heal the arteries will reduce the risk that penetrating the scab will cause a clot/rupture.

In any case, following Pauling's vitamin C advice is warranted.

And it is probably wise to be wary of just taking a lot of lysine - without vitamin C. Take both.