Talk:Atherosclerosis/Archive 1

Initial comments

Some of the text on this page has been taken from the public domain document at http://www.4woman.gov/faq/atheroscle.htm

Cellular Atherogenesis; The first and secound paragraphs should be swapped around as the initial damage occurs (2nd para) and then foramtion of fatty streaks occur (1st para). As it stands it could create confusion that fatty streak formation precedes the inflammation response and formation of foam cells.

Red wine

No mention of it reducing plaque. Why? —Preceding unsigned comment added by 69.155.110.28 (talk) 16:56, 31 March 2008 (UTC)

Enhanced Oral Chelation the ultimate cure (?)

They say EDTA contained in Chelation theraphy removes all the plaque from arteries. Can somebody please tell us, is this true? In the Wikipedia article it says EDTA chelation is NOT proven to be effective so there is obvious error somewhere. Source: http://www.healthresources.net/, who is lying here? Wikipedia or Healthresources? IEEE 13:26, 18 April 2007 (UTC)

In the chelation therapy discussion / talk page I wrote a blurb on a TV show that I saw 15 to 20 years ago. I remember phonetically writing down the word "key-lation" at the time in order to remember the specific topic.

I have copy+pasted my section below:

There is no scientific evidence that oral chelation reduces plaque or helps with clogged arteries. If you read the article, you'll see that calcium actually has very little to do with the atheromatous plaques and consequent thrombi that cause 90% of heart attacks. If you do a Google search for "oral chelation plaque" the only sites that come up are so called "natural medicine" websites that have a product to sell. --Geekish 02:29, 21 September 2007 (UTC)

TV Show 15 to 20 Yeas Ago

I recall seeing a talk show on Canadian TV. It had one host, and multiple guests. The show was about anti-aging or something.

It stuck with me that one of the guests explained that hardening of the arteries (atherosclerosis) involved a calcification process of the blood vessel walls, and that Calcium was a metal. Even back then the guest stated that it was very difficult to locate a doctor who would administer chelation therapy to reduce the calcification of a patient's circulatory system to fix heart disease or poor circulation troubles.

He explained that the chelation therapy treatment had no horrendous side-effects, since, after all, it was already being used as a safe, effective treatment method for heavy metal poisoning. It was extremely frustrating and puzzling to him how illogical the American Medical Association (AMA) treated this practice issue. Most doctors would refuse to treat atherosclerosis using chelation therapy because it was not a listed protocol for its treatment. Using a protocol not listed as standard operating procedure for a given disease is grounds for medical malpractice. As such doctors who are timid about lawsuits or worse, losing their license to practice medicine are forced to comply with the established protocols of surgery or administering drug therapy instead.

The TV guest listed several US states where some doctors could be eventually found to prescribe this treatment without it being a case of heavy metal poisoning. He explained also that even those friendly doctors did not want to use the procedure very often on the same patient. He explained that calcium was added back in order to reduce thinning of bone. He also explained that the post-treatment adding back of calcium and other vitamins and minerals done to prevent unnecessary losses of this nature, made patients "feel" great as much if not more so than had they only just been treated with the chelating agent. The patients so treated, the guest claimed remarkably, would have virtually all of their heavy plaque deposits stripped away, leaving their blood vessels / heart / valves free to operate almost as effectively as a young healthy athlete.

He or another guest were also heavily endorsing anti-oxidants. I seem to recall that it was folic acid--and that several vegetables and plants were mentioned that contained this substance.

Ketosis and ketones were also explained.

From chemistry I seem to remember that Calcium is a fairly reactive metal, and that trying to chelate it might be a tough job so that any agent used to grab it might easily grab other less reactive metals from one's system. It is not quite as reactive as sodium, but quite nasty if not found in ionic solution or in salt form.

In the TV show, to my recollection of it now, did not have any specifics about the chelating agent used for the atherosclerosis treatment. From the description of the various chelating agents listed, specifically that different agents more specifically target certain metals, then calcium as a highly reactive metal would be more troublesome to specifically chelate. If a double-blind study were used with inappropriate chelating agents being used, the conclusions would be forgone that failure would be the outcome of such an exercise: ie., chelating is no more effective than placebo--which would be inaccurate and biased. Oldspammer 18:16, 27 May 2007 (UTC)

Arteriosclerosis / Atherosclerosis

As described here here, and here, Arteriosclerosis / Atherosclerosis are not the same. Arteriosclerosis is the more general term describing many diseases involving the cardiovascular system and its associated arteries and vessels which go along with it. Atherosclerosis is a term used to describe diseases that affect the vessel walls, in other words, "hardening of the arteries". Therefore Arteriosclerosis should not be redirected to Atherosclerosis, but a better idea would be to create an individual article for Arteriosclerosis. Would it be best to create two seperate articles for this purpose? --Bryan986 05:40, 28 Feb 2005 (UTC)

I'd recommend two different articles, with a note at top of each linking to the other. --Arcadian 22:32, 8 September 2005 (UTC)

As a temporary measure, I've added the following paragraph: Some sources draw a distinction between "Arteriosclerosis", "Atherosclerosis", and "Arteriolosclerosis". In these contexts, "Atherosclerosis" is used when referring to larger arteries, and "Arteriolosclerosis" is used when referring to arterioles, with "Arteriosclerosis" used as a parent of both terms. --Arcadian 23:50, 2 November 2005 (UTC)

I think you'll find "Arteriosclerosis", is by definition, a hardening (and loss of elasticity) of the artery (in Latin, Arterio meaning artery and sclerosis meaning hardening), "Atherosclerosis" is an artery hardened by an atherosclerotic plaque (in Latin Athero means porrige-like) and "Arteriolosclerosis" is by definition, Arteriosclerosis mainly affecting the arterioles. Therefore, Atherosclerosis is a condition symptomatic of, and a form of, arteriosclerosis and artiolosclerosis. Please change your article so it makes this clear. -- Rutigor 21:00 GMT, 26/12/05

Arcadian's temporary paragraph (see above) replaced with a new paragraph using the phrasing provided by Rutigor to improve clarity and accuracy. --68.162.219.226 14:24, 5 July 2006 (UTC)

References

These references could not be traced back to information in the article:

• Steven Nissen: Atherosclerosis Development, Clinical Cardiology Vol 27 (Suppl IV), 17-20, July 2004
• Peter Libby: Atherosclerosis: The New View, Scientific American Vol 286, No. 5, May 2002

The Libby article is a good overview, but perhaps a more scholary source would be better to explain the inflammation - atherosclerosis link. JFW | T@lk 22:48, 23 March 2006 (UTC)

Here is the Libby article in PDF. JFW | T@lk 22:51, 23 March 2006 (UTC)

Patent as a source

I strongly oppose moves by WetBandit (talk · contribs) to link to a patent owned by Rath and Pauling (U.S. patent 5,278,189) with regards to vitamin C. There are much better sources for this information - a patent is a secondary source which contains legal, not medical proof. The patent identifies Rath & Pauling as owners of the intellectual property, but does not itself provide proof of the clinical efficacy of vitamin C in atherosclerosis. I have asked WetBandit for a better source, with reinsertion of the patent in response. Does Anyone else have views on this? JFW | T@lk 10:12, 26 March 2006 (UTC)

agree with jfdwolff. citation should be a primary source. Anlace 23:04, 28 March 2006 (UTC)

Astroid studies?

MAlvis, can you clarify for us what you were referring to in your edit summary when you mentioned (an) Asteroid study? I can't find anything to do with that in the actual article? Was that referring to several articles? Thanks Dieter Simon 17:09, 28 March 2006 (UTC)

I am sorry, but there is only one reference to the Asteroid trial which in the article only once refers to "the Asteroid trial..."

"The ASTEROID trial, mentioned above and in reference 3, has been the first to show actual disease volume regression, however, by design, was not large enough and long enough to statistically "prove" the mortality reduction issue. The trials to test this issue with this agent are currently in progress; all current evidence and signs are that the outcomes will be very favorable."

The ASTEROID study had no placebo group, could not prove clinical benefit and used a drug dose Health Canada issued a caveat about, i.e rosuvastatin a.k.a Crestor 40 mg. Crestor trials have never included a significant placebo group to show if the drug harms or benefits anyone over placebo. It likely causes a massive reduction in CoQ10 and may seriously harm those with heart failure and promote muscle and nerve damage. I propose any reference to ASTEROID be removed: it showed a volume reduction but gave no clue as to if the artery became stronger or weaker, it simply became thinner, as did the lumen, the opening for blood flow [picture on page 8]. Eddie at: vos@health-heart.org

Can you point us to the relevant prior section, because I can't find it. Dieter Simon 23:40, 30 March 2006 (UTC)

Don't get me wrong, I really do admire the article, it is extremely informative, just if you could clear up that point for us. Dieter Simon 11:23, 31 March 2006 (UTC)

Prevention

I'd be really interested in seeing a section on prevention, information on how to make healthier choices to minimize atherosclerosis.

There are 2 subjects here:

1. how to prevent structural decline of the artery and I propose that 'corrosion' of relevant proteins is caused by homocysteine, a general protein corrosive [reduced by 1/2 dozen B vitamins or once called vitamins] and by similar 'glycation' caused be excess blood sugar in diabetes. These are the 2 main causal factors in protein decline, including the artery. Moreover, homocysteine promotes cell migration and clotting.

2. how to prevent heart attack and dying thereof once structural / architectural decline of the artery wall is present, something the age-old International Atherosclerosis Project showed is the case in vertually all individuals from all regions examined. Pre-fatal fibrillation may be reduced or prevented by adequate electrolyte [arguably most relevant being magnesium] status, and certainly both the plant omega-3 found in canola, flax and soy oils, and the longer chain omega-3's found in any fish oil [studies: Lyon Diet Heart, and GISSI].

Statin drugs are used in such prevention strategy but they are not approved for such purpose in most countries: FDA approval only covers 'dyslipidemia' treatment; same in Canada. One of their side effects, even in low-dose, is mimicking nitroglycerin via the NO-synthase pathway, and they have mild antiinflammatory roles. In either department we have approved and safe alternatives without the side effects, cost and lack of mortality or effecacy benefit that statins suffer from and where heart attack and mortality benefit is simply absent in women of any age. Eddievos 13:59, 25 December 2006 (UTC) Eddie at: vos@health-heart.org

Atheroma vs. Atherosclerosis

I find the information presented in this article and in atheroma to be quite redundant and the distinction between the two topics is not clear to me. What are the non-atheroma aspects of atherosclerosis? If atheromas are one of the symptoms of atherosclerosis, then this article says very little on the other aspects. It seems a good amount of the information here should move to the atheroma article. This article ought to give a higher level view of atherosclerosis that includes a summary on atheroma formation (with a "for more information see the article on atheroma" link ), and focus more on the disease aspects. --128.36.196.58 16:22, 12 June 2006 (UTC)

The Plaque

In all textbooks I've come across, the fibrous cap is considered part of the plaque.

CFTR gene variations susceptible

as conductance of membranes is one of anatomical features of artery , why not dig also around this gene? 83.12.255.234 22:22, 26 February 2007 (UTC)

Given that PubMed does not yield anything, perhaps you should ask this question to health researchers, not a bunch of strangers on the internet. It bears remembering that CTFR-related membrane problems only really feature in epithelium, not the tissues of which blood vessels are built. Don't make things more difficult than they already are. JFW | T@lk 19:18, 15 July 2007 (UTC)

Foam Cells

Since Foam cells are macrophages and this are usually are able to move, why do they stay at the walls of the artery. Why not dot they simple phagocytose the colesterol and leave to die at the skyn or be expleled from the body. The macrophages would then clean the artery all and all would be ok. Maybe, they could be instruted to leave the walls using some chemical signal.

Tell a researcher at a university, not us. JFW | T@lk 19:18, 15 July 2007 (UTC)

This article was reviewed by a leading academic in the field

In PCPro on 12th July 2007 Dr Oliver Downing, Lecturer in Pharmacology (retired), at the University of Aston is quoted as saying "Wikipedia performs well on this subject. Dr Downing suggests its entry would be of more benefit to the serious student than its Encarta and Britannica equivalents." Lumos3 21:36, 13 July 2007 (UTC)

This is already noted in the template at the top and is covered by Wikipedia:External peer review/PCPRO154. violet/riga (t) 13:35, 27 July 2007 (UTC)

Three-vessel disease

An editor has proposed, at Wikipedia:Drawing board, that there be a separate article on Three-vessel disease. Comments there (or here) are welcome. -- John Broughton (♫♫) 22:34, 13 August 2007 (UTC)

Detecting Atherosclerosis Early

A study led by a team of researchers at Oregon Health & Science University has demonstrated for the first time that molecular imaging with contrast-enhanced ultrasound and targeted microbubbles is effective in detecting at a very early stage inflammatory processes that lead to atherosclerosis.[1] Brian Pearson 01:43, 21 August 2007 (UTC)

Trials don't support this claim, but that's because they suck.

From the treatment section:

"High dose supplements of vitamin E or C, with the goal of improving antioxidant protection, have failed to produce any beneficial trends in human, double blind, clinical research trials. However, these trials have consistently used lower doses than those claimed to be effective and have ignored the short half life of high intakes of vitamin C in the body."

No sources are provided to substantiate this paragraph. I am aware that the Heart Protection Study (HPS) into Vitamin supplementation involved prescribing 40 times the RDA of Vitamin E (As well as 4 times the RDA of Vitamin C) and found that the supplementation "...did not produce any significant reductions in the 5-year mortality from, or incidence of, any type of vascular disease, cancer, or other major outcome" in a Randomised Double-Blind Controlled trial of over 20,000 subjects.

I can only suspect that this paragraph is to rationalise / excuse the absence of evidence, thusly:

"High doses of Vitamins C and E reduce Vascular Disease."

"We gave thousands of people increased supplementation over many years and found no evidence that they do."

"Obviously, you didn't give them enough."

"Well, how much is enough?"

"More than what you gave them." —Preceding unsigned comment added by 172.188.68.42 (talk) 11:02, August 29, 2007 (UTC)

Well there's this paradox. Population studies show that people that get more vitamin E in their diets have better heart health and longer lives. But in studies where patients are given supplements, no benefit is seen. Maybe the population studies have it wrong - Vitamin E is correlated with something we're not measuring or taking into account. Or, my favorite theory, is that all the Vitamin E trials have used only one form of Vit E – α tocopherol – out of the eight different forms found naturally. (No, they don't interconvert in the body.) So I take modest supplements (400 mg / week) of the mixed tocopherols/tocotrienols. (and eat my vegetables) I'd really like to see some trials run with the full spectrum.

• Huang HY, Appel LJ (2003). "Supplementation of diets with alpha-tocopherol reduces serum concentrations of gamma- and delta-tocopherol in humans". J. Nutr. 133 (10): 3137–40. PMID 14519797. Retrieved 2007-11-22.

David.Throop (talk) 04:49, 23 November 2007 (UTC)

1. The studies with artificial Vit. E and Vit A were worse. I haven't been able to see studies with anything but natural vit E. (RRR) Enantiomerically pure alpha tocopherol. But there's some evidence that high levels of Vit. E depletes Vit. K. The result of this would be a temporary thinning of the blood (Vit. K causes coagulation) but a longterm increase in calcification (Vit K. is very interesting in terms of reducing calcification. Particularly menaquinone, as mentioned in the article.)

Order of Events in Main Image

Atherosclerosis Picture

The main image for this article may have an incorrect order of events for the pathogenesis of the disease covered in this article. The image is quite good because of its clear delineation of the events in atherosclerosis's development, but I am not sure that the events are depicted in the correct order.

My main question is whether or not it is correct to depict an inflammatory response involving macrophage (and eventually foam cells) occurring prior to the depositing of lipids in the vessel's intima. In my understanding, the inflammatory cells appear in response to toxic, oxidized lipoproteins that have accumulated due to binding with extracellular constituents.

Can anyone provide any clarification on why the image describes these events (lipid accumulation and inflammatory response) happening in the opposite order?

Green453 04:34, 24 October 2007 (UTC)

My reading of the Stitzinger piece (currently reference 19 in the article) on pp 13-14 indicates that you're correct. First comes increased vasopermeability, then LDL lodges in the endothelium, then it oxidizes, and only then are the monocytes recruited.

As for why the text reads as it does — because our understanding of all this is rapid flux right now?

David.Throop (talk) 05:06, 19 November 2007 (UTC)

Do you have any suggestions about how best the image could be edited to reflect this process more clearly? Also, does anyone know if there is a SVG file instead of the PNG that could be edited?

Green453 (talk) 03:09, 20 November 2007 (UTC)

Contact User:Grahams Child or User:Jrockley, who created it. I showed you a reference that gives one order of events; they may have a ref that says something else.

David.Throop (talk) 04:30, 23 November 2007 (UTC)

Not totally accurate, have a look at Davidsons for a proper timeframe.

Contact User:Antetz Two opposite theories currently exist related to the causality of inflammatory and oxydative phenomenons. The first one places the inflammatory phenomenon as the one that leads to the oxydative positive loop. The second one says the oxydative reaction causes an inflammatory response. Thus, the order of the events is not well known yet (information from my med school course about atherosclerosis).

I would say that what we don't clearly see in the image is the Fibroateroma part. Where are the fibers or calcification? —Preceding unsigned comment added by Antetz (talk • contribs) 20:07, 6 October 2008 (UTC)

Ornish Esselstyn and Gould

The sentence in the artice: "Dietary changes to achieve benefit have been more controversial, generally far less effective and less widely adhered to with success." lacks a citation. Ornish Esselstyn and Gould have succeeded in regressing atheroma in most of their patients. Should not this be mentioned? robert2957 (talk) 14:39, 23 November 2007 (UTC)

Sure, mention it. But could you get a citation from a peer-reviewed journal, rather than heartattackproof.com?

You might try scholar.google.com.

David.Throop (talk) 16:55, 23 November 2007 (UTC)

Hyaline arteriolosclerosis

The following data was pulled from the creation of Hyaline arteriolosclerosis to be included here, but since I'm no expert, someone with knowledge needs to palce it appropriately into the article. Thanks! - CobaltBlueTony™ _talk 15:19, 12 March 2008 (UTC)

Hyaline arteriolosclerosis is a kind of degenerative change in the walls of large and medium arteries. It is associated with aging, but is more severe in hypertension patients, and in long term can potentiate both aortic dissection and cerebrovascular haemorrhage.

Under microscope, a homogeneous pink hyaline thickening of the arteriole walls, and thus narrowing of lumen, can be observed.

References

• Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease. St. Louis, Mo: Elsevier Saunders. ISBN 0-7216-0187-1.

Chinese linked wrongly

The Chinese page linking to Atherosclerosis links to the Chinese for Arteriosclerosis, and the Arteriosclerosis page (English) does not link to this (or any other Chinese page). Not sure how to fix the links, help please! Atherosclerosis = 动脉粥样硬化； Arteriosclerosis = 动脉硬化. —Preceding unsigned comment added by 70.225.168.116 (talk) 22:55, 4 February 2009 (UTC)

Stiffness and elasticity of calcifications?

I noticed this sentence in the Visible Features section is contradictory, because higher elasticity should equate to higher stiffness: "In addition, the calcification deposits between the outer portion of the atheroma and the muscular wall, as they progress, lead to a loss of elasticity and stiffening of the artery as a whole." Since I don't know much about elasticity changes during atherosclerosis, I suggest someone with more knowledge clean this section up. Femtoamy (talk) 16:01, 23 February 2009 (UTC)

Image suggestion

I've uploaded a very simple diagram that shows atherosclerosis (right). If someone thinks there's a good spot for it, please add it to the article. (EhJJ)^TALK 19:40, 23 February 2009 (UTC)

I like this image more than the main image. The main image belongs in a section on disease progression. This sums up the disorder nicely. 99.132.249.24 (talk) 11:25, 19 July 2009 (UTC)

"Hemorheologic-Hemodynamic Theory"

A Google web search returned 9 results; a Google Scholar search returned six results.

I've not removed the section from the article for the moment, to get comments of other editors. But I think that until citations are added for the second paragraph, where the theory is actually described, needs citations; otherwise, this is bordering on original research. And I don't understand why the second paragraph isn't first: describe the theory, then (next paragraphs) explain why it explains things that the mainstream theory does not, rather than starting out with an attack paragraph. -- John Broughton (♫♫) 01:24, 9 April 2009 (UTC)

In reply: I have added five references to the second paragraph dealing with the hemorheologic-hemodynamic theory. These papers themselves have been referenced a total of 68 times. The paper which put forth the theory, "A unifying theory..." has been referenced 20 times. Another reference, "A critical analysis of the role of cholesterol in atherogenesis" has been referenced 22 times. These numbers are from a Google Scholar search. I was unaware of this resource. Thanks for turning me on to it. Most importantly, I have put a link to the article devoted to the H-H theory, which has references by quite a number of authors.

The second paragraph is where it is because intellectual honesty suggests that the limitations of a theory should be listed after it is put forth. Thus, I think the proper location for the "attack" paragraph is immediately after the mainstream theory. As noted at the end of the article on "Atheroma," "in spite of popular belief, cholesterol is not the villain that causes atherosclerosis." For practical reasons, I think it is appropriate to place that material before putting forth the H-H theory because otherwise, why else would one read on?

Finally, I object to the word "attack." This material is simply a dispassionate listing of shortcomings of the mainstream theory, with supporting references. It is my belief that there is no place for negative emotional words such as "attack" in evaluation of scientific material, especially in Wikipedia, which epitomizes neutrality.

Bigdaddypathologist (talk) 02:51, 11 April 2009 (UTC)

Homogenization of milk

I removed this section from this and other pages - strong claims were made about milk and health, substantiated only by a blog post from some conspiracy theory site. —Preceding unsigned comment added by 74.229.230.122 (talk) 00:43, 14 April 2009 (UTC)

Why atherosclerosis doesn't occur in veins.

The reasoning for why atherosclerosis does not occur in veins put forth in this article is extremely dubious. Sure, pO2 in veins is lower than in arteries. However, my understanding of oxidative damage blames products of cellular metabolism, not pO2. I'd like to see a reference documenting that oxidative modification does not occur below a certain threshold of pO2. If one has ever harbored doubts about the validity of in vitro oxLDL data in atherosclerosis, please check out "The distribution of oxidatively-modified lysine in the human vasculature", Atherosclerosis 2000;148: 255-63. There is a photomicrograph of an endothelial cell in a human vein full of oxidatively-modified protein. Unfortunately, this paper has been ignored, being referenced only a single time according to Google Scholar. Perhaps, Thomas Kuhn would not be surprised. He knew that discrepant observations are ignored by the mainstream to preserve a paradigm. As stated in the Wikipedia article on Kuhn, "the failure of a result to conform to the paradigm is seen not as refuting the paradigm, but as the mistake of the researcher, contra Popper's refutability criterion." Hopefully, the failure of intensive LDL lowering therapy and torcetrapib will make mainstream atherogenesis theorists ready for a paradigm shift. Bigdaddypathologist (talk) 21:05, 25 April 2009 (UTC)

Blood pressure is very low in veins. The much higher pressure in arteries leads to more initial lesions(that the body tries to repair causing atherosclerosis) . Thats also a reason for increase risk from higher blood pressure. —Preceding unsigned comment added by 70.255.81.160 (talk) 08:08, 1 July 2009 (UTC)

Physiologic Factors

I added a peer-reviewed reference re: CRP and heart attack risk. DanielGlazer (talk) 05:37, 20 June 2009 (UTC)

Rupture and Stenosis

I rewrote information in this section to more accurately represent the pathophysiclogy of clot development and heart attack. DanielGlazer (talk) 05:49, 20 June 2009 (UTC)

What happened to horrible artery picture

My recollection is that there was a picture of an artery here? 99.132.249.24 (talk) 11:24, 19 July 2009 (UTC)

Assessment comment

The comment(s) below were originally left at Talk:Atherosclerosis/Comments, and are posted here for posterity. Following several discussions in past years, these subpages are now deprecated. The comments may be irrelevant or outdated; if so, please feel free to remove this section.

Rated "top" as topic of general/medical interest. - tameeria 04:00, 19 February 2007 (UTC)

Last edited at 04:00, 19 February 2007 (UTC). Substituted at 08:35, 19 April 2016 (UTC)