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I want to help improve this article[edit]

I appreciate all the hard work that has been done to get this article acknowledged as "B" class. That being said, I've spent the last seventeen years of my professional life studying the celluar and molecular mechanisms of atherogenesis and I would like this article to be much better. I want to help make this article be a better article. And *that* being said, I know zip about editing Wikipedia articles so I ask for help from mpiano but wat opiano|Cyclopiano]] (talk) —Preceding undated comment added 07:17, 12 May 2010 (UTC).

Hemorheologic-Hemodynamic Theory[edit]

This section really looks like a combination of spam and soapboxing. To attract the attention of more contributors, I have posted a notice at WT:MED (here). I have trimmed a small amount, but it really reads as if it is written, for the most part, as a speculative piece with minimal mainstream support (i.e. within the medical community it is a fringe theory). Right now I'm tempted to remove it, the only thing that's keeping me from doing so is the lack of access to sources. If the articles cited don't mention the theory specifically, this section is very much a synthesis, and therefore inappropriate for wikipedia per our policy on original research. A bit of digging on google scholar, google and google books turns up very few hits - far fewer than I would expect of a mainstream, heavily debated hypothesis (though about what I would expect of a pet theory published by a single researcher). Any thoughts? I posted a notice on the MED wikiproject pointing to this discussion (thus); this was mentioned once in the past, with minimal discussion. WLU (t) (c) Wikipedia's rules:simple/complex 18:19, 8 March 2010 (UTC)

It might be appropriate to split this idea off into its own article, so that this apparently non-mainstream idea can be reduced to WP:DUE weight for this article while still WP:PRESERVEing good information. Offhand, I'd guess that "due weight" would give this idea about one paragraph. (Shouldn't there be a standard pathogenesis section in this article? I didn't see one when I skimmed the TOC.) WhatamIdoing (talk) 03:14, 9 March 2010 (UTC)
It apparently was an article before, Bongomatic merged from it here, it looked like this before. Lots of references, but they don't seem to actually discuss the theory itself - they are primary references that are synthesized to advance a theory.
I really can't support the section. There are almost no references in google. The sources used to justify the section were mostly primary, and didn't seem to use the words "Hemorheologic-hemodynamic theory" anywhere. The few that actually use the terms for the most part have a uniting factor in being by a single author - Gregory D. Sloop (formerly of the LSUHSC department of pathology, not any more). The search term gets 10 hits on google scholar. The first, second, seventh and tenth are all by Sloop, the first sourced to Medical hypotheses (which is the biggest red flag you can get for a medical topic that it's a fringe theory). The second, seventh and tenth are all by Sloop and published in a single journal - Atherosclerosis. I'd really like to get a copy of their editorial review board membership between 1999 and 2002 to see if he's on it. The third, fifth and sixth aren't references to the theory, the two words just happen to be next to each other in a sentence. 4, 8 and 9 seem legitemate, but that's still only three independent publications discussing the theory. 8 and 9 are essentially throwaway references to the theory stating that it exists, with no substantive discussion (and 8 is an animal model, and both are proposing alternative models of atherosclerosis that don't actually "endorse" the HHT). 4 is, like 8, a primary source.
The entire section is the product of essentially a single editor - Bigdaddypathologist, with less than 150 edits and most of those on this topic (both atherosclerosis, but more specifically the HHT within that page). I am really, really, REALLY uncomfortable with this remaining on a main page as if it were a serious, contemporary and accepted contender for the explanation of atherosclerosis. It may be true, but right now it is not seriously or substantially cited, referenced, mentioned, researched or discussed anywhere. This looks like classic soapboxing, and even if it is true, wikipedia is niether a crystal ball nor a publisher of original research. It's well-written, it certainly seems theoretically interesting, but it's still mostly an original research justification for the theory, with only a few legitemately used sources that are used to justify an enormous amount of undue weigth (in my mind). The following is what I could retain after trimming out most of the OR, and I'm still uncomfortable with keeping it until I can get a better look at the references to see if they actually mention HHT. The conventional explanation may be flawed, but it seems very obvious to me at least, that this isn't currently accepted as the answer. I would even be cautious in re-creating the old pages discussing the HHT for these reasons again. Simply put - how many pages do we have on medical subjects where the total number of references (including all primary sources, all speculative papers, and all "mere mentions") can be counted on less than two hands? Below is what remains, and note that the last reference to Heart is actually a letter to the editor. I really don't think this is appropriate as a section in the header-page for a major health topic. I really don't think it was appropriate to have such a lengthy section before I trimmed it, and I think at best this could be a separate stub. That's at best, I'd actually rather have it left out and the redirects deleted. WLU (t) (c) Wikipedia's rules:simple/complex 14:24, 10 March 2010 (UTC)
Given the lack of general discussion about this idea, I support the removal. When/if we get (substantially) more than a single person talking about it, then we can deal with it then. WhatamIdoing (talk) 04:16, 17 March 2010 (UTC)

Hemorheologic-hemodynamic theory[edit]

The hemorheologic–hemodynamic theory holds that atherosclerosis is a disease of stasis of blood, which promotes the organization of a thrombus into an atherosclerotic plaque.[1] The hemorheologic-hemodynamic theory posits that thrombosis leads to both plaque development and its complication, superimposed thrombosis and infarction. The name reflects the fact that the interaction of hemorheologic, i.e., blood flow, and hemodynamic, i.e., blood velocity, pulsatility, and arterial geometry, factors lead to atherosclerosis. Mainstream theory provides no explanation for accelerated atherosclerosis associated with hypertension[2] and cannot explain the presence of fibrous plaques in synthetic arteriovenous grafts.[3] The hemorheologic-hemodynamic theory predicts that low-density lipoprotein (LDL) should increase blood viscosity and high-density liporotein (HDL) should decrease blood viscosity, which has been demonstrated experimentally.[4] The hemorheologic-hemodynamic theory explains the existence of atherosclerotic plaques in synthetic arteriovenous grafts.[3] Being largely inanimate, the capacity of these vessels to respond to an injury with an inflammatory response, the inciting cause of atherosclerosis according to mainstream atherogenesis theory, would be very limited. Further, this theory explains the benefit of blood donation.[5]

  1. ^ Sloop GD (1999). "A critical analysis of the role of cholesterol in atherogenesis". Atherosclerosis. 142 (2): 265–8. PMID 10030376.  Unknown parameter |month= ignored (help)
  2. ^ Perret RS, Sloop GD. Increased peak blood velocity in association with elevated blood pressure. Ultrasound in Medicine and Biology 2000;26: 1387-91.
  3. ^ a b Sloop GD, Fallon KB, Zieske AW. Atherosclerotic plaque-like lesions in synthetic arteriovenous grafts: implications for atherogenesis. Atherosclerosis 2002;1260: 133-9.
  4. ^ Sloop GD, Garber DW. The effects of low-density lipoprotein and high-density lipoprotein on blood viscosity correlate with their association with risk of atherosclerosis in humans. Clinical Science 1997;92:473-9.
  5. ^ Sloop GD. Possible association of a reduction in cardiovascular events with blood donation. Heart 1998;79:422.

atherosclrosis ia a diseaseaffecting arteries . it is commonly reffered to as a "narrowing" of the arteries. it is a chronic disease in which there is accumulation of fatty materials , abnormal amounts of smooth muscles , cholestrol , or fibrin in the arteries . "mishi" — Preceding unsigned comment added by (talk) 14:26, 1 January 2012 (UTC)


Calling LDL a "hollow molecule for carrying cholesterol" is plain wrong. More correct would be to say that the lipoproteins have formed a micelle, which is of low density because of a high cholesterol/lipid content. Anything else is humbug. Source: Biochemistry; Berg, Tymoczko, Stryer; sixth edition; page 744 —Preceding unsigned comment added by (talk) 22:34, 8 March 2010 (UTC)

Thank you for your suggestion. When you believe an article needs improvement, please feel free to make those changes. Wikipedia is a wiki, so anyone can edit almost any article by simply following the edit this page link at the top. The Wikipedia community encourages you to be bold in updating pages. Don't worry too much about making honest mistakes—they're likely to be found and corrected quickly. If you're not sure how editing works, check out how to edit a page, or use the sandbox to try out your editing skills. New contributors are always welcome. You don't even need to log in (although there are many reasons why you might want to). WhatamIdoing (talk) 03:07, 9 March 2010 (UTC)


Should atheromatosis be a redirect to this article and cited inside it? I'm not sure if they are perfect synonyms. --capmo 17:57, 19 April 2010 (UTC)

Research section would benefit from structure[edit]

The Research section seems a random collection. Can we find a review and structure it by approach and then chronology ? Rod57 (talk) 12:21, 24 November 2010 (UTC)


The diagram appears to be a modification of one in a published paper: The effects of angiotensin-converting enzyme inhibition on endothelial dysfunction: Potential role in myocardial ischemia Original Research Article The American Journal of Cardiology, Volume 82, Issue 10, Supplement 1, 19 November 1998, Pages S23-S27 Carl J. Pepine

which is in turn based on these American Heart Associate guidelines: (Circulation. 1995;92:1355-1374.)

I suspect that this means that it is available under the "Creative Commons Attribution-Share Alike 3.0 Unported license." as stated. There is also a typo - "Clinical Collerlation" should be "Clinical correlation" or "clinical manifestation" or similar. AndyDScott (talk) 14:18, 22 December 2010 (UTC)

Cocaine and arrythmias[edit]

In light of cocaine being one of the causes of Ms Houston's death, we might consider adding a section on recreational drugs & cardio-vascular disease. "There is also evidence that cocaine can trigger cardiac arrhythmias, probably as a result of the enhanced sympathetic state and the direct effects of cocaine on the heart. The mechanisms are not fully understood, but several theories have been proposed..." (talk) 22:05, 24 March 2012 (UTC)

Cocaine & heart disease[edit],0,6229065.story

"Cocaine’s negative effects on cardiac health are well-established. Writing in the New England Journal of Medicine in 2001, Dr. Richard A. Lange and Dr. L. David Hillis..." (talk) 18:18, 26 March 2012 (UTC)

Re Panoramic radiograph#Detection of carotid atherosclerosis[edit]

It seems that there has been some research interest into the use of panoramic radiographs to detect carotid atheromas. There is general agreement on WP:DENT that (i) this is not an indication to take a panoramic radiograph (the selection criteria from my country do not mention this either) and (ii) radiographs taken for other reasons are never screened for this condition in modern practice. We are thinking of deleting this content from panoramic radiograph as per WP:UNDUE (and possibly also WP:COI, since there is a recurring name cropping up on every reference) and reducing it to a few sentences if a suitable secondary source can be found. The content might be more at home on this article or on a nested article of panoramic radiograph or a nested page of this article. Thoughts? Lesion (talk) 02:37, 11 March 2013 (UTC)

Detection is via ultrasounds or CT with contrast typically. Plain radiographs one we need a good ref. Doc James (talk · contribs · email) (if I write on your page reply on mine) 21:03, 12 April 2013 (UTC)
I have picked up a AAA on plain X ray but plain X ray is not for diagnosis AAA. Doc James (talk · contribs · email) (if I write on your page reply on mine) 21:07, 12 April 2013 (UTC)

Mummies and atherosclerosis[edit]

Isn't it wrong to draw a conclusion that "atherosclerosis isn't lifestyle related, because Ancient mummies have atherosclerosis"?! We don't know what the particular people ate, but because they were the day's royalty, they probably ate very well, like kings, and had little exercise, just as people in the developed countries (where atherosclerosis is widespread) eat very well and exercise little today. That's a ridiculous conclusion...! Of course atherosclerosis is caused by the environment, that means, lifestyle. The lifestyle is the same. -- (talk) 17:01, 6 June 2013 (UTC)

Oestrogen Receptors[edit]

Information on how 27-hydroxy cholesterol at high concentrations acts as an antagonist for the oestrogen receptors, preventing their normal function of keeping arteries elastic by preventing normal nuclear receptor function would be greatly appreciated. Added a lead reference here: [1] Lenny (talk) 07:45, 13 June 2013 (UTC)

Gut flora? Vitamin A, D, K1, K2 ratios?[edit]

Is there some new information on gut flora? Vitamin A, D, K1, K2 ratios? That could pertain to this article. GeoFan49 (talk) 23:33, 25 October 2013 (UTC)

New content[edit]

"In 1913 Russian Pathologist Nikolai N. Anichkov fed purified cholesterol to rabbits and produced the same lesions that had been seen in the arteries of humans on autopsy. A hundred years later in 2013 Dr. William C. Roberts, MD, Executive Director, Baylor Heart and Vascular Institute concluded that atherosclerosis had a single cause - cholesterol. "1) Atherosclerosis is easily produced experimentally in herbivores (monkeys, rabbits) by giving them diets containing large quantities of cholesterol (egg yolks) or saturated fat (animal fat). Indeed, atherosclerosis is one of the easiest diseases to produce experimentally, but the recipient must be an herbivore. It is not possible to produce atherosclerosis in carnivores (tigers, lions, dogs, etc.). In contrast, it is not possible to produce atherosclerosis simply by raising a rabbit's blood pressure or blowing cigarette smoke in its face for an entire lifetime. 2) Atherosclerotic plaques contain cholesterol. 3) Societies with high average cholesterol levels have higher event rates (heart attacks, etc.) than societies with much lower average cholesterol levels. 4) When serum cholesterol levels (especially the low-density lipoprotein cholesterol [LDL-C] level) are lowered (most readily, of course, by statin drugs), atherosclerotic events fall accordingly and the lower the level, the fewer the events (“less is more”). Although most humans consider themselves carnivores or at least omnivores, basically we humans have characteristics of herbivores" From his article Some Facts and Principles Learned after Spending 50 Years investigating Coronary Heart Disease."

First of all we do not do large quotes as there are copyright issues with them. Why is this placed before the systematic reviews? It appears to be of undue weight. Doc James (talk · contribs · email) (if I write on your page reply on mine) 00:33, 24 March 2014 (UTC)

Potential drugs for treating atheriosclerosis[edit]

(This text was removed for no apparent reason)

Akcea Therapeutics, announced positive results from a phase 2 study of ISIS-APO(a)Rx in which patients with high lipoprotein(a), or Lp(a) (a known driver of cardiovascular disease), achieved reductions in Lp(a) of up to 94%, with a mean reduction of 71%. They also announced results from a phase 1/2a study of ISIS-APO(a)-LRx in which subjects with elevated Lp(a) achieved dose-dependent reductions in Lp(a) of up to 99%.[1] ISIS-APO(a)Rx represents the first specific and potent drug in clinical development to lower Lp(a) levels and may be beneficial in reducing cardiovascular disease events and progression of calcific aortic valve stenosis. They are specifically targeted second generation antisense oligonucleotides (ASOs) that inhibit apo(a) mRNA translation.[2][3]

The sugar, cyclodextrin, removed cholesterol that had built up in the arteries of mice fed a high-fat diet.[4][5][6] Cyclodextrin works via two mechanisms. The first is to dissolve cholesterol crystals so the body can excrete them, and the second is to reduce the inflammatory response in artery walls when macrophages soak up cholesterol crystals.

Cyclodextrin, which is a type of sugar, has already been approved by the US Food and Drug Administration for use in humans. But because it has been in existence for some time, it cannot be patented. That makes it harder to get a drug company interested in developing cyclodextrin to treat heart disease, but it also will make it easier to get the drug approved to treat heart disease if the clinic trials support the research findings.

Cyclodextrin could be used in combination with other drugs, such as AEM-28 (Ас-hE18A-NH2 peptide) that binds to all of the atherogenic lipoproteins to enhance the uptake of these lipoproteins by the liver[7] But this option needs to be explored in clinical trials. Dmitry Dzhagarov (talk) 08:00, 21 April 2016 (UTC)

External links modified[edit]

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  1. ^ Isis Pharma announces positive results from phase 2 study of ISIS-APO(a)Rx
  2. ^ Graham, M. J., Viney, N., Crooke, R., & Tsimikas, S. (2015). Antisense Inhibition of Apolipoprotein (a) to Lower Plasma Lipoprotein (a) Levels in Humans. Journal of lipid research, jlr-R052258. doi:10.1194/jlr.R052258
  3. ^ Stein, E. A., & Raal, F. (2016). Future Directions to Establish Lipoprotein (a) as a Treatment for Atherosclerotic Cardiovascular Disease. Cardiovascular Drugs and Therapy, 30(1), 101-108. doi:10.1007/s10557-016-6654-5
  4. ^ Sebastian Zimmer, Alena Grebe, Siril S. Bakke et al., and Eicke Latz (Apr 2016). Cyclodextrin promotes atherosclerosis regression via macrophage reprogramming. Science Translational Medicine: 8(333), 333ra50 doi:10.1126/scitranslmed.aad6100
  5. ^ A sugar can melt away cholesterol. Science News
  6. ^ New hope for treating atheriosclerosis ScienceDaily
  7. ^ Anantharamaiah, G. M., & Goldberg, D. (2015). Novel method for reducing plasma cholesterol: a ligand replacement therapy. Clinical lipidology, 10(1), 83-90. , doi: 10.2217/clp.14.63