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WikiProject Medicine / Cardiology (Rated B-class, Mid-importance)
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Atheroma vs. Atherosclerosis[edit]

I find the information presented in this article to be beyond the scope of its subject. About half the article is on the clinical aspects of atherosclerosis and therefore belongs in the atherosclerosis article. The ICD codes belong there too. On the other had there is a lot of information in that article that would enrich this one. --InfoCan 16:29, 12 June 2006 (UTC)

POV - Prevalence[edit]

despite the opening sentence containing the addendum typical for most humans, there is neither cross-cultural nor within America's cultural data on the prevalence of the disease. If this were any other article, that would have already been grounds for a full POV review. <spetz>. 17:56, 30 March 2007 (UTC)

How to keep normal blood glucose levels low?[edit]

What are specific methods to keep normal blood glucose levels low, (glycosylated hemoglobin, also called HbA1c, values < 5.0)? —The preceding unsigned comment was added by (talk) 05:42, 12 April 2007 (UTC).

Esselstyn Ornish And Gould[edit]

Ornish Esselstyn and Gould have succeeded in regressing atheroma in most of their patients. Should not this be mentioned? robert2957 (talk) 14:41, 23 November 2007 (UTC)

I also think this is worth a mention. I don't know Gould's work, but a one line summary of the other two would be that Ornish proved that lifestyle changes (diet, relaxation, exercise...) can reverse cardiovascular disease and Esselstyn later proved that it was the dietary changes which got the job done (avoid all animal products and refined oils, eat cruciferous veg multiple times a day). Great floors (talk) 00:59, 20 January 2017 (UTC)

pictures would be nice[edit]

would be nice —Preceding unsigned comment added by (talkcontribs) 01:21, 22 July 2007

Atheroma and Acne[edit]

Has anyone out there ever noticed a correlation of acne with patients who develop atheroma. One could simply say that artheroma is acne of the arteries. Sounds like nonsense, but why do cultures that do not develop acne, do not develop artheroma - (until individuals move the Western cultures and then they suffer from both). Onset in time is about the same, just before pubety. Men suffer from acne much more than women, until women reach menopause (READ ARTICLE ON ACNE). Women develop acne and artheroma typically after menopause. Won't go into further medical/chemical details, but there sure is a lot of very similar factors in both cases. And as for the Western culture effect, everybody points to diet as being the major factor, however, are we overloooking environmental factors, such as pollutents from our industrialized Western countries. Such pollutents include tobacco smoking as well as exhausts from energy plants and automobiles. Now someone will jump in and say that Wiki is only for referenced work and original thoughts have no place here. The problem is that if you give someone informaton in one area and they see similar information in another area, they start to think. The nature of man 2+2 = something greater than 4. Ok, now pleae tell me why acne and artheroma are not similar. Wiseoldowl (talk) 04:57, 14 April 2008 (UTC)

I'm taking a neurobiology class. Acne and atheroma may both be very much related--inflammation is an important aspect of both.—Preceding unsigned comment added by (talkcontribs) 18:55, 1 May 2008
Errm not directly. A kick to a shin will result in localised inflammation, but that does not mean person will then have greater inflammatory process happening in their coronary arteries. Likewise acne may have infective component (treated afterall often with antibiotics), yet no more directly means that someone with acne has a chest infection - albeit that both are infectious processes. David Ruben Talk 10:08, 29 November 2008 (UTC)

Section names[edit]

re my edit - I've removed capitalised case to sentance case, also had unwheldy long titles - so I've shortened and drifted them somewhat closer to common section name style per WP:MEDMOS. David Ruben Talk 10:13, 29 November 2008 (UTC)


I can't help but wonder where did most of the information in this article originate. The references don't lead me to an abstract/synopsis about atheromas. I do believe the article is a good read, but the original source would be great to have, as I'm interested in the material.

I agree; especially the info regarding the statement atheroma's only marginally decrease the lumen size of the blood vessels they inhabit as this goes against a lot of what I have been taught (I possess a biology degree and now study medicine) and is not referenced. I have asked my lecturer and will modify the article when and if necessary. —Preceding unsigned comment added by (talk) 01:35, 10 April 2009 (UTC)

Having consulted my lecturer and several articles I have no idea where the information regarding the fact that atheroma's can increase (!) lumen size or only marginally decrease it and is not the source of atheromas symptoms. It goes against common sense and contradicts everything I know (I have a biology degree and study medicine). I do not have time to replace this section with anything particuarly outstanding but this is just wrong. —Preceding unsigned comment added by Mat8989 (talkcontribs) 15:42, 19 April 2009 (UTC)

The work by Glagov et al 1987 demonstrated that early stage plaques result in expansion of the vessel wall to compensate. Lumen size is therefore maintained in many plaques. AndyDScott (talk) 12:13, 30 June 2010 (UTC)

Link to pri-med[edit]

"Pathogenesis of Acute MI" - links to the pri-med website. I can't find the discussed video even searching for it. Remove? AndyDScott (talk) 12:17, 30 June 2010 (UTC)

I just removed it; thanks for checking on that. -- Beland (talk) 17:04, 27 April 2015 (UTC)


The scientific consensus is that there is a causal link between cholesterol and atheroma. There are good references in the lipid hypothesis article if anyone wishes to examine them. So, unless the claim that there is no connection between cholesterol and atheroma is given a good citation soon I am going to remove it. (talk) 05:11, 22 July 2010 (UTC)

IMT measurements in the carotid artery[edit]

I suggest this information is too detailed for this page and this section should be abbreviated or incorporated into the body text and additional material merged with the page on Intima-media thickness. Adh (talk) 18:12, 16 April 2012 (UTC)

Agreed; I added a merge tag on both articles. -- Beland (talk) 17:06, 27 April 2015 (UTC)

Mechanism of atheroma formation[edit]

This is located in Vulnerable plaque. Perhaps it should be shifted here (talk) 06:43, 8 June 2013 (UTC)

Agreed; it seems like that article should be merged into this one. I added merge tags on both. -- Beland (talk) 17:15, 27 April 2015 (UTC)
Agree - some redundancy between articles. should be merged. BakerStMD 16:09, 22 May 2015 (UTC)

Typical heart attack occurs at 20% stenotic arteries?[edit]

I am removing unsubstantiated claims (bolded) from this paragraph:

Most artery flow-disrupting events occur at locations with less than 50% lumen narrowing. From clinical studies published in the late 1990s to IVUS (in-the-artery-ultrasound) to visualize disease status, the typical heart attack occurs at locations with about 20% stenosis (narrowing), prior to sudden lumen closure and resulting myocardial infarction.[citation needed] Cardiac stress testing, traditionally the most commonly performed noninvasive testing method for blood flow limitations, generally only detects lumen narrowing of ~75% or greater, although some physicians advocate nuclear stress methods that can sometimes detect as little as 50%.[citation needed]

Justification: Whether most ACSs arise at locations with mild or severe stenosis is a somewhat contentious issue in cardiology (see this article for both sides of the issue), but not even the "mild stenosis" side (which I believe is in the minority) says that the typical MI is caused by a 20% stenosis. The paragraph gave no references for its bold claims. There have been studies in the 1990s that seemed to show mild stenoses were responsible for most ACSs, but the degree of stenosis was checked a long time before the actual ACS. I believe it is best to refrain from taking sides until there is consensus. See also this article by William Fearon. (talk) 08:55, 24 February 2016 (UTC)

Why does atheroma develop only in arteries and why does it accumulate even though the hemodynamic pressure is higher?[edit]

The introduction of the article says "Veins do not develop atheromata, because they are not subjected to the same hemodynamic pressure that arteries are".

Mechanically speaking, that doesn't make any sense. Atheroma shouldn't "accumulate" in the arteries because the hemodynamic pressure is higher. Just like deposits will be less likely to accumulate in a pipe where the dynamic pressure is the highest.

The cited ref ([1]) says "The present experiment showed that the wall thickness of GCCA (arteries, used as veins in the study) decreased continuously and possessed similar structures as that of veins 12 weeks post surgery".

So it really doesn't seem like a mechanical accumulation of sand, but more like the targeted patching of wall weaknesses. Patches that are no longer necessary and thus are removed when the artery is used as a vein. How many years will we have to wait for that kind of "groundbreaking discovery" from the medical community? The RedBurn (ϕ) 13:19, 28 March 2017 (UTC)

History of Research, paragraph 5, line 1[edit]

The first line of this section starts "Yet not in yield to despite these medical advances" Does this mean anything? If it does can it be expressed more clearly? (talk) 12:49, 17 September 2017 (UTC)