Talk:Atherosclerosis
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![]() | This article was reviewed by PC Pro on June 2007. Comments: Overview: Very (perhaps too) comprehensive article. Britannica "fares poorly" and "Encarta earns the Dunce's Cap". Please examine the findings. For more information about external reviews of Wikipedia articles and about this review in particular, see this page. |
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]
- ^ Sloop GD (1999). "A critical analysis of the role of cholesterol in atherogenesis". Atherosclerosis. 142 (2): 265–8. PMID 10030376.
{{cite journal}}
: Unknown parameter|month=
ignored (help) - ^ Perret RS, Sloop GD. Increased peak blood velocity in association with elevated blood pressure. Ultrasound in Medicine and Biology 2000;26: 1387-91.
- ^ a b Sloop GD, Fallon KB, Zieske AW. Atherosclerotic plaque-like lesions in synthetic arteriovenous grafts: implications for atherogenesis. Atherosclerosis 2002;1260: 133-9.
- ^ 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.
- ^ 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 109.63.37.16 (talk) 14:26, 1 January 2012 (UTC)
Micelle
[edit]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 193.190.253.146 (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)
Atheromatosis
[edit]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)
- Indeed, the Research section needs to be cleaned from obsolete data, filled with modern trends and re-structured. Apparently, it was not done since 2010, let's do it now. 92.0.216.66 (talk) 09:51, 5 February 2018 (UTC)
Diagram
[edit]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)
- I agree. According to the labelling of the diagram in the original 1998 article by Carl J Pepine, MD, Clinical Collerlation in the Wikipedia (EN) article is indisputably a typo. It should be CLINICAL CORRELATION in bold Roman type, upper case, as for the other headings for the diagram. Please would an editor with greater graphical editing skill than I possess fix this? 82.15.254.27 (talk) 23:59, 30 May 2021 (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.
https://www.mja.com.au/journal/2002/177/5/cocaine-use-and-cardiovascular-complications "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..."
151.204.190.111 (talk) 22:05, 24 March 2012 (UTC)
Cocaine & heart disease
[edit]"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..." 151.204.190.111 (talk) 18:18, 26 March 2012 (UTC)
- cocaine can cause abuses in drug wastage and other new digestive disorders in alchohol hydrogenation by alcholase enzyme by new oxidase and hydrogenase enzyme 202.65.173.51 (talk) 08:10, 25 August 2024 (UTC)
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)
- 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)
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. --94.22.37.52 (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)
References
- ^ Isis Pharma announces positive results from phase 2 study of ISIS-APO(a)Rx
- ^ 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
- ^ 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
- ^ 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
- ^ A sugar can melt away cholesterol. Science News
- ^ New hope for treating atheriosclerosis ScienceDaily
- ^ 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
External links modified
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did cut some BS, or how to say that politely
[edit]"The key to the more effective approaches has been better understanding of the widespread and insidious nature of the disease" this sentence (i guess it was in Treatment section) seems to say next to nothing. i suggest (at least) to remove the adjectives. Though it still lacks substance.
Also i miss some additional clues from "diet" section (particularly oat), or at least some more links beyond the mediterranean diet which is already mentioned.
changed the aforementioned (half-) sentence to this: "The key to the more effective approaches has been better understanding of the disease...". Thugh i still dont really like it, it still sounds like a political or sales management blah-blah. 80.98.79.37 (talk) 23:27, 21 July 2017 (UTC).
Where does this ref
[edit]Say Hypomagnesemia[1] causes atherosclerosis? Doc James (talk · contribs · email) 04:45, 4 October 2017 (UTC)
References
Lead
[edit]Per WP:LEAD the lead should be 3 or 4 paragraphs. Also per WP:MEDMOS we do not tend to have a section called overview. Doc James (talk · contribs · email) 05:20, 6 October 2017 (UTC)
4 paragraphs works best for this article. I'm not sure what the other editor is trying to accomplish. QuackGuru (talk) 05:23, 6 October 2017 (UTC)
You’re making things up. The lead should be ONE paragraph, providing a dictionary-like definition WITHOUT going into detail. — Preceding unsigned comment added by 2605:A000:F8C8:1800:3998:2658:B49D:4A6A (talk) 03:54, 10 October 2017 (UTC)
References
The journal that this is from has an impact factor of zero.[3]
Need a better source. Doc James (talk · contribs · email) 12:35, 3 January 2018 (UTC)
- This is a primary source[4]
- Need secondary sources. Doc James (talk · contribs · email) 01:09, 5 January 2018 (UTC)
Verification request
[edit]@Doc James: Can you help verify if the source of this edit is reliable and placed at the proper section of "Modifiable
"? Since this source is not secondary source which got me curious about if there exists a template called {{secondary source needed}}? Thanks!! --It's gonna be awesome!✎Talk♬ 11:42, 14 May 2018 (UTC)
- User:It's gonna be awesome as a primary source ( a small study in mice ) it is not sufficient IMO for teh claims presented. Will see if I can find a better one. Doc James (talk · contribs · email) 16:17, 14 May 2018 (UTC)
- We have this review[5] Doc James (talk · contribs · email) 16:19, 14 May 2018 (UTC)
- Thank you for this! --It's gonna be awesome!✎Talk♬ 16:20, 14 May 2018 (UTC)
- Have adjusted here. User:It's gonna be awesome what do you think? Doc James (talk · contribs · email) 16:23, 14 May 2018 (UTC)
- Nice work! Thanks for the time and effort! --It's gonna be awesome!✎Talk♬ 16:24, 14 May 2018 (UTC)
- Have adjusted here. User:It's gonna be awesome what do you think? Doc James (talk · contribs · email) 16:23, 14 May 2018 (UTC)
- Thank you for this! --It's gonna be awesome!✎Talk♬ 16:20, 14 May 2018 (UTC)
- We have this review[5] Doc James (talk · contribs · email) 16:19, 14 May 2018 (UTC)
- User:It's gonna be awesome as a primary source ( a small study in mice ) it is not sufficient IMO for teh claims presented. Will see if I can find a better one. Doc James (talk · contribs · email) 16:17, 14 May 2018 (UTC)
Discussion of Acceptable Sources
[edit]@Doc James: As best I can discern, source selection on this topic is particularly difficult. There appear to be a great heterogeneity of sources on atherosclerosis with substantial variance in level of detail and accuracy, many contradictory. For example:
- there is no uniform definition of atherosclerosis, a problem which makes a page like this particularly difficult: some define it as a disease of accumulation despite the existence of lesions without abnormal accumulation both in early lesions in main coronaries and in later potentially fatal lesions of the branch coronaries supplying the conduction system of the heart.
- the NIH NHLBI page on atherosclerosis doesn't mention the proliferative aspect of the disease which is a central characteristic of early atherogenesis -- many investigators consider the proliferative aspect of the disease to be the primary characteristic and the accumulation and degeneration secondary/subsequent. For example, Ross et al 1984 state: "Contrary to earlier beliefs, atherosclerosis is not initially a degenerative process. Instead, the lesions of atherosclerosis are proliferative, particularly during their development and progression. The degenerative changes so commonly observed are a manifestation principally of changes that occur in relatively advanced lesions."[1]
I've done a good deal of reading on this topic and I'm wondering whether a more focused approach to source material would help improve the quality of this page. For example, a few high quality sources:
- The Natural History of Coronary Atherosclerosis by Constantin Velican published by CRC Press 1989: a comprehensive summary of the field written by a Romanian pathologist with over 300 peer reviewed publications on atherosclerosis including about a dozen in Atherosclerosis in the US.
- Atherosclerosis VI: summary of the sixth Saratoga international conference.
These seem to provide a more consistently thorough overview of the disease, particularly the non-lipoprotein aspects of the disease like the proliferative aspect, early changes, really solid explanation of basic pathology (and things like a comprehensive analysis of progression and incidence by age bracket), description and hypotheses behind gelatinous lesions (which are relatively poorly understood and not explained by most mainstream hypotheses of atherogenesis), role of proteoglycans and the stimuli which could result in abnormal retention, etc. Nickandre (talk) 20:35, 12 December 2019 (UTC)
Missing Citation - found?
[edit]There's a missing citation in the last paragraph of the Signs and Symptoms section, about findings in Viet Nam War casualties. I suspect this may be it, but can't be certain without the full text of the article. If someone at a library that has it can look, that gap may be filled.
JAMA. 1971 May 17;216(7):1185-7. Coronary artery disease in combat casualties in Vietnam J J McNamara, M A Molot, J F Stremple, R T Cutting PMID: 5108403 — Preceding unsigned comment added by Giraldus6 (talk • contribs) 18:54, 24 March 2021 (UTC)
Are Atherosclerosis and Arteriosclerosis the same thing?
[edit]Apologies if this is a naive question, but are atherosclerosis and arteriosclerosis the same thing? According to the Mayo Clinic, they are not.[7]. They are covered by two separate articles in Wikipedia but it's not clear from reading the lede of these articles that they are not synonyms but are related. The names are quite similar and for some (myself included) it's easy to conflate the two. Could someone more knowledgeable about these subjects alter the ledes to avoid confusion? 80.41.95.252 (talk) 14:45, 5 May 2021 (UTC)
- Atherosclerosis is a specific type of Arteriosclerosis in which lipid core plaques build up against the artery walls. Arteriosclerosis is a general term that describes any type of hardening of the arteries. I found a good description of it in Robin's Basic Pathology [8] but I'm not sure if a textbook is the best source to link since it is not accessible to most readers. This is their definition "Atherosclerosis is characterized by intimal lesions called atheromas (or atheromatous or atherosclerotic plaques ) that impinge on the vascular lumen and can rupture to cause sudden occlusion." MrTeratoma (talk) 01:12, 6 May 2021 (UTC) [1]
References
- ^ Kumar V, Abbas AK, Aster JC, Perkins JA. Robbins Basic Pathology 10th Ed. / [Edited by] Vinay Kumar, Abul K. Abbas, Jon C. Aster ; Artist, James A. Perkins. Tenth edition. Elsevier; 2018. Accessed May 6, 2021. https://www.elsevier.com/books/robbins-basic-pathology/kumar/978-0-323-35317-5
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