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{{Infobox medical condition (new)
| name = Atheroma
| synonyms = atheromata (''plural''), atheromas (''plural''), atheromatous plaque, plaque
| image = Carotid Plaque.jpg
| caption = Atherosclerotic plaque from a [[carotid endarterectomy]] specimen. This shows the division of the [[common carotid artery|common]] into the [[internal carotid artery|internal]] and [[external carotid artery|external carotid arteries]].
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| field =
| symptoms =
| complications = [[Thrombosis]], [[embolism]], [[atherosclerosis]], [[arteriosclerosis]]
| onset =
| duration =
| types =
| causes = [[Hyperlipidemia]], [[hypertriglyceridemia]], [[hypercholesterolemia]]
| risks =
| diagnosis =
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| deaths =
}}
An '''atheroma''', or '''atheromatous plaque'''
The material consists of mostly [[macrophage|macrophage cells]],<ref name="pmid20376052">{{cite journal |last1=Hotamisligil |first1=Gökhan S |title=Endoplasmic reticulum stress and atherosclerosis |journal=Nature Medicine |date=April 2010 |volume=16 |issue=4 |pages=396–399 |doi=10.1038/nm0410-396 |pmid=20376052 |pmc=2897068 }}</ref><ref name="pmid22356914">{{cite journal |last1=Oh |first1=Jisu |last2=Riek |first2=Amy E. |last3=Weng |first3=Sherry |last4=Petty |first4=Marvin |last5=Kim |first5=David |last6=Colonna |first6=Marco |last7=Cella |first7=Marina |last8=Bernal-Mizrachi |first8=Carlos |title=Endoplasmic Reticulum Stress Controls M2 Macrophage Differentiation and Foam Cell Formation |journal=Journal of Biological Chemistry |date=6 April 2012 |volume=287 |issue=15 |pages=11629–11641 |doi=10.1074/jbc.M111.338673 |pmid=22356914 |pmc=3320912 |doi-access=free }}</ref> or debris, containing [[lipids]], calcium and a variable amount of fibrous [[connective tissue]]. The accumulated material forms a swelling in the artery wall, which may intrude into the [[Lumen (anatomy)|lumen]] of the artery, [[stenosis|narrowing]] it and restricting blood flow. Atheroma is the [[pathological]] basis for the disease entity [[atherosclerosis]], a subtype of [[arteriosclerosis]].<ref>{{
==Signs and symptoms==
For most people, the first symptoms result from atheroma progression within the [[coronary arteries|heart arteries]], most commonly resulting in a [[myocardial infarction|heart attack]] and ensuing debility. The heart arteries are difficult to track because
==Mechanism==
The healthy epicardial coronary artery consists of three layers, the [[tunica intima]], media, and [[adventitia]].<ref name=Emed>{{EMedicine|article|153647|Coronary Artery Atherosclerosis}}</ref><ref>{{cite journal |last1=Waller |first1=Bruce F. |last2=Orr |first2=Charles M. |last3=Slack |first3=John D. |last4=Pinkerton |first4=Cass A. |last5=Van Tassel |first5=James |last6=Peters |first6=Thomas |title=Anatomy, histology, and pathology of coronary arteries: A review relevant to new interventional and imaging techniques-Part I |journal=Clinical Cardiology |date=June 1992 |volume=15 |issue=6 |pages=451–457 |doi=10.1002/clc.4960150613 |pmid=1617826 |s2cid=12034096 |doi-access=free }}</ref> Atheroma and changes in the artery wall usually result in small [[aneurysm]]s (enlargements) just large enough to compensate for the extra wall thickness with no change in the lumen diameter. However, eventually, typically as a result of rupture of [[vulnerable plaque]]s and clots within the lumen over the plaque, [[stenosis]] (narrowing) of the vessel develops in some areas. Less frequently, the artery enlarges so much that a gross aneurysmal enlargement of the artery results. All three results are often observed, at different locations, within the same individual.<ref>{{
===Stenosis and closure===
Over time, atheromata usually progress in size and thickness and induce the surrounding muscular central region (the media) of the [[artery]] to stretch out, which is termed ''remodeling''. Typically,
[[File:Atheroma.jpg|thumb|302x302px|Narrowed arterial blood vessel blocked with an atheroma (artist's conception).]]
If the muscular wall enlargement eventually fails to keep up with the enlargement of the atheroma volume, or a clot forms and organizes over the plaque, then the
The [[endothelium]] (the cell monolayer on the inside of the vessel) and covering tissue, termed [[fibrous cap]], separate atheroma from the blood in the
While clots at the rupture site typically shrink in volume over time, some of the clot may become organized into fibrotic tissue resulting in narrowing of the artery
===Artery enlargement===
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==Histology==
The accumulation (swelling) is always in the '''tunica intima''', between the [[endothelium]] lining and the smooth muscle [[tunica media|middle layer]] of the artery wall. {{cn|date=February 2021}}While the early stages, based on gross appearance, have traditionally been termed [[fatty streaks]] by pathologists, they are not composed of [[fat cells]] but of accumulations of [[white blood cells]], especially [[macrophages]], that have taken up oxidized [[low-density lipoprotein]] (LDL).{{cn|date=February 2021}}
After they accumulate large amounts of cytoplasmic membranes (with associated high cholesterol content) they are called [[foam cell]]s. When foam cells die, their contents are released, which attracts more macrophages and creates an extracellular lipid core near the centre to inner surface of each atherosclerotic plaque. {{cn|date=February 2021}}
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Interventional and non-interventional methods to detect atherosclerosis, specifically '''[[vulnerable plaque]]''' (non-occlusive or soft plaque), are widely used in research and clinical practice today.{{cn|date=February 2021}}
[[Carotid]] [[Intima-media thickness]] Scan (CIMT can be measured by B-mode [[ultrasonography]]) measurement has been recommended by the [[American Heart Association]] as the most useful method to identify atherosclerosis and may now very well be the gold standard for detection.<ref>{{
[[Intravascular ultrasound]] is the current most sensitive method detecting and measuring more advanced atheroma within living individuals, but has had limited applications due to cost and body invasiveness.<ref>{{cite journal|title=American College of Cardiology Clinical Expert Consensus Document on Standards for Acquisition, Measurement and Reporting of Intravascular Ultrasound Studies (IVUS)|last1=Mintz|first1=Gary S.|last2=Nissen|first2=Steven E.|journal=[[Journal of the American College of Cardiology]]|date=April 2001|volume=37|issue=5|page=1485|doi=10.1016/S0735-1097(01)01175-5|pmid=11300468|doi-access=free|issn=0735-1097}}</ref><ref>{{cite journal|title=The Dilemma of Diagnosing Coronary Calcification: Angiography Versus Intravascular Ultrasound|last1=Tuzcu|first1=E. Murat|last2=Berkalp|first2=Berktan|last3=de Franco|first3=Anthony C.|last4=Ellis|first4=Stephen G.|last5=Goormastic|first5=Marlene|last6=Whitlow|first6=Patrick L.|last7=Franco|first7=Irving|last8=Raymond|first8=Russell E.|last9=Nissen|first9=Steven E.|journal=[[Journal of the American College of Cardiology]]|date=March 1996|volume=27|issue=4|
[[CT scan]]s using state of the art higher resolution spiral, or the higher speed [[Electron beam tomography|EBT]], machines have been the most effective method for detecting calcification present in plaque. However, the atheroma have to be advanced enough to have relatively large areas of calcification within them to create large enough regions of ~130 [[Hounsfield scale|Hounsfield units]] which a CT scanner's software can recognize as distinct from the other surrounding tissues. Typically, such regions start occurring within the heart arteries about 2–3 decades after atheroma start developing. The presence of smaller, spotty plaques may actually be more dangerous for progressing to acute [[myocardial infarction]].<ref>{{cite journal |last1=Ehara |first1=Shoichi |last2=Kobayashi |first2=Yoshiki |last3=Yoshiyama |first3=Minoru |last4=Shimada |first4=Kenei |last5=Shimada |first5=Yoshihisa |last6=Fukuda |first6=Daiju |last7=Nakamura |first7=Yasuhiro |last8=Yamashita |first8=Hajime |last9=Yamagishi |first9=Hiroyuki |last10=Takeuchi |first10=Kazuhide |last11=Naruko |first11=Takahiko |last12=Haze |first12=Kazuo |last13=Becker |first13=Anton E. |last14=Yoshikawa |first14=Junichi |last15=Ueda |first15=Makiko |title=Spotty Calcification Typifies the Culprit Plaque in Patients With Acute Myocardial Infarction: An Intravascular Ultrasound Study |journal=Circulation |date=30 November 2004 |volume=110 |issue=22 |pages=3424–3429 |doi=10.1161/01.CIR.0000148131.41425.E9 |pmid=15557374 |s2cid=11917149 |doi-access=free }}</ref>
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==Treatment==
{{More medical citations needed|section| date = October 2019 | reason = Out of ten points, only 4 are referenced, and among those only one is a primary, peer-reviewed reference. Without the medical refs, it's unclear how reliable each advised approach is pertaining to treating the disease, even if it is a good general advice}}
Many approaches have been promoted{{by whom|date=June 2014}} as methods to reduce or reverse<ref name=":0">{{cite news |title=Ask the doctor: Reversing atherosclerosis? |url=https://www.health.harvard.edu/heart-health/ask-the-doctor-reversing-atherosclerosis
* eating a diet of raw fruits, vegetables, nuts, beans, berries, and grains;<ref name=":0" /><ref name=":1" />
* consuming foods containing [[
* abdominal fat reduction;
* aerobic exercise;<ref name=":0" />
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* maintaining normal, or healthy, blood pressure levels;
* aspirin supplement
* mouse studies indicated that subcutaneous administration of [[cyclodextrin|oligosaccharide 2-hydroxypropyl-
==History of research==
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According to United States data, 2004, for about 65% of men and 47% of women, the first [[symptom]] of cardiovascular disease is [[myocardial infarction]] (heart attack) or sudden death (death within one hour of symptom onset).{{Citation needed|date=August 2009}}
A significant proportion of artery flow-disrupting events occur at locations with less than 50% [[Lumen (anatomy)|lumenal]] narrowing. [[Cardiac stress test]]ing, traditionally the most commonly performed
The sudden nature of the complications of pre-existing atheroma, [[vulnerable plaque]] (non-occlusive or soft plaque), have led, since the 1950s, to the development of intensive care units and complex medical and surgical interventions. [[Angiography]] and later [[cardiac stress testing]] was begun to either visualize or indirectly detect [[stenosis]]. Next came [[Coronary artery bypass surgery|bypass surgery]], to plumb transplanted [[vein]]s, sometimes [[arteries]], around the stenoses and more recently [[angioplasty]], now including [[stent]]s, most recently drug coated stents, to stretch the stenoses more open.{{citation needed|date=June 2014}}
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* {{cite journal |last1=Ornish |first1=D. |last2=Brown |first2=S.E. |last3=Billings |first3=J.H. |last4=Scherwitz |first4=L.W. |last5=Armstrong |first5=W.T. |last6=Ports |first6=T.A. |last7=McLanahan |first7=S.M. |last8=Kirkeeide |first8=R.L. |last9=Gould |first9=K.L. |last10=Brand |first10=R.J. |title=Can lifestyle changes reverse coronary heart disease? |journal=The Lancet |date=July 1990 |volume=336 |issue=8708 |pages=129–133 |doi=10.1016/0140-6736(90)91656-u |pmid=1973470 |s2cid=4513736 }}
* {{cite journal |last1=Gould |first1=K. Lance |last2=Ornish |first2=D |last3=Scherwitz |first3=L |last4=Brown |first4=S |last5=Edens |first5=RP |last6=Hess |first6=MJ |last7=Mullani |first7=N |last8=Bolomey |first8=L |last9=Dobbs |first9=F |last10=Armstrong |first10=WT |title=Changes in Myocardial Perfusion Abnormalities by Positron Emission Tomography After Long-term, Intense Risk Factor Modification |journal=JAMA |date=20 September 1995 |volume=274 |issue=11 |pages=894–901 |doi=10.1001/jama.1995.03530110056036 |pmid=7674504 }}
* {{cite journal |last1=Ornish |first1=Dean |last2=Scherwitz |first2=LW |last3=Billings |first3=JH |last4=Brown |first4=SE |last5=Gould |first5=KL |last6=Merritt |first6=TA |last7=Sparler |first7=S |last8=Armstrong |first8=WT |last9=Ports |first9=TA |last10=Kirkeeide |first10=RL |last11=Hogeboom |first11=C |last12=Brand |first12=RJ |title=Intensive Lifestyle Changes for Reversal of Coronary Heart Disease |journal=JAMA |date=16 December 1998 |volume=280 |issue=23 |pages=2001–7 |doi=10.1001/jama.280.23.2001 |pmid=9863851 |s2cid=21508600 }}
* {{cite journal |last1=Ornish |first1=Dean |title=Avoiding revascularization with lifestyle changes: the multicenter lifestyle demonstration project |journal=The American Journal of Cardiology |date=November 1998 |volume=82 |issue=10 |pages=72–76 |doi=10.1016/s0002-9149(98)00744-9 |pmid=9860380 }}
* {{cite journal |last1=Dod |first1=Harvinder S. |last2=Bhardwaj |first2=Ravindra |last3=Sajja |first3=Venu |last4=Weidner |first4=Gerdi |last5=Hobbs |first5=Gerald R. |last6=Konat |first6=Gregory W. |last7=Manivannan |first7=Shanthi |last8=Gharib |first8=Wissam |last9=Warden |first9=Bradford E. |last10=Nanda |first10=Navin C. |last11=Beto |first11=Robert J. |last12=Ornish |first12=Dean |last13=Jain |first13=Abnash C. |title=Effect of Intensive Lifestyle Changes on Endothelial Function and on Inflammatory Markers of Atherosclerosis |journal=The American Journal of Cardiology |date=February 2010 |volume=105 |issue=3 |pages=362–367 |doi=10.1016/j.amjcard.2009.09.038 |pmid=20102949 }}
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[[Category:Diseases of arteries, arterioles and capillaries]]
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