400:, the tests most commonly performed clinically with the goal of predicting susceptibility to future heart attack. In contrast to conventional angiography, cardiac CT angiography does enable visualization of the vessel wall as well as plaque composition. Some of the CT derived plaque characteristics can help predict for acute coronary syndrome. In addition, because these lesions do not produce significant stenoses, they are typically not considered "critical" and/or interventionable by interventional cardiologists, even though research indicates that they are the more important lesions for producing heart attacks.
422:) in portions of larger arteries closest to the skin, such as the carotid or femoral arteries. While stability vs. vulnerability cannot be readily distinguished in this way, quantitative baseline measurements of the thickest portions of the arterial wall (locations with the most plaque accumulation). Documenting the IMT, location of each measurement and plaque size, a basis for tracking and partially verifying the effects of medical treatments on the progression, stability, or potential regression of plaque, within a given individual over time, may be achieved.
411:, near-infrared spectroscopy, careful clinical follow-up, and other methods, to predict these lesions and the individuals most prone to future heart attacks. These efforts remain largely research with no useful clinical methods to date (2006). Furthermore, the usefulness of detecting individual vulnerable plaques by invasive methods has been questioned because many "vulnerable" plaques rupture without any associated symptoms and it remains unclear if the risk of invasive detection methods is outweighed by clinical benefit.
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431:''poor lipid plaque'' present in the stable plaque. In case of a vulnerable plaque, this results in a larger diameter of the Artery Lumen, which means that patient's life style is not affected, however, when the thin fibrous cap breaks, this causes a prompt activation of platelets which causes the occlusion of the artery, which causes a sudden heart attack if it occurs in the coronary artery.
22:
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185:, making it prone to rupture. Increased hemodynamic stress, e.g. increased blood pressure, especially pulse pressure (systolic blood pressure vs. diastolic blood pressure difference), correlates with increased rates of major cardiovascular events associated with exercise, especially exercise beyond levels the individual does routinely.
430:
The factors involved to promote either a vulnerable plaque or a stable plaque are not clear yet, however, the major differences between a vulnerable and stable plaque are that vulnerable plaques have a ''rich-lipid core'' and a ''thin fibrous cap'' in comparison with the ''thick fibrous cap'' and the
365:
downstream. In this, the usual situation, the debris obstruct smaller downstream branches of the artery resulting in temporary to permanent end artery/capillary closure with loss of blood supply to, and death of, the previously supplied tissues. A severe case of this can be seen during angioplasty in
281:
The macrophages sometimes become so overloaded with oxidized lipoprotein particles, the cholesterol contained therein and membrane-laden that they are called foam cells. Some of these cells die in place, releasing their fat and cholesterol-laden membranes into the intercellular space. This attracts
656:
Abela, GS; Kalavakunta, JK; Janoudi, A; Leffler, D; Dhar, G; Salehi, N; Cohn, J; Shah, I; Karve, M; Kotaru, VPK; Gupta, V; David, S; Narisetty, KK; Rich, M; Vanderberg, A; Pathak, DR; Shamoun, FE (31 August 2017). "Frequency of
Cholesterol Crystals in Culprit Coronary Artery Aspirate During Acute
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When this inflammation is combined with other stresses, such as high blood pressure (increased mechanical stretching and contraction of the arteries with each heart beat), it can cause the thin covering over the plaque to split, spilling the contents of the vulnerable plaque into the bloodstream.
298:
The clotting system reacts and forms clots both on the particles shed into the blood stream and locally over the rupture. The clot, if large enough, can block all blood flow. Since all the blood, within seconds, passes through 5-micrometre capillaries, any particles much larger than 5 micrometres
259:
particles become oxidized and this attracts macrophages that uptake the particles. This process typically starts in childhood. To be specific: oxidized lipoprotein particles in the artery wall are an irritant which causes the release of proteins (called
434:
Concerning stable plaques, the thick fibrous cap avoids the breaking risks, however, it reduces significantly the artery diameter which causes the cardiovascular problems related to the decreasing of vessel's diameter (this is determined by the
313:
The clot organizes and contracts over time, leaving behind narrowing(s) called stenoses. These narrowing(s) are responsible for the symptoms of the disease and are identified, after the fact, by the changes seen on
295:
Mechanical stretching and contraction of the artery, with each heart beat, i.e. the pulse, results in rupture of the thin covering membrane, spewing clot-promoting plaque contents into the blood stream.
288:
In some regions of increased macrophage activity, macrophage-induced-enzymes erode away the fibrous membrane beneath the endothelium so that the cover separating the plaque from blood flow in the
361:
Upon rupture, atheroma tissue debris may spill into the blood stream; this debris has cholesterol crystals and other material which is often too large (over 5 micrometers) to pass on through the
234:
Hyperlipidemia, hypertension, smoking, homocysteine, hemodynamic factors, toxins, viruses, and/or immune reactions results in chronic endothelial injury, dysfunction, and increased permeability.
403:
The tests most commonly performed clinically with the goal of testing susceptibility to future heart attack include several medical research efforts, starting in the early to mid-1990s, using
373:
rupture may allow bleeding from the lumen into the inner tissue of the atheroma, making the atheroma size suddenly increase and protrude into the lumen of the artery, producing lumen
32:
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While a single ruptured plaque can be identified during autopsy as the cause of a coronary event, there is currently no way to identify a culprit lesion before it ruptures.
455:), stay slender, eat a proper diet, quit smoking, and maintain a regular exercise program. Researchers also think that obesity and diabetes may be tied to high levels of
744:"The myth of the "vulnerable plaque": transitioning from a focus on individual lesions to atherosclerotic disease burden for coronary artery disease risk assessment"
597:
343:
within the plaque play a key role in splitting the plaque and also inducing inflammation. The sticky cytokines on the artery wall capture blood cells (mainly
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The cytokines induce the endothelial cells lining the artery wall to display adhesion molecules that attract immune-system white blood cells (to be specific,
302:
Most ruptures and clotting events are too small to produce symptoms, though they still produce heart muscle damage, a slow progressive process resulting in
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Another approach to detecting and understanding plaque behavior, used in research and by a few clinicians, is to use ultrasound to non-invasively measure
1135:
703:"Additive value of semi-automated quantification of coronary artery disease using cardiac CT-angiography to predict for future acute coronary syndrome"
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223:, in the walls of the arteries leads to the development of "soft" or vulnerable plaque, which when released aggressively promotes blood clotting.
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Smooth muscle cells migrate from the media to the intima, proliferate, and develop an extracellular matrix made up of collagen and proteoglycans.
188:
Generally an atheroma becomes vulnerable if it grows more rapidly and has a thin cover separating it from the bloodstream inside the arterial
347:) that accumulate at the site of injury. When these cells clump together, they form a thrombus, sometimes large enough to block the artery.
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Patients can lower their risk for vulnerable plaque rupture in the same ways that they can cut their heart attack risk: Optimize
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568:. Kumar, Vinay, 1944-, Abbas, Abul K.,, Aster, Jon C.,, Perkins, James A. (Ninth ed.). Philadelphia, PA. 2014.
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196:. However, a repeated atheroma rupture and healing is one of the mechanisms, perhaps the dominant one, that creates
173:, and intra-plaque hemorrhage. These characteristics together with the usual hemodynamic pulsating expansion during
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Because artery walls typically enlarge in response to enlarging plaques, these plaques do not usually produce much
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the slow clearance of injected contrast down the artery lumen. This situation is often termed non-reflow.
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264:) which attract monocyte white blood cells (white blood cells are the inflammatory cells within the body).
166:, large lipid-rich necrotic core, increased plaque inflammation, positive vascular remodeling, increased
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617:"Cholesterol crystal induced arterial inflammation and destabilization of atherosclerotic plaque"
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Janoudi, Abed; Shamoun, Fadi E.; Kalavakunta, Jagadeesh K.; Abela, George S. (1 July 2016).
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The defining characteristics of a vulnerable plaque include but are not limited to: a thin
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which explains how flow-rate is related to the radius of the vessel to the fourth power).
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The most frequent cause of a cardiac event following rupture of a vulnerable plaque is
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Current research and thinking relating to the formation of vulnerable plaques (see
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Myocardial
Infarction and Their Relation to Inflammation and Myocardial Injury".
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Moreno, P. R. (2010). "Vulnerable Plaque: Definition, Diagnosis, and
Treatment".
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block blood flow. (most of the occlusions are too small to see by angiography).
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Heart
Disease and Stroke Statistics – 2006 update, American Heart Association.
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The monocytes squeeze into the artery wall. Once inside, they transform into
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477:"Atherosclerotic plaque in arteries overview • Heart Research Institute"
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on top of the site of the ruptured plaque that blocks the lumen of the
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if you can. Unsourced or poorly sourced material may be challenged and
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contribute to a high mechanical stress zone on the fibrous cap of the
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539:"Vulnerable Plaque - Texas Heart Institute Heart Information Center"
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more macrophages and smooth muscle cell migration and proliferation.
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portion of the blood stream, are absorbed into the intima, past the
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of the artery lumen. Therefore, they are not detected by
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which will ingest the oxidized lipoprotein particles.
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patterns, keep blood glucose levels low normal (see
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243:particles, which carry fats (including the fat
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46:Please review the contents of the article and
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748:Journal of the American College of Cardiology
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211:Researchers have found that accumulation of
247:made by every human cell) within the water/
1136:Reproductive endocrinology and infertility
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596:: CS1 maint: location missing publisher (
1477:Bachelor of Medicine, Bachelor of Surgery
811:
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718:
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177:and elastic recoil contraction during
793:"Requiem for the 'vulnerable plaque'"
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1376:Physical medicine and rehabilitation
742:Arbab-Zadeh, A.; Fuster, V. (2015).
560:
558:
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701:Versteylen MO; et al. (2013).
1512:Medical Scientist Training Program
791:Libby, P.; Pasterkamp, G. (2015).
659:The American Journal of Cardiology
426:Vulnerable plaque vs stable plaque
14:
192:. Tearing of the cover is called
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1502:Doctor of Osteopathic Medicine
936:Oral and maxillofacial surgery
48:add the appropriate references
1:
671:10.1016/j.amjcard.2017.07.075
1482:Bachelor of Medical Sciences
1249:Neurosurgical anesthesiology
306:, the most common basis for
543:www.texasheartinstitute.org
377:or even total obstruction.
33:reliable medical references
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760:10.1016/j.jacc.2014.11.041
720:10.1016/j.jacc.2013.02.065
339:Recent studies have shown
1600:
514:10.1016/j.ccl.2009.09.008
437:Hagen–Poiseuille equation
292:becomes thin and fragile.
39:or relies too heavily on
1436:Transplantation medicine
1327:Clinical neurophysiology
1244:Obstetric anesthesiology
1164:Interventional radiology
924:Digestive system surgery
813:10.1093/eurheartj/ehv349
634:10.1093/eurheartj/ehv653
481:Heart Research Institute
405:intravascular ultrasound
308:congestive heart failure
1671:Cardiovascular diseases
1307:Intensive care medicine
1281:Mass gathering medicine
1126:Maternal–fetal medicine
899:Cardiothoracic surgery
800:European Heart Journal
621:European Heart Journal
304:ischemic heart disease
1550:Personalized medicine
1409:Reproductive medicine
1334:Occupational medicine
1288:Evolutionary medicine
600:) CS1 maint: others (
418:(usually abbreviated
1570:Traditional medicine
1530:Alternative medicine
1397:Addiction psychiatry
1211:Transfusion medicine
1206:Medical microbiology
1121:Gynecologic oncology
973:Reproductive surgery
394:cardiac stress tests
341:cholesterol crystals
255:lining, some of the
147:) in the wall of an
1592:History of medicine
1575:Veterinary medicine
1382:Preventive medicine
1234:Adolescent medicine
1076:Infectious diseases
322:, and treated with
129:atheromatous plaque
62:"Vulnerable plaque"
1540:Molecular oncology
1497:Doctor of Medicine
1487:Master of Medicine
1404:Radiation oncology
1276:Emergency medicine
1229:Addiction medicine
1196:Clinical chemistry
1191:Clinical pathology
983:Transplant surgery
941:Orthopedic surgery
919:Colorectal surgery
502:Cardiology Clinics
457:C-reactive protein
330:, with or without
171:neovascularization
131:– a collection of
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1492:Master of Surgery
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1441:Tropical medicine
1387:Prison healthcare
1302:Hospital medicine
1266:Disaster medicine
1256:Aviation medicine
1071:Hospital medicine
978:Surgical oncology
963:Pediatric surgery
957:
904:Endocrine surgery
806:(43): 2984–2987.
713:(22): 2296–2305.
707:J Am Coll Cardiol
665:(10): 1699–1707.
627:(25): 1959–1967.
213:white blood cells
133:white blood cells
125:vulnerable plaque
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1271:Diving medicine
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58:Find sources:
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29:This article
27:
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1560:Rural health
1545:Nanomedicine
1096:Rheumatology
1027: /
946:Hand surgery
931:Neurosurgery
803:
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409:thermography
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316:stress tests
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168:vasa-vasorum
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153:heart attack
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37:verification
30:
1630:Wikiproject
1419:Venereology
1364:Neonatology
1261:Dermatology
1116:Gynaecology
1108:gynaecology
1091:Pulmonology
909:Eye surgery
871:Specialties
508:(1): 1–30.
449:lipoprotein
398:angiography
363:capillaries
328:angioplasty
320:angiography
276:macrophages
253:endothelium
245:cholesterol
238:Lipoprotein
217:macrophages
164:fibrous cap
145:cholesterol
143:(including
137:macrophages
135:(primarily
31:needs more
1665:Categories
1392:Psychiatry
1378:(PM&R)
1371:Phlebology
1359:Pediatrics
1186:Anatomical
1151:Diagnostic
1131:Obstetrics
1081:Nephrology
1066:Hematology
1061:Geriatrics
1054:Hepatology
1039:Cardiology
1029:Immunology
548:2017-03-28
486:2024-08-29
463:References
443:Prevention
73:newspapers
1676:Neurology
1580:Physician
1464:education
1322:Neurology
1317:Narcology
1181:Pathology
1159:Radiology
1034:Angiology
998:Andrology
592:cite book
584:879416939
381:Detection
375:narrowing
345:platelets
269:monocytes
262:cytokines
219:, termed
207:Formation
1610:Category
1086:Oncology
1017:medicine
1015:Internal
863:Medicine
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778:25601032
729:23562925
679:28867129
643:26705388
522:19962047
407:(IVUS),
390:stenosis
371:atheroma
201:stenosis
183:atheroma
179:diastole
1650:Outline
1620:Commons
1565:Therapy
1462:Medical
1025:Allergy
993:Urology
886:Surgery
769:4344871
326:and/or
175:systole
87:scholar
52:removed
1640:Portal
1507:MD–PhD
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290:lumen
190:lumen
94:JSTOR
80:books
818:PMID
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725:PMID
675:PMID
639:PMID
602:link
598:link
580:OCLC
570:ISBN
518:PMID
318:and
66:news
35:for
956:ENT
874:and
808:doi
764:PMC
756:doi
715:doi
667:doi
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