Coronary heart disease (CHD) and other manifestations of atherosclerosis were not among the most common causes of death until the beginning of the 20th century, but thereafter a dramatic increase was observed in industrialized countries, including Western Europe and the United States, peaking around 1960 to 1980.1 Comparable increases in the incidence of CHD have later occurred or are currently occurring in many other parts of the world mainly because of population growth and an increased avera…
However, in young patients and females, plaque erosions are a more common cause of coronary thrombosis underlying myocardial infarction . et al.
However, recently the neovascularisation at the base of the atheroma and in the shoulder parts of advanced plaques attracted renewed attention in this respect. Kume
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They have no clinical implications at least on the short term, but may stimulate plaque growth through thrombin and PDGF related stimulation of smooth muscle growth and matrix synthesis. vector art, clipart and stock vectors. Hansson
7 and Fig. The continued recruitment of T-cells and macrophages at sites of ‘dysfunctional endothelium’ appears to be a constant feature of lesion initiation and progression as it accentuates the chronic inflammatory nature of atherosclerosis .
Lathérosclérose est une atteinte fréquente, qui se développe avec lâge, a fortiori chez les personnes exposées à certains comportements liés à lhygiène de vie (sédentarité, tabagisme) et présentant des facteurs de risque cardiovasculaires (hypercholestérolémie, hypertension artérielle, ). (From Listgarten MA, Mayo HE, Tremblay R: Development of dental plaque on epoxy resin crowns in man. (Abstract). Katz
P.L. Asterisk is in the lipid core of the plaque. Becker
Même si la physiopathologie de la plaque d’athérome est commune, il s’agit donc bien de deux situations distinctes, résumées sur la figure 1. In this respect inflammation is closely related to a process of repair. Holm
Stable plaques also tend to have less inflammation than is present in unstable plaques. On the other hand, smooth muscle cell proliferations and collagen synthesis exert reparative and stabilizing effects. Tang
Any combination of cap thickness and atheroma size may occur. J.H.
An interesting relationship between the type of remodelling of the vessel wall and the tissue composition of the local plaque was found: lipid-rich plaques with many inflammatory cells were often associated with local arterial dilation.
et al. Fishbein
A clue to the mechanism of increased vasoreactivity of the culprit lesion in unstable angina, Differential expression of tissue factor protein in directional atherectomy specimens from patients with stable and unstable coronary syndromes, Macrophages, smooth muscle cells, and tissue factorin unstable angina. P.T. For example, phagocytosis of lipids is basically a protective mechanism, but unlimited uptake and foam cell death may lead to expansion of the soft atheroma. M.
et al. K.D. L.
de Boer OJ, van der Wal AC, Becker AE. The defining characteristics of a vulnerable plaque include but are not limited to: a thin fibrous cap, large lipid-rich necrotic core, increased plaque inflammation, positive vascular … This was in contrast to the overall morphology of the ruptured lesions, which was heterogeneous both with respect to plaque architecture (lipid or fibrous) and presence or absence inflammation . A.L. The plaque is largely fibrocellular/fibrosclerotic and contains only small deeply located atheromas (hematoxylin–eosin stain). Yao
Asmaa ROUILLI 2 1- Décrivez la répartition des roches métamorphiques dans la région d’Uzerche. Un article de la revue M/S : médecine sciences (Volume 20, numéro 3, mars 2004, p. 259-381) diffusée par la plateforme Érudit. (Anti-CD68/anti-α-actin immunodouble stain). Author information: (1)Department of Cardiology, Larissa University Hospital, Larissa, Greece. Loree
et al. The majority of coronary thrombi (∼75%) is caused by plaque rupture.1,2 Prototype of the rupture-prone plaque contains a large, soft, lipid-rich necrotic core with a thin and inflamed fibrous cap, so-called thin-cap fibroatheroma (TCFA) (Figure 1).3,4 Other common features include expansive remodelling, large plaque size, plaque haemorrhage, neovascularization, adventitial inflammation, and ‘spotty’ calcifications.4 Thin-cap fibroatheroma caps are usually <65 µm thick.4Figure 2 summarizes factors co… Aux limites, c’est-à-dire aux bordures des plaques a lieu une forte activité sismique et volcanique.
33–42. A.K. O.J. Ellis
Stable plaque formation in the cerebral artery stock vector 86283254 from Depositphotos collection of millions of premium high-resolution stock photos, vector images and illustrations. Asthénosphère : Partie du globe terrestre située sous la lithosphère, moins rigide mais pas liquide, qui s’étend jusqu’à 700 km. There is abundant anti HLA-DR reactivity on plaque cells indicating active inflammation. On the right side is a fibrous plaque. G.
"Making plaque disappear is not possible, but we can shrink and stabilize it," says cardiologist Dr. Christopher Cannon, a Harvard Medical School professor. Atherosclerosis continues to be one of the main subjects in pathology research. Le gravier ou les gravillons restent compacts grâce à la structure en nid d'abeilles de la plaque pour gravillons. In contrast, other plaques … Several mediators produced by activated T-lymphocytes and macrophages in plaques promote destabilizing effects. J Am Coll Cardiol 1998;31:420.
D. van der Wal
The intriguing complexity of its pathogenesis as well as the importance of its clinical sequelae provide a rationale for this .
Deep intimal tears which extend into the highly thrombogenic lipid core of lesions, and sometimes showing extrusion of parts of the atheroma are often associated with massive thrombus formation. Formation stable de plaques dans l'artère cérébrale, 86283254, parmi la collection de millions de photos stock, de dessins vectoriels et d'illustrations, de qualité supérieure et en haute définition, de Depositphotos. M.A. C.M.
Lendon et al. Ongoing inflammation or a rapid progression of growth due to thrombus organization could imply a progression to unstable syndromes [18, 42]. 7), and a fibrous lesion of which the cellular component consists almost solely of smooth muscle cells (typically stable, Fig. M.
It would be more likely the plaque is hard, stable plaque.
In conclusion, it appears that during the ongoing process of lesion formation, and also in mature clinically relevant plaques, two major tissue remodeling forces may be operative. Leucocyte recruitment in rupture prone regions of lipid-rich plaques: a prominent role for neovascularization? Libby
Armonk, NY: Futura Publishing Company, Inc, 1996, pp. Les phénomènes géologiques accompagnant la formation des chaines de montagnes et leur relation avec la tectonique des plaques Pr. Illustration about Stable plaque formation in the human artery.
The preference of inflammatory cells for lipid plaques as alluded to earlier is not coincidental, and presently there are several arguments in support of an intriguing relationship between lipids and inflammation. Farb
TGF-β and other growth factors, including platelet derived growth factor (PDGF) and basic fibroblast growth factor (bFGF), play an important role in wound healing and the reparative stage of many chronic inflammatory diseases. Atherosclerosis, the formation of life-threatening plaques in blood vessels, is a form of cardiovascular disease.
The recruitment appears to be specific for macrophages, T lymphocytes and mast cells [24–27], and the arterial endothelium covering the plaque surface is considered as the principal site of entrance for these cells . These biologic features of the plaque determine to a large extent whether or not a plaque will be vulnerable, and set the stage for rupture triggers to induce a rupture event. S.
M.R. R.D. (B) Detail of the boxed area in (A).
Moreover, the association between inflamed lipid lesions and local vessel dilation provides another clue why many mildly stenotic lesions do rupture. A.E.
Interesting clinicopathological correlations, demonstrating that inflammation can be seen as a marker for plaque instability. In human plaques, clusters of lymphocytes are regularly observed in close proximity of ceroid pigments , which are considered as an end product of lipid oxidation . van der Wal
•destruction of the underlying vessel wall → aneurysm formation → secondary rupture and / or thrombosis. E.P. de Boer
However, in the advanced lipid plaque which needs the support of an intact fibrous cap the same effect appears to be dangerous. Passeri
Microvessels create an alternative and probably more easily accessible pathway for leukocytes to enter the so called ‘rupture prone’ sites of advanced plaques. have provided a description of the histology of 448 plaques in coronary arteries of 54 men with stable angina. Slowly growing plaques expand gradually due to accumulation of lipid in foam cells and migration and proliferation of smooth muscle cells. 2 Stable and unstable plaques Atherosclerotic plaque formation results from complex cellular interactions in the intima of arteries, which take place between resident cells of the vessel wall (smooth muscle cells and endothelial cells) and cells of the immune system (leukocytes). Dirksen MT, van der Wal AC, van den Berg FM, van der Loos CM, Becker AE. These plaques tend to stabilize and are not prone to rupture. Basically the leukocytes have a protective function and serve in host defense by eliminating injurous agents, but their secretory products may also augment injury by damaging surrounding tissue components. Haudenschild
Patients with low serum levels of HDL and high LDL had more vulnerable plaques according to the criteria above. And search more of iStock's library of royalty-free vector art that features Anatomy … Moreno
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A.P. Studies using computer modeling of plaques have identified circumferential tensile stress on the fibrous cap as the most important intrinsic mechanical stress factor involved in plaque rupture [15, 21]. S.
J.H. The stenotic areas tend to become more stable despite increased flow velocities at these narrowings. L.D. How Doctors Measure Plaque Stability A CT scan can show how stable plaques are (American Journal of Roentgenology, March 2015;204(3):W249-W260). Carotid plaque composition in stable and unstable coronary artery disease.
Dental Plaque is defined as a BioFiolm of Structured Resilient Yellow Greyish substance that adheres to intra oral tooth surface or other hard surface in the oral cavity including removal and fixed restoration..
Atherosclerosis. (B) shows a detail of the erosion underneath the thrombus. An overall impression emerging from these investigations is that the biological (inflammatory) state of lesions must be considered of prime importance in determining the clinical outcome of patients with coronary atherosclerosis. Das
J.A. G.T. Escaned
The role of complex stenosis morphology, Immune and inflammatory mechanisms in the development of atherosclerosis, Inflammation in atherosclerotic plaques: a clinically crucial event, Molecular bases of acute coronary syndromes, Arterial smooth muscle: a multifunctional mesenchymal cell, Cytokines and growth factors positively and negatively regulate interstitial collagen gene expression in human vascular smooth muscle cells, Transforming growth factor B is increased in human vascular restenosis lesons, Molecular and cell biology of native coronary and vein graft atherosclerosis: regulation of plaque stability and vessel remodelling by growth factors and cell-extracellular matrix interactions, Apoptosis is abundant in human atherosclerotic lesions, especially in inflammatory cells (macrophages and T cells), and may contribute to the accumulation of gruel and plaque instability, Evidence for apoptosis in advanced human atheroma: co-localization with interleukin-beta converting enzyme, Apoptosis in human atherosclerosis and restenosis, Localization of stromelysin gene expression in atherosclerotic plaques by in situ hybridization, Increased expression of matrix metalloproteinases and matrix degrading activities in vulnerable regions of human atherosclerotic plaques, Matrix metalloproteinases and cardiovascular disease, Macrophage foam cells from experimental atheroma constitutively produce matrix degrading proteinases, Macrophages and ceroid in human atherosclerosis, Cell mediated immunity in atherosclerosis, Induction of T cell activation by oxidized low density lipoprotein, T lymphocytes from human atherosclerotic plaques recognize oxidized low density lipoprotein, Evidence of a local immune response in atherosclerosis CD4, Haemostatic risk factors for cardiovascular diseases, Morphology of the endothelium over atherosclerotic plaques in human coronary arteries, Factors influencing the presence or absence of acute thrombi insudden ischemic death, Plaque rupture with wevere preexisting stenosis precipitating coronary thrombosis: characteristics of coronary atherosclerotic plaques underlying fatal occlusive thrombi, Angiographic progression of coronary artery disease and the development of myocardial infarction, Five year follow up factors associated with progression of coronary artery disease in the Coronary Artery Surgery Study, Compensatory enlargment of human atherosclerotic coronary arteries, Paradoxical arterial wall shrinkage may contribute to luminal narrowing of human atherosclerotic femoral arteries, Remodelling of the atherosclerotic arterial wall: a determinant of luminal narrowing in human coronary arteries, The relation of arterial geometry with luminal narrowing and histological markers for plaque vulnerability: the remodeling paradox, Medial thinning and atherosclerosis B evidence for a local inflammatory effect, An overview of the quantitative influence of several risk factors on progression of atherosclerosis in young people in the United States, Coronary risk factors and plaque morphology in men with coronary disease who died suddenly, The PDAY Collaborating Investigators. R.J.A.G.M. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide, This PDF is available to Subscribers Only. formation de l’ Himalaya La lithosphère océanique qui séparait l’inde et l’Asie a été absorbée par une subduction, l’océan s’est fermé ; lorsque les deux lithosphères continentales se sont affrontées , l’inde a embouti le continent asiatique l’Himalaya s’est formé .
Smoking did not influence the composition of the plaques with respect to features of vulnerability, but appeared to be highly thrombogenic. The pathogenesis of coronary artery disease and the acute coronary syndromes. Molecular processes such as inflammation, lipid accumulation, apoptosis, proteolysis, thrombosis and angiogenesis have shown to be highly related with plaque vulnerability. Keaney
J.S.T. The atherectomy specimens are grouped according to the type of coronary syndrome. Discontinuity of the endothelium allows a contact between the blood stream and highly thrombogenic plaque materials (collagen fibrils and lipid debris insulated with Tissue Factor), which initiates activation of the coagulation system with at least some degree of thrombus formation 4. Unlimited phagocytosis of oxidized LDL by macrophages through scavenger receptors with a high ligand specificity for ox-LDL results in the formation of foam cells, which is another hallmark of atherosclerosis . Dental Pellicle forms within seconds after brushing. 5). Rosenschein
Although the major risk factors for coronary heart disease (age, gender, hypercholesterolemia, hypertension, smoking, diabetes) clearly correlate with the extent of plaque formation in coronary arteries , little is known about whether, and if so, how they influence the composition and vulnerability of plaques. High blood levels of cholesterol encourage the formation and growth of vascular plaques that put you at risk for heart attack and stroke.
Atherosclerosis is a lipoprotein-driven disease that leads to plaque formation at specific sites of the arterial tree through intimal inflammation, necrosis, fibrosis, and … G.V.R. Arrow to the right indicates the reparative effects of smooth muscle cells, leading to the formation of a stable fibrous plaque. X.
Fuster V, Badimon L, Badimon JJ, Chesebro JH.
It can be anticipated from the extensive experimental work in this field that local differences in arterial flow or shear stress over a bulging plaque surface may induce local variations in endothelial function (expression of adhesion molecules, production of growth factors) within one and the same plaque, with local differences in leukocyte recruitment and platelet adherence as a consequence [82–84]. Disruptions in these cases were either deep ruptures (60%) (see also Fig. N.
The disruption of atherosclerotic plaques and the subsequent formation of thrombi are currently recognized as the primary mechanisms of myocardial and cerebral infarctions (1). N.
C.E. The result is a reparative and stabilizing effect on the plaque structure [46, 47, 51].
S.M. But they may become vulnerable, there is a risk of rupture and lead to thrombosis. Chen
 tested the mechanical strength of human fibrous cap tissue and observed significantly reduced maximum stress at fracture when fibrous caps are infiltrated with macrophages. Recent investigations by this group give more insight in this paradoxical situation.
(Anti-CD68/anti-α-actin immunodouble stain). Henney
C.M. When compared with lesions underlying chronic stable angina, the lesions of patients with unstable coronary syndromes contain significantly larger amounts of inflammatory cells [17, 18, 33], including activated inflammatory cells, as indicated by the expression of HLA-DR molecules on cells .
Bentz van de Berg
On the other hand, lipid associated inflammation introduces tissue degrading effects. Carpenter
Larger, but apparently clinically silent ruptures have been observed also at autopsy in coronary arteries of 9% of persons who died of non-cardiac disease, increasing to 22% in those with diabetes or hypertension. G.
Atherosclerotic thrombosis Critical stenosis •demand ˃ supply •coronary artery circulation rest → adequate cardiac perfusion exertion → chest pain = stable angina •chronic arterial hypoperfusion: bowel ischemia, sudden cardiac death, chronic IHD, ischemic encephalopathy, in
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These lesions, which occur more often in younger individuals and in women, have less often or smaller foci of inflammation .
Lipid related inflammation in the plaque leads to degradation and weakening of the plaque tissue. Essentially clinically stable are fibrous plaques, composed of solid fibrous or fibrocellular tissue, and only small amounts of extracellular lipid or no lipid at all. Large mural thrombi due to large surface erosions or superficial fissures in the fibrous cap have found in many of the lesions underlying unstable angina. Zarins
A gradual increase in macrophage and T cell content can be noticed from the lesions of patients with chronic stable angina to the severest types of unstable angina. Maximum accumulation of Plaque takes place in 21 days. M.
Moreover, 69% of deep plaque ruptures reaching into a lipid core were found in man, whereas in a previous study of the same group , 69% of superficial erosions was reported in women (in plaques composed of smooth muscle cells and matrix proteins rather than lipids and macrophages), indicating sex-related differences in the type of rupture, which could have been the result of differences in plaque composition. Skalli
In both sections the same immunodouble staining is applied (anti-CD68/anti-α-actin immunodouble stain).
Vulnerable plaques. Piek
But they may become vulnerable, there is a risk of rupture and lead to thrombosis. In these retrospective comparative studies several histopathological parameters of plaque inflammation have been analyzed and quantified in tissue specimens of culprit lesions and correlated with the clinical status of the patient (either chronic stable angina or one of the various forms of unstable angina).
... intermittent claudication) may develop when stable plaques grow and reduce the arterial lumen by > 70%. J.H. J.Y.
In contrast, a gradual decline in the average tissue areas occupied is noticed in the same series of patients from stable angina to the severest types of unstable angina  (Fig. Hangartner
Syndromes of atherosclerosis. Lee
Apoptose et syndromes coronariens aigus.
An interesting relationship was seen between the amounts of inflammatory cells in the lesions and the severity of various unstable ischemic syndromes [18, 33, 40]. Schoneveld
There is focal accumulation of macrophages (red), creating a vulnerable site in the periphery of the fibrous cap.
D.B. (B) Adjacent section stained with Picro Sirius Red (collagen red, media yellow) shows a decrease in collagen density where the macrophages have accumulated. Burke
These external factors will not be discussed, but still some other plaque features require attention.
van der Loos
Search for other works by this author on: The pathogenesis of atherosclerosis: a perspective for the 1990s, Plaque fissuring the cause of acute myocardial infarction, sudden ischemic death and crescendo angina, Morphologic features of unstable atherothrombotic plaques underlying acute coronary syndromes, Significance of plaque ulceration in symptomatic patients with high grade carotid stenosis, A macro and microview of coronary vascular insult in ischemic heart disease, Stability and instability: two faces of coronary atherosclerosis, Lipoproteins and atherogenesis: current concepts, Evidence that the death of macrophage foam cells contributes to the lipid core of atheroma, Risk of thrombosis in human atherosclerotic plaque: role of extracellular lipid, macrophages and smooth muscle cell content, Fibrous and lipid-rich plaques atherosclerotic plaques are part of interchangeable morphologies related to inflammation B. This study revealed on the average larger tissue areas infiltrated with macrophages and larger amounts of lymphocytes in patients with unstable angina, and larger tissue areas occupied by smooth muscle cells in patients with stable angina. Stable plaque formation in the human artery.
Email this page; Link this page ; Print; Please describe! Illustration of Stable plaque formation in the human artery. Most of these are intra plaque hemorrhages, due to entrance of blood into the lipid core of the lesion and followed by healing of the rupture . In this paper, we analyze a simplified model of plaque growth to derive physically meaningful results about the growth of plaques. Gown
Fully developed plaques contain highly variable amounts of inflammatory cells, but largest concentrations can be found in lipid-rich lesions where they occupy the attenuated cap, the shoulder parts of the lesions or both [12, 13]. van der Loos
Z.S. T.O. Foam cell death plays an important role in the formation and growth of the atheroma, together with extracellular binding of lipids to collagen fibers and proteoglycans [10, 11].
Studies on experimental atheromas have endorsed these observations: isolated lipid laden macrophages obtained from the aortic wall of cholesterol fed rabbits spontaneously synthesize and release metalloproteinases, whereas alveolar macrophages derived from the same animals and under the same circumstances do not . Still, it is presently unclear what impact the various biologically active mediators released from eroded aortic surfaces may have on the human body. Xu c, Glagov S. clinical correlations of atherosclerosis: correlations of atherosclerosis: correlations of clinical and... Or a rapid progression of growth due to accumulation of T-cells macrophages and smooth muscle cells typically... Growth to derive physically meaningful results about the growth of native plaques and also of plaque.. Vulnerable lipid-rich plaque in a coronary artery disease loss associated with platelet thrombi are present the! 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