Repeated plaque ruptures, ones not resulting in total lumen closure, combined with the clot patch over the rupture and healing response to stabilize the clot is the process that produces most stenoses over time. A.C. S. (A) Example of an intact (non-ruptured) eccentric lipid-rich plaque in a coronary artery. Cybulsky Becker van der Wal G.K. (Anti-CD68/anti-α-actin immunodouble stain). However, recently the neovascularisation at the base of the atheroma and in the shoulder parts of advanced plaques attracted renewed attention in this respect. M.J. Fuster V, Badimon L, Badimon JJ, Chesebro JH. Apoptose et syndromes coronariens aigus. J.H. Mann Zhou Manderson X. Indeed, many plaques that underlie coronary thrombus are high grade stenotic lesions. Stable & Unstable Plaques. 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 [58]. 6. Once activated by plasmin or mast cell products, they initiate a cascade of proteolytic activities with a very broad substrate specificity, including all the extracellular matrix components of the fibrous cap [57]. A.J. G.T. Molecular and cellular mechanisms that underlie risk factor dependent differences in plaque composition, and related types of plaque disruption are not sufficiently understood. Patients with low serum levels of HDL and high LDL had more vulnerable plaques according to the criteria above. S. R. A.C. Initial plaque formation takes as long as 2 hours to start forming. E.L. (Abstract). Fibrous tissue provides the structural integrity of a plaque. T. By Tefi. Less well known are the quantitative differences in these structural components: histopathologic examinations of a large series of plaques have revealed substantial variations in the thickness of fibrous caps, in the size of atheromas, in the extent of dystrophic calcification and, as has been shown more recently, in the relative amounts of major cell types: and inflammatory cells [12, 13]. Apoptosis, an intrinsically programmed mode of cell death, can be activated by inflammatory mediators, and is recognized as a mechanism of foam cell death in plaques. Moreover, inflammation appears to be associated also with the initiation of plaque rupture, a notion derived from several clinicopathological investigations using autopsy materials and atherectomy specimens. Fisher D. Stemme Ongoing inflammation or a rapid progression of growth due to thrombus organization could imply a progression to unstable syndromes [18, 42]. During inflammation another series of events is initiated that must lead to the healing of injured tissue, either by regeneration or by scarring (fibrosis). Much attention has been devoted to the rate of luminal stenosis and plaque volume of lesions that underlie coronary thrombosis. J. Kaartinen Henney de Boer OJ, van der Wal AC, Becker AE. 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. A.I. In contrast, in small diameter vessels such as coronary arteries, occlusive thrombosis is a frequent and often fatal complication of plaque rupture, and even smaller not occluding thrombi may lead to clinical symptoms [5, 6]. - Acheter ce vecteur libre de droit et découvrir des vecteurs similaires sur Adobe Stock The most common of these manifestations is coronary heart disease, including stable angina pectoris and the acute coronary syndromes. Still, it is presently unclear what impact the various biologically active mediators released from eroded aortic surfaces may have on the human body. A.E. de Boer R.M. ... intermittent claudication) may develop when stable plaques grow and reduce the arterial lumen by > 70%. Normal CIMT and presence of plaque. et al. van der Loos Additional support for the influence of risk factors on plaque disruption stems from autopsies on diabetic patients with coronary thrombosis, which revealed erosion of the plaque surface as the most common type of plaque disruption (66% of diabetic infarct patients) [8]. They also observed dilation at sites of atherosclerotic plaques, but in other instances (plaques) shrinkage of the vessel wall leading to lumen narrowing could be objectivated [73, 74]. New insights have emerged on a possible role for inflammation and repair also in local arterial wall remodeling in terms of dilation and shrinkage, with consequences for the geometry of the entire vessel [75]. C.K. But they may become vulnerable, there is a risk of rupture and lead to thrombosis. G.R. Charlston A.C. van der Wal J.A. 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. Des milliers de nouvelles images de grande qualité ajoutées chaque jour. Smooth muscle cells increase the structural strength by producing the connective tissue matrix of a plaque. Kume van der Wal Plaque lithosphérique : zone stable faisant partie de la lithosphère à la surface de la Terre. Ellis Ischemic stroke in the cerebral artery. II. An adjacent tissue section shows accumulations of macrophages (red cells) at the rupture site. Atherosclerosis is a lipoprotein-driven disease that leads to plaque formation at specific sites of the arterial tree through intimal inflammation, necrosis, fibrosis, and calcification. M.I. Corley S.D. 2.10. In: Fuster V, editor. E.C. Gown Inflammation is involved in the formation and growth of a stable plaque but also plays an important role in the transformation into the unstable plaque by stimulating metalloproteinase, macrophages and thrombotic activity. A. In coronary arteries, therefore, plaque disruption has been studied most extensively, and a number of correlations have emerged between the morphology of the culprit plaques, the degree of thrombus formation and types of ensuing ischemic coronary syndromes of patients [5, 6, 8]. Interesting clinicopathological correlations, demonstrating that inflammation can be seen as a marker for plaque instability. Wakeley Whether a plaque tends to stability or instability will depend on which mechanism dominates the course of plaque formation in a given period of time. It might explain the angiographically detected rapid progression of stenosis and the onset of acute events in patients with stable angina who were placed on a waiting list for non-urgent coronary angioplasty [43, 44]. et al. (Pico Sirius red stain: collagen red). Richardson Circulation 1998 (in press). 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. G.K. Horrigan Resnick 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. This is illustrated in Figs. 5). Expression of adhesion molecules on neovessels in atherosclerotic plaques. (B) Adjacent section shows abundant stromelysin-1 (MMP3) staining of foam cell macrophages around the lipid core, and to a lesser extent some smooth muscle cells in the fibrous cap (anti-MMP3 immunostain). Lefvert Palmer Bohle In coronary arteries most of these lesions remain clinically silent, or on the long term, may lead to stable angina pectoris [5]. L’himalaya est le résultat de la collision de la plaque indienne et de la plaque eurasienne . S. This notion is of importance, since only specific types of lesions in this spectrum of morphologic variants appear to be associated with acute manifestations of atherosclerotic disease. et al. Koch M.Y. O.J. 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G.K. Falk E. Advanced lesions and acute coronary syndromes: a pathologist's view. 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). et al. Holm G. A.C. Most plaques rupture at sites of high calculated circumferential stress, which is often at the periphery of eccentric plaques. Hansson In early lesions and in restenosis lesions, smooth muscle cell apoptosis could have beneficial effects and promote regression, but in the fibrous cap of advanced lesions it introduces another potential of plaque destabilization through the loss of repair cells. How Doctors Measure Plaque Stability A CT scan can show how stable plaques are (American Journal of Roentgenology, March 2015;204(3):W249-W260). An observation of particular interest is that synthesis as well as lytic activity of these enzymes is most abundant in the lipid laden macrophages and in the extracellular space around lipid cores of plaques [56]. Apart from the undisputable role of atherosclerosis in abdominal aneurysm formation [7], mural thrombosis leads to a surprisingly low rate of clinically significant complications in these patients, although cholesterol emboli can be regularly found in their kidneys and skin at autopsy. Apoptosis of cells has been observed in atherosclerotic plaques and in restenosis lesions after PTCA [53, 54]. N.J. P. Mitchinson J.Y. Asthénosphère : Partie du globe terrestre située sous la lithosphère, moins rigide mais pas liquide, qui s’étend jusqu’à 700 km. Differences in histological composition inside the plaque and its relation to the geometry of the arterial wall have implications for the biomechanical properties of plaques. Becker D. van der Wal Bramucci Slowly growing plaques expand gradually due to accumulation of lipid in foam cells and migration and proliferation of smooth muscle cells. Passeri Leucocyte recruitment in rupture prone regions of lipid-rich plaques: a prominent role for neovascularization? J. 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. In situ immunophenotypic analysis suggesting an immune mediated response, Accumulation of activated mast cells in the shoulder region of human coronary atheroma, the predilection site of atheromatous rupture, Neovascular expression of E-selectin, intercellular adhesion molecule-1, and vascular adhesion molecule-1 in human atherosclerosis and their relation to intimal leukocyte content, Infiltrates of activated mast cells at the site of coronary atheromatous erosion or rupture in myocardial infarction, Activated inflammatory cells are associated with plaque rupture in carotid artery stenosis, Coronary plaque erosion without rupture into a lipid core: a frequent cause of coronary thrombosis in sudden coronary death, Macrophage infiltration in acute coronary syndromes: implications for plaque rupture, Identification of 92 Kd gelatinase in human coronary atherosclerotic lesions; association of active enzyme synthesis with unstable angina, Mast cell infiltration in acute coronary syndromes: implications for plaque rupture, The expression of angiotensin-1 converting enzyme in human atherosclerotic plaques is not related to the deletion/inserton polymorphism but to the risk of restenosis after coronary interventions, Tissue endothelin-1 immunoreactivity in the active coronary atherosclerotic plaque. et al. 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. H. van der Wal atherosclerosis detailed illustration. A.V. But they may become vulnerable, there is a risk of rupture and lead to thrombosis. The plaque is largely fibrocellular/fibrosclerotic and contains only small deeply located atheromas (hematoxylin–eosin stain). On the left side is a lipid-rich plaque. Stowers M.J. In both sections the same immunodouble staining is applied (anti-CD68/anti-α-actin immunodouble stain). Smooth muscle cells (blue) are in the media and focally in the fibrous cap where they cover the site of macrophage accumulation. E. And search more of iStock's library of royalty-free vector art that features Anatomy … Allen Weisenberg Intrinsic mechanical forces clearly contribute to the process of plaque rupture, but of equal importance is the tissue composition of the fibrous cap. Atherosclerotic plaque formation. Download royalty-free Atherosclerosis. On the other hand, the atheroma is soft, weak and highly thrombogenic. G.K. Farb J. Le gravier ou les gravillons restent compacts grâce à la structure en nid d'abeilles de la plaque pour gravillons. 7 and Fig. 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 [18]. Many research efforts have been devoted to the identification of such unstable plaques; this article tends to emphasize the central role of intrinsic plaque features in the process of plaque rupture and thrombosis. Moreno In the test group, 29 and 80 frames were stable and unstable plaques, respectively. N. G. C.L. van der Loos Image 38564558. On the other hand, lipids pools appear to be not the only determinant of plaque instability. Fibrosis related contraction (a well known phenomenon in wound healing) could explain why many highly stenotic lesions are fibrous. Arbustini The onset of plaque rupture is a complex process. M.A. et al. Atherosclerosis detailed illustration. Once an atherosclerotic plaque has formed, it shows the highly characteristic architecture of a fibrous cap encaging a central core of extracellular lipids and debris: the ‘atheroma'. Davies N. However, the actual sites of rupture were also influenced by variations in the mechanical strength of the fibrous cap due to accumulations of lipid-laden macrophages. M.J. Gimbrone Cybulsky H.M. The clinical significance of these findings is unknown. Pickering P.J.W. In another study which included 47 patients who died of myocardial infarction, a total of 103 ruptured plaques were identified and only 40 of these ruptures could be associated with the infarct related coronary thrombosis [69]. Pepper 81–104. 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 [18] (Fig. 8 show a completely different cellular composition. et al. S. Correlations between the cellular composition of atherectomy specimens taken from coronary culprit lesions and the corresponding clinical symptoms of 58 patients with ischemic coronary syndromes. 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… Kaartinen C.K. P.D. Isner Galis Bortman Arrow to the left indicates the destabilizing effects of lipids and inflammation, thus creating a vulnerable lipid-rich plaque. Les phénomènes géologiques accompagnant la formation des chaines de montagnes et leur relation avec la tectonique des plaques Pr. Stable plaque Unstable plaque Pathological intimal thickening Fibroatheroma Thin-cap fibroatheroma Fibrocalcific plaque Plaque rupture Plaque erosion Calcified nodule This is a preview of subscription content, log in to check access. These plaques tend to stabilize and are not prone to rupture. T. Carr Ball A. (A) High grade stenosing lesion with occlusive thrombosis of a 32 year old male who died instantly of acute myocardial infarction. Macrophage contents, visualized by immunostaining with anti-CD68, were found to be significantly higher in the upstream parts of plaques than in their downstream parts. 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.. Kovanen van der Loos Z.S. Hemodynamic factors such as local disturbances in flow velocity and alterations in shear stress form another risk factor for plaque initiation and growth [81]. G.V.R. P. Dollery R.Y. R.D. Virmani There is focal accumulation of macrophages (red), creating a vulnerable site in the periphery of the fibrous cap. Related keywords. Although basically expressions of the same disease, the plaques in Fig. In these plaques, easily accessible for quantitative investigations, a critical threshold for vulnerability to rupture of more than 50 volume percent of extracellular lipids was established by Davies et al. J. For this reason, large plaques may angiographically be visualized as only mildly stenotic. Rennick The so-called fibrin cap on the lesion matures. Thickening of the intima-media complex implies occult plaque formation, but plaque may, of course, be seen directly with ultrasound when it achieves sufficient size to protrude into the carotid artery lumen. ... Les manifestations de l'activité du globe terrestre (séismes, volcans, formation de montagnes ou d'océans) sont le résultat du mouvement des différentes plaques lithosphériques ou tectonique des plaques qui a souvent des conséquences désastreuses sur notre vie et notre environnement. 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. 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 [20]. C.C. Smooth muscle cells produce by far most of the extracellular matrix components of a plaque, including collagens, elastin and various types of proteoglycans [48]. P. However, in the PDAY investigations smokers had more lipids in their plaques, particularly oxidized lipoproteins, than non-smokers [80]. Cross-section of an atherosclerotic plaque, which is heavily infiltrated with macrophages (red) and contains only scarce smooth muscle cells (blue) in the fibrous cap (anti-CD68/anti-α-actin immunodouble stain). W. Kovanen et al. The stable plaques are less likely to rupture because they have a thick fibrous cap with a small lipid core (LC) area (van der Wal, 1999). 1). 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. Recent investigations by this group give more insight in this paradoxical situation. This view is illustrated in Fig. Atherosclerosis is a lipoprotein-driven disease that leads to plaque formation at specific sites of the arterial tree through intimal inflammation, necrosis, fibrosis, and … Bland (B) shows a detail of the erosion underneath the thrombus. 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 … Chen Hibbs 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). Keaney P.M. T.G. Stable atherosclerotic plaque formation in the human artery, they tend to be asymptomatic. S.M. J. Certainly, external factors including systemic thrombotic factors and ‘rupture triggers’ such as vasospasms or elevated blood pressure will play a role in the ultimate thrombotic occlusion of the vessel or reduction of flow between a critical threshold [6, 65, 66]. M.A. Haberbosch 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, ). A.H. J Am Coll Cardiol 1998;31:420. Holm Kolettis But, despite these differences an overlap in the extent of inflammation was noticed between the groups of stable and unstable patients; at least a number of stable patients had considerable amounts of inflammatory cells in their culprit lesions. Atherogenesis: Unstable Plaque Formation Variant Image ID: 3377 Add to Lightbox. T. The purpose of this study was to determine whether bone formation and extensive dystrophic calcification are associated with stable plaques and protective against ischemic vascular events. A.L. While unstable and vulnerable plaques have been characterized by several studies which indicate that they have a thin fibrous cap (< 65 µm) and its LC is substantial (Libby, 2001; Andrews et al., 2018). Role of smooth muscle cell death in advanced coronary primary lesions: implications for plaque instability, Biphasic pattern of cell turnover characterizes the progression from fatty streaks to ruptured human atherosclerotic plaques, Mechanisms of plaque rupture: mechanical and biologic interactions. In fact, most patients had mixtures of plaque types in varying proportions [19]. M.J. P.K. Cell death leads to the spill of lipids and, hence, the enlargement of the soft lipid core [52]. Lipid plaques, therefore, are considered ‘rupture prone'. Dirksen MT, van der Wal AC, van den Berg FM, van der Loos CM, Becker AE. et al. Other findings of interest concern the various inflammatory products released by cells in unstable plaques: increased numbers of macrophages producing the proteolytic enzyme gelatinase B (MMP9) [34, 35], the inflammatory cytokine TNF- and tryptase-producing mast cells [28], vasoactive substances such as angiotensin I [36] and endothelin [37], larger amounts of the thrombosis initiator Tissue Factor [38, 39], and increased numbers of Interleukin-2 receptors on T cells (as marker for acute T cell activation in unstable lesions) [40]. G.C. Pathologic analysis of coronary atherectomy specimens allowed the further investigation of the relationship between plaque inflammation and acute plaque events, also in patients with less severe coronary artery disease. extended these observations by identifying in addition neutral proteases releasing mast cells as participants in the inflammatory process, providing another indication for active inflammation at rupture sites [30]. Lopez-Cuellar 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. In only 15% of these patients, all the plaques causing >50% stenosis were fibrous, while in 13% of patients virtually all plaques had a lipid core. Stable atherosclerotic plaque formation in the human artery, they tend to be asymptomatic. R. Stable atherosclerotic plaque formation in the human artery, they tend to be asymptomatic. 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