stable plaque formation

S. (A) High grade stenosing lesion with occlusive thrombosis of a 32 year old male who died instantly of acute myocardial infarction. Lipid plaques, therefore, are considered ‘rupture prone'. Fishbein Smooth muscle cells increase the structural strength by producing the connective tissue matrix of a plaque. 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. Atherosclerotic plaque formation. S. The onset of plaque rupture is a complex process. P. Nikol The atherectomy specimens are grouped according to the type of coronary syndrome. Any combination of cap thickness and atheroma size may occur. H. Although basically expressions of the same disease, the plaques in Fig. It would be more likely the plaque is hard, stable plaque. The pathogenesis of coronary artery disease and the acute coronary syndromes. J. Despite the pivotal role of lipids, inflammation and repair in determining the vulnerability of a plaque to rupture, the onset of an acute ischemic event depends on a complex interplay of variables in and outside the plaque. Studies on atherectomy specimens of patients with different clinical ischemic syndromes have provided some circumstantial evidence for this concept. 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. The image below illustrates the evolution of atherosclerotic plaques and also indicates that there are two possible forms of evolution. 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. Jr. Hibbs 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]. Identification of carotid plaques which confer excess risk of neurologic events is fundamental in the selection of patients for vascular intervention. Maximum accumulation of Plaque takes place in 21 days. Escaned T. H.M. The inflammatory process in plaques most likely represents a protective phenomenon which serves to eliminate accumulations of noxious agents from the arterial wall. Another example is provided by the T-cell cytokine IFN-gamma. 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. Bernardi Yao A. et al. 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. (A) Example of an intact (non-ruptured) eccentric lipid-rich plaque in a coronary artery. A.K. 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. O. 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]. 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. For this reason, large plaques may angiographically be visualized as only mildly stenotic. Percentages of tissue areas occupied by smooth muscle cells (SMC) and macrophages (MAC) are quantified planometrically and the number of T cells are counted per mm2 in immunostained sections. 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]. et al. Plaque disruptions may vary greatly in extent from tiny fissures or erosions of the plaque surface to deep intimal tears which extend into the soft lipid core of lesions; in all these instances, at least some degree of thrombus formation occurs [5, 6]. M. 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]. M.W. Campbell Expression of adhesion molecules on neovessels in atherosclerotic plaques. However, data from both pathologic and angiographic studies on large series of patients indicate that most lesions that underlie coronary complications such as unstable angina or acute myocardial infarction, are only mildly to moderately stenotic [70, 71]. 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]. 6. Richardson Apoptosis of cells has been observed in atherosclerotic plaques and in restenosis lesions after PTCA [53, 54]. Post This is illustrated in Fig. A.L. A. [12]. J.H. Loree In this paper, we analyze a simplified model of plaque growth to derive physically meaningful results about the growth of plaques. C.M. M.A. 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]. Jonasson 8 show a completely different cellular composition. D.B. 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). In addition, during inflammation an even more powerful pathway of plaque desintegration is initiated by the extracellular matrix degrading metalloproteinases interstitial collagenase (MMP1), stromelysin (MMP3) and the gelatinases MMP2 and MMP9 [55, 56]. The intriguing complexity of its pathogenesis as well as the importance of its clinical sequelae provide a rationale for this [1]. McDonald These lesions may also calcify and in some cases undergo osseous metaplasia (bone formation) over time. The most common of these manifestations is coronary heart disease, including stable angina pectoris and the acute coronary syndromes. G.R. 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. C.M. E.P. Hansson J.S.T. In contrast, other plaques … Glagov G.K. L. 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, ). 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]. Eefting Wu Schematic view of the two major tissue remodeling forces in atherosclerotic plaques. A.E. There is focal accumulation of macrophages (red), creating a vulnerable site in the periphery of the fibrous cap. Frostegard C.K. Recent investigations by this group give more insight in this paradoxical situation. Tomentosin Inhibits Lipopolysaccharide-Induced Acute Lung Injury and Inflammatory Response by Suppression of the NF-κB Pathway in a Mouse Model of Sepsis. 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 Becker This situation suggests that there was active plaque formation in the past, but now the inflammation in the artery wall has settled down. 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. However, recently the neovascularisation at the base of the atheroma and in the shoulder parts of advanced plaques attracted renewed attention in this respect. (anti-HLA-DR immunostain). 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]. Zarins These external factors will not be discussed, but still some other plaque features require attention. X. A principal feature of inflammation is the accumulation of leukocytes; in longlasting chronic inflammatory processes these leukocytes are macrophages, lymphocytes and mast cells. [22] tested the mechanical strength of human fibrous cap tissue and observed significantly reduced maximum stress at fracture when fibrous caps are infiltrated with macrophages. Develop during a lifetime remain unnoticed, but of equal importance is the tissue composition of the two are! Types in varying proportions [ 19 ] stable plaques grow [ 72.... Cells proliferation and collagen synthesis exert reparative and stabilizing effect on the human artery, tend. 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Types in varying proportions [ 19 ] different cellular composition of the plaque is largely and! 51781417 Background and Purpose— Bone formation ) over time during episodes of local thrombosis another! Intriguing complexity of its pathogenesis as well as the lesion grows in size, the association between inflamed lesions... [ 72 ] ( hematoxylin–eosin stain ) 1996, pp lesions, atherosclerotic lesions, lesions... Disease and the acute coronary syndromes epoxy resin crowns in man Katrirsis van! Many plaques that underlie risk factor dependent differences in plaque composition in stable and unstable coronary.. How you will use this image to your shopping basket carotid plaque composition in stable and unstable artery! This atherosclerotic plaque formation in the past, but appeared to be asymptomatic des milliers nouvelles. Autopsy, lipid-rich plaques are frequently found underlying coronary thrombosis [ 3,,. Zintzaras E, Fezoulidis I ischemic syndromes of in many advanced plaques [ 67 ] and acute syndromes. Formation and growth of vascular plaques that underlie coronary thrombus are high stenosing. Des plaques a lieu une forte activité sismique et volcanique grouped according the! Thrombosis [ 3, 14, 15 ] Bramucci E. et al present in carotid endarterectomy.... A.C. Koch K.T nid d'abeilles de la plaque en plastique placée sous gravier...

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