Zeiher
It would be more likely the plaque is hard, stable plaque. Atherosclerosis continues to be one of the main subjects in pathology research. M.C.
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D.
Resnick
Libby
A.E. S.
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]. E.
Dirksen MT, van der Wal AC, van den Berg FM, van der Loos CM, Becker AE. A.C.
M.A. 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.
how you will use this image and then you will be able to add this image to your shopping basket. G.K. Falk E. Advanced lesions and acute coronary syndromes: a pathologist's view.
An adjacent tissue section shows accumulations of macrophages (red cells) at the rupture site. C.K. de Boer
Clarijs
A.E.
Disruptions in these cases were either deep ruptures (60%) (see also Fig. Baseline patient characteristics of the two groups are shown in Table Table2. Lark
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).
Tsukada
et al. Katz
K.D. Thrombin generated during episodes of local thrombosis is another stimulator of smooth muscle cell growth. Stable plaque formation in the human artery. Becker
H.
Brown
Ischemic stroke in the cerebral artery.
E.
van der Loos
et al. J.
L.
R.
Cell death leads to the spill of lipids and, hence, the enlargement of the soft lipid core [52]. Zhou
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. R.T. Lendon
Oxford University Press is a department of the University of Oxford. O.J. J.S.T. The atherectomy specimens are grouped according to the type of coronary syndrome. Moreover, 69% of deep plaque ruptures reaching into a lipid core were found in man, whereas in a previous study of the same group [32], 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. In mature human plaques these mechanisms have not been investigated thus far, but a recent study in our laboratory revealed a relationship between the direction of arterial flow and local differences in macrophage and smooth muscle cells densities in entire carotid artery plaques which were taken at autopsy. W.H. Farb
Fishbein
A concept, Influence of plaque configuration and stress distribution on fissuring of coronary atherosclerotic plaques, Comparing of histopatologic features of coronary lesions obtained from directional atherectomy in stable versus acute coronary syndromes, Comparison of coronary lesions obtained by directional atherectomy in unstable angina, stable angina and restenosis after either atherectomy or angioplasty, Clinically stable angina is not necessarily associated with histologically stable atherosclerotic plaques, Morphological characteristics of clinically significant coronary artery stenosis in stable angina, Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology, Distribution of circumferential stress in ruptured and stable atherosclerotic lesions: a structural analysis with histopathologic correlation, Atherosclerotic plaques are locally weakened when macrophage density is increased, The pathogenesis of atherosclerosis. et al. Atherosclerosis is a lipoprotein-driven disease that leads to plaque formation at specific sites of the arterial tree through intimal inflammation, necrosis, fibrosis, and … But they may become vulnerable, there is a risk of rupture and lead to thrombosis.
Filamentous bacteria (f) appear to be invading cocci microcolonies. Stable atherosclerotic plaque formation in the human artery, they tend to be asymptomatic. In a study on 20 thrombosed coronary arteries in our laboratory, the classical lipid-rich morphology was found indeed in 50% of the underlying ruptured plaques, but the other 50% had either a substantial fibrous cap (25% or more of the entire plaque thickness) or were almost completely fibrous in composition, albeit all with surface erosions [20]. Kearney
Accordingly, in extreme cases that occur at both ends of the spectrum, plaques may arise with a totally different cellular composition. M.R. Becker
van der Wal
33–42. Manderson
The most common of these manifestations is coronary heart disease, including stable angina pectoris and the acute coronary syndromes. Tigges
P. Dollery
Davies
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. Lendon et al.
Piek
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. A.C.
G.
S.
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. Avec la plaque stabilisatrice EuroGravel, vous obtenez très facilement une surface de gravier stable et sans traces. Stowers
Transforming growth factor beta (TGF-β) is one of the most potent stimulators of connective tissue production by smooth muscle cells [49]. A.
Giscombe
Isner
S.
McDonald
Cybulsky
{"152344379":{"content_id":"152344379","title":"Stable atherosclerotic plaque formation in the human artery, they tend to be asymptomatic. Triposkiadis F(1), Sitafidis G, Kostoulas J, Skoularigis J, Zintzaras E, Fezoulidis I. These lesions, which occur more often in younger individuals and in women, have less often or smaller foci of inflammation [32]. A.E. J.M.
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. 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.
No membership needed. E.C. C.L. C.E. 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]. II.
Glagov
J.G. In this large diameter vessel the process of plaque disruption and thrombosis is not ended by luminal occlusion, and may lead to extensive surface ulcerations comprising large areas of the aortic wall, as can be observed in many autopsy cases at older age.
P. Nikol
[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. E.L.
H.
In the test group, 29 and 80 frames were stable and unstable plaques, respectively. Maximum accumulation of Plaque takes place in 21 days.
3). Une plaque lithosphérique est une zone stable délimitée par des zones actives. Born
S.
(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). 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]. compared morphologic plaque features with the profile of risk factors of corresponding patients [79]. 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].
Initial plaque formation takes as long as 2 hours to start forming. J.
A.V. (B) Detail of the boxed area in (A). 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]. Expression of adhesion molecules on neovessels in atherosclerotic plaques.
F.D. But, despite this broad spectrum of clinical disease, most of the acute manifestations of atherosclerosis share a common pathogenetic feature: rupture of an atherosclerotic plaque [2–4]. et al. 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. R. van der Wal
Microvessels create an alternative and probably more easily accessible pathway for leukocytes to enter the so called ‘rupture prone’ sites of advanced plaques. M.I. Most plaques rupture at sites of high calculated circumferential stress, which is often at the periphery of eccentric plaques. Hansson
8 show a completely different cellular composition.
Plaque lithosphérique : zone stable faisant partie de la lithosphère à la surface de la Terre. van der Loos
M.J.
Holm
... intermittent claudication) may develop when stable plaques grow and reduce the arterial lumen by > 70%.
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. Holm
"Making plaque disappear is not possible, but we can shrink and stabilize it," says cardiologist Dr. Christopher Cannon, a Harvard Medical School professor. 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. These observations provide a link between lipids and inflammation, and furthermore could give at least one explanation why the lytic effects of inflammation are most prominent in lipid-rich plaques (Fig. Asmaa ROUILLI 2 1- Décrivez la répartition des roches métamorphiques dans la région d’Uzerche. Stable atherosclerotic plaque formation in the human artery, they tend to be asymptomatic. Ongoing inflammation or a rapid progression of growth due to thrombus organization could imply a progression to unstable syndromes [18, 42]. 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. Fragale
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). 8). Kovanen et al. 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. Becker
This atherosclerotic plaque contains almost solely smooth muscle cells (blue) nd is practically devoid of macrophages. van Suylen
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. A.
Wu
Bentz van de Berg
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). Smooth muscle cells increase the structural strength by producing the connective tissue matrix of a plaque. S. Sterpetti
But they may become vulnerable, there is a risk of rupture and lead to thrombosis. Rosenschein
Therefore, clinical stability does not always indicate biologic stability in terms of (absence of) inflammation and thrombus formation. Moreover, this study and several other atherectomy investigations documented fragments of thrombus in substantial numbers (up to 20%) of apparently stable plaques [16–18, 33, 41, 42].
Apoptosis of cells has been observed in atherosclerotic plaques and in restenosis lesions after PTCA [53, 54].
van der Wal
Atherogenesis: Unstable Plaque Formation Variant Image ID: 3377 Add to Lightbox.
On the other hand, the atheroma is soft, weak and highly thrombogenic. Most major blood-flow-stopping events occur at large plaques, which, prior to their … Ehsani
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. Smooth muscle cells produce by far most of the extracellular matrix components of a plaque, including collagens, elastin and various types of proteoglycans [48]. 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]. U.
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