ライフサイエンスコーパス: fibrous cap

1 th macrophages in both the necrotic core and fibrous cap.

2 rast enhancement improves delineation of the fibrous cap.

3 nd by lumen-derived microvessels through the fibrous cap.

4 ome thrombi may occur without rupture of the fibrous cap.

5 ia compared with fibrous plaque or an intact fibrous cap.

6 ty by increasing the collagen content of the fibrous cap.

7 id core, many inflammatory cells, and a thin fibrous cap.

8 in the normal media as well as the plaque's fibrous cap.

9 evaluate therapy intended to "stabilize" the fibrous cap.

10 ruptured area of the plaques but not in the fibrous cap.

11 sis by favoring collagen accumulation in the fibrous cap.

12 agenous extracellular matrix of the plaque's fibrous cap.

13 plaque that had undergone ulceration of its fibrous cap.

14 that can contribute to the weakening of the fibrous cap.

15 icial, for example preventing rupture of the fibrous cap.

16 behavior and provide tensile strength to the fibrous cap.

17 lipid core, intensive inflammation and thin fibrous cap.

18 an underlying necrotic core with a ruptured fibrous cap.

19 plaques with a low-signal intensity core and fibrous cap.

20 atrix that provides physical strength to the fibrous cap.

21 he use of OCT for identifying macrophages in fibrous caps.

22 les the quantification of macrophages within fibrous caps.

23 improved lesional efferocytosis, and thicker fibrous caps.

24 nt resolution to identify thin (< 65 microm) fibrous caps.

25 vealed a distinct localization of miR-210 in fibrous caps.

26 s of regional formation of plaques with thin fibrous caps.

27 plaques in segments with low ESS had thinner fibrous cap (115 mum [63-166] versus 170 mum [107-219];

28 sus 853.4 +/- 570.8, P<0.001), and a thinner fibrous cap (70.2 +/- 20.2 microm versus 103.3 +/- 46.8

29 ologically characterized by a thin, inflamed fibrous cap, a dense lipid core, and mural thrombus.

30 Extracellular matrix loss in the fibrous cap, a prelude to rupture, is attributed to matr

31 a measure of the mechanical fidelity of the fibrous cap and can enable the identification of high-ri

32 areas, enhanced VSMC apoptosis, and reduced fibrous cap and collagen content.

33 in lipid-rich plaques with rupture of a thin fibrous cap and contact of the thrombus with a pool of e

34 as VSMC-specific TRF2 increased the relative fibrous cap and decreased necrotic core areas.

35 Specimens with thin fibrous cap and intense expression of CD3, CD68, and vas

36 s on facets of plaque development, including fibrous cap and lipid core formation.

37 ntraplaque hemorrhage with disruption of the fibrous cap and luminal thrombus.

38 th alpha smooth muscle actin (aSma)-positive fibrous cap and Mac3-expressing macrophage-like plaque c

39 A thicker fibrous cap and stiffer plaque that is less likely to ru

40 Higher signal on T2-W MRI identifies the fibrous cap and thrombus within AAA.

41 ce, who developed more advanced lesions (eg, fibrous caps and acellular areas).

42 Thin fibrous caps and large lipid pools are important determi

43 rlying most myocardial infarctions have thin fibrous caps and large necrotic cores; however, these fe

44 s of inflammation and more plaques had thick fibrous caps and no signs of inflammation, compared with

45 atients being treated with fish oil had thin fibrous caps and signs of inflammation and more plaques

46 c structural features of the atherosclerotic fibrous cap, and high-resolution microscopic and spectro

47 associated with larger lipid burden, thinner fibrous cap, and higher prevalence of thin-cap fibroathe

48 The integrity of the fibrous cap, and thus its resistance to rupture, depends

49 ement for this to occur is an extremely thin fibrous cap, and thus, ruptures occur mainly among lesio

50 m inefficient apoptotic cell clearance, thin fibrous caps, and focal inflammation.

51 ferocytosis, smaller necrotic cores, thicker fibrous caps, and increased ratio of proresolving versus

52 by their large necrotic cores, thin-inflamed fibrous caps, and positive remodeling.

53 unica media, the base of the plaque, and the fibrous cap are increased in ruptured atherosclerotic pl

54 containing large lipid pools with only thin fibrous caps are most at risk.

55 intraplaque haemorrhage, or thin or ruptured fibrous caps, are increasingly believed to be associated

56 esion size but markedly reduces the relative fibrous cap area in plaques and increases VSMC apoptosis

57 It also significantly increased fibrous cap area, reduced necrotic core area, and increa

58 esis, but alters plaque phenotype inhibiting fibrous cap areas in advanced lesions.

59 However, VSMC DNA damage reduced relative fibrous cap areas, whereas accelerating DSB repair incre

60 advance a hypothesis for the rupture of thin fibrous cap atheroma, namely that minute (10-mum-diamete

61 lesions with pathologic intimal thickening, fibrous-cap atheromas with cores in an early or late sta

62 esions with pathologic intimal thickening or fibrous-cap atheromas with cores in an early stage of ne

63 resulted in development of plaques with thin fibrous caps because of decreased smooth muscle cell mig

64 small microcalcifications within the plaque fibrous cap can lead to sufficient stress accumulation t

65 Rupture of the fibrous cap causes most fatal myocardial infarctions.

66 tudies that examine the relationship between fibrous cap changes and clinical outcome and to permit t

67 studies will determine the predictive value fibrous cap characteristics, as visualized by MRI, for r

68 The unique capabilities of OCT for fibrous cap characterization suggest that this technolog

69 The tear in the fibrous cap could be identified in 157 of 254 patients;

70 A tear in the fibrous cap could be identified in 59% of plaques; in 70

71 macrophage content and developed protective fibrous caps covering the plaque core.

72 rentiation and proliferation, and lesion and fibrous cap development.

73 poptosis, but increased collagen content and fibrous cap development.

74 e of the IEL as an independent predictor for fibrous cap disruption (P=0.0001).

75 well as increased lesion fibrin staining and fibrous cap disruption (P=0.06 for both).

76 Sudden fibrous cap disruption of 'high-risk' atherosclerotic pl

77 expression causes intraplaque hemorrhage and fibrous cap disruption, features associated with human p

78 Thickness of the fibrous cap emerged as the best discriminator of plaque

79 VSMCs in fibrous caps expressed markers of senescence (senescence

80 esonance imaging (CEMRI) have shown that the fibrous cap (FC) in atherosclerotic carotid plaques enha

81 stics of the necrotic core (NC) covered by a fibrous cap (FC), intraplaque hemorrhage (IPH), and calc

82 less mature, and have a reduced frequency of fibrous cap formation as compared with PDGF-B +/+ chimer

83 t prevent, accumulation of smooth muscle and fibrous cap formation.

84 Contrast enhancement helped discriminate fibrous cap from lipid core with a contrast-to-noise rat

85 l is capable of distinguishing intact, thick fibrous caps from intact thin and disrupted caps in athe

86 o be capable of distinguishing intact, thick fibrous caps from thin and ruptured caps in human caroti

87 ongly support the hypothesis that nearly all fibrous caps have microCalcs, but only a small subset ha

88 core, increased inflammatory milieu and thin fibrous caps, have been well characterized through patho

89 wed extensive macrophage infiltration of the fibrous cap, in particular at rupture sites contrary to

90 fine structure of the lesion, including the fibrous cap, in vivo.

91 reased plaque stability, including a thinner fibrous cap, increased necrotic core area, and increased

92 o rupture were defined as those with a thin, fibrous cap infiltrated by macrophages and were quantita

93 igatory component of plaque vulnerability is fibrous cap inflammation; molecular imaging is best suit

94 Cells of the fibrous cap, intima, and underlying media showed complet

95 mately 50% of mice, as well as disruption of fibrous caps, intraluminal thrombosis, neovascularizatio

96 MRI identification of a ruptured fibrous cap is highly associated with a recent history o

97 45 weeks, smooth muscle cell accumulation in fibrous caps is indistinguishable in the two groups.

98 ed with a high-risk plaque, including a thin fibrous cap, large necrotic core, macrophage infiltratio

99 hDTR Apoe-/- mice induced marked thinning of fibrous cap, loss of collagen and matrix, accumulation o

100 Of 21 IVOCT TCFAs (fibrous cap <65 mum, lipid arc >1 quadrant), only 8 were

101 by histology as presence of lipid pool, thin fibrous cap (<65 microm by ocular micrometry), and infla

102 between OCT and histological measurements of fibrous cap macrophage density (r=0.84, P<0.0001) and a

103 Macrophage degradation of fibrous cap matrix is an important contributor to athero

104 that subcellular microcalcifications in the fibrous cap may promote material failure of the plaque,

105 terized by a necrotic core with an overlying fibrous cap measuring <65 microm, containing rare smooth

106 for 16 weeks developed advanced lesions with fibrous caps, necrotic cores, and cholesterol clefts in

107 The fibrous cap of an atherosclerotic plaque may become thin

108 Increased biomechanical stresses in the fibrous cap of atherosclerotic plaques contribute to pla

109 The fibrous cap of atherosclerotic plaques is composed predo

110 farction, and also in the degradation of the fibrous cap of atherosclerotic plaques, thereby contribu

111 of enzymes that may cause degradation of the fibrous cap of coronary plaque; shear stress; circadian

112 ression, including in cells that compose the fibrous cap of the lesion and in medial cells in proximi

113 hat microcalcifications that form within the fibrous cap of the plaques lead to the accrual of plaque

114 cifications (microCalcs) >/= 5 microm in the fibrous caps of 22 nonruptured human atherosclerotic pla

115 lar matrix is the principal component of the fibrous caps of atherosclerotic plaques and intimal hype

116 in all plaques (r = 0.67, p < 0.001) and in fibrous caps of necrotic core fibroatheromas (r = 0.68,

117 asurement of birefringence in plaques and in fibrous caps of necrotic core fibroatheromas.

118 thin the vessel wall could digest and weaken fibrous caps of vulnerable plaques, thus provoking throm

119 ue containing large necrotic cores with thin fibrous caps often precipitates these acute events.

120 hick, (2) an intact, thin, or (3) a ruptured fibrous cap on MRI, gross, and histological sections.

121 h such plaques are considered to have a thin fibrous cap overlying a lipid pool, imaging modalities i

122 from rupture of a vulnerable plaque (a thin fibrous cap overlying a lipid-rich core), and 18 resulti

123 n the Western world, usually occurs when the fibrous cap overlying an atherosclerotic plaque in a cor

124 plication often culminates in rupture of the fibrous cap overlying this lipid core.

125 Ruptured plaques usually have thin fibrous caps overlying a large thrombogenic lipid core r

126 es was more frequent than in areas of intact fibrous cap (P = 0.028).

127 s with severe macrophage infiltration at the fibrous cap (P=0.0001) and at the shoulders of the plaqu

128 Nine patients had a fibrous cap pathologically, which was visualized as a di

129 Compared with patients with thick fibrous caps, patients with ruptured caps were 23 times

130 t macrophages were seen to accumulate in the fibrous cap, potentially promoting its focal erosion, as

131 Eu-P947 was particularly present in the fibrous cap region of plaques.

132 lls, vascular smooth muscle cells within the fibrous cap region of the plaque, and macrophages within

133 aque shoulders (1.6 +/- 1.1, p < 0.001), and fibrous cap regions (1.6 +/- 1.1, p < 0.001).

134 c lesion, to the rupture of the "vulnerable" fibrous cap, resulting in the acute coronary syndrome an

135 ymptomatic plaques had a higher incidence of fibrous cap rupture (P = .007), juxtaluminal hemorrhage

136 f coronary artery thrombosis with or without fibrous cap rupture in sudden coronary death is unknown.

137 Although fibrous cap rupture is the primary cause of coronary thr

138 tense lipid accumulation, inflammation, thin fibrous cap, severe internal elastic lamina degradation,

139 degrading proteases promotes thinning of the fibrous cap, severe internal elastic lamina fragmentatio

140 lating miR-210 in vitro and in vivo improved fibrous cap stability with implications for vascular dis

141 en, artery wall, and main plaque components; fibrous cap status (thick, thin, or ruptured); American

142 Calcification does not increase fibrous cap stress in typical ruptured or stable human c

143 enosis and has a large lipid core and a thin fibrous cap that is often infiltrated by inflammatory ce

144 a necrotic core and thinning of a protective fibrous cap that overlies the core.

145 osclerosis suggest that the thickness of the fibrous cap that overlies the necrotic core distinguishe

146 and cellular debris, typically covered by a fibrous cap that separates the thrombogenic core from th

147 onstrated an independent association between fibrous cap thickening and improved CEC that may contrib

148 e improved using lipid arc >/=80 degrees and fibrous cap thickness </=85 mum over 3 continuous frames

149 Combining VH-defined fibroatheroma and fibrous cap thickness </=85 mum over 3 continuous frames

150 =0.30), the number of continuous frames with fibrous cap thickness </=85 mum was higher in TCFA (6.5

151 ation (15.4% versus 34.4%; P=0.008), whereas fibrous cap thickness (105.2+/-62.1 versus 96.1+/-40.4 m

152 dality with sufficient resolution to measure fibrous cap thickness (FCT) in vivo.

153 Baseline OCT minimal fibrous cap thickness (FCT) was 100.9 +/- 41.7 mum, whic

154 ments of plaque collagen (R=0.73, P<0.0001), fibrous cap thickness (R=0.87, P<0.0001), and necrotic c

155 s in plaque morphology including increase in fibrous cap thickness and decrease in the prevalence of

156 ogy and gross tissue examination to identify fibrous cap thickness and rupture.

157 mulation of macrophages along with increased fibrous cap thickness and smooth muscle cell numbers.

158 Fibrous cap thickness and thin-cap fibroatheroma showed

159 f plaque stability, including an increase in fibrous cap thickness as compared to wild-type controls.

160 a larger area of calcification and increased fibrous cap thickness in complex lesions.

161 Because clinical assessment of fibrous cap thickness is not possible by noninvasive ima

162 source laser are often used for identifying fibrous cap thickness of plaques, yet cannot provide ade

163 Fibrous cap thickness was not significantly different be

164 On OCT, although minimal fibrous cap thickness was similar (71.8+/-44.1 mum versu

165 increased atherosclerosis, reduced relative fibrous cap thickness, and medial degeneration.

166 id arc, lipid-core length, lipid index (LI), fibrous cap thickness, and thin-cap fibroatheroma.

167 acute carotid stroke, including wall volume, fibrous cap thickness, number and location of lipid clus

168 The hierarchical importance of fibrous cap thickness, percent luminal stenosis, macroph

169 ncreased number of macrophages and decreased fibrous-cap thickness.

170 s features of plaque vulnerability including fibrous cap thinning and extensive necrotic core areas.

171 Potential mechanisms of fibrous cap thinning are also addressed, in particular e

172 s to determine whether MRI identification of fibrous cap thinning or rupture is associated with a his

173 mooth muscle actin-positive cell population, fibrous cap thinning, and decreased collagen content.

174 ity, including elastic fiber degradation and fibrous cap thinning, by heightening metalloprotease pro

175 important mechanism for formation of a thick fibrous cap to protect the atherosclerotic plaque from r

176 osclerotic lesion, RNA was prepared from the fibrous cap versus adjacent media of 13 patients undergo

177 Fibrous cap VSMCs exhibited markedly shorter telomeres c

178 median value of the minimum thickness of the fibrous cap was 47.0, 53.8, and 102.6 microm, respective

179 The appearance of the fibrous cap was categorized as (1) an intact, thick, (2)

180 Using previously reported MRI criteria, the fibrous cap was categorized as intact-thick, intact-thin

181 An atherosclerotic plaque with a fibrous cap was identified on 27 (42%) of 64 images of v

182 In plaque ruptures, the fibrous cap was infiltrated by macrophages in 100% and T

183 sions, the overall incidence of apoptosis in fibrous caps was significantly greater in ruptured plaqu

184 acrophage content and the presence of buried fibrous caps, were significantly reduced by RAdTIMP-2.

185 within lesions and SMC investment within the fibrous cap, which may result from impaired SMC migratio

186 ollagen content and a marked thinning of the fibrous cap, which suggests that plaque progression was

187 of cholesterol or necrotic debris and a thin fibrous cap with a dense infiltration of macrophages.

188 Plaque rupture of a fibrous cap with communication of the thrombus with a li