ライフサイエンスコーパス: fibrous cap

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

2 atrix that provides physical strength to the fibrous cap.

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

4 rast enhancement improves delineation of the fibrous cap.

5 nvestment and/or retention in the protective fibrous cap.

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

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

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

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

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

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

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

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

14 sis by favoring collagen accumulation in the fibrous cap.

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

16 plaque that had undergone ulceration of its fibrous cap.

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

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

19 and increased differentiation of SMCs in the fibrous cap.

20 behavior and provide tensile strength to the fibrous cap.

21 the formation or maintenance of a protective fibrous cap.

22 lipid core, intensive inflammation and thin fibrous cap.

23 an underlying necrotic core with a ruptured fibrous cap.

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

25 les the quantification of macrophages within fibrous caps.

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

27 plaque burden, large lipid content, and thin fibrous caps.

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

29 improved lesional efferocytosis, and thicker fibrous caps.

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

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

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

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

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

35 osis, increased plaque necrosis, and thinner fibrous caps - all signs of vulnerable plaques in humans

36 en with a well-formed necrotic core and thin fibrous cap and are metabolically active.

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

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

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

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

41 n an eccentric lesion that traverses a thick fibrous cap and ends in a small necrotic core.

42 at generate extracellular matrix to form the fibrous cap and hence stabilize plaques.

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

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

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

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

47 TREM2+ phenotype within border zones of the fibrous cap and necrotic core.

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

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

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

51 Thin fibrous caps and large lipid pools are important determi

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

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

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

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

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

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

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

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

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

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

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

63 nd a thicker extracellular matrix (ECM)-rich fibrous cap are more stable, but there are major ambigui

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

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

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

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

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

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

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

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

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

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

74 bated with calcifying EVs were used to mimic fibrous cap calcification in vitro, while an ApoE(-/-) m

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

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

77 f smooth muscle cells (SMC) and other ACTA2+ fibrous cap cells destabilizes atherosclerotic plaques a

78 part by impacting phenotypic transitions of fibrous cap cells.

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

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

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

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

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

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

85 gression and stabilize VPs by thickening the fibrous cap, decreasing atheroma and necrotic core volum

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

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

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

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

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

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

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

93 VSMCs in fibrous caps expressed markers of senescence (senescence

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

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

96 tomography (IVOCT) enables identification of fibrous cap (FC), measurement of FC thicknesses, and ass

97 BM showed improvements in necrotic core and fibrous cap formation and reduced NETs.

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

99 The contribution of secreted 25-HC to fibrous cap formation was analyzed using a smooth muscle

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

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

102 Our method accurately detected the fibrous cap from the detected lipid plaque.

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

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

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

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

107 A ruptured fibrous cap (HR: 4.91; 95% CI: 1.31-18.45; P = 0.018) an

108 e fibrous cap (RFC) and erosion of an intact fibrous cap (IFC) are the two predominant mechanisms cau

109 ables real-time detection of ACS with intact fibrous cap (IFC, plaque erosion) and ACS due to rupture

110 stic TREM2 antibody (4D9) markedly increased fibrous caps in both control and LAB mice, eliminating t

111 arly fibroatheroma with thick and protective fibrous caps in mice and humans.

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

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

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

115 formation while increasing the thickness of fibrous caps, indicating that it stabilized plaques.

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

117 Plaques with collagen-poor thin fibrous caps infiltrated by macrophages and lymphocytes

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

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

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

121 In ruptures, a thin fibrous cap is disrupted and associated with significant

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

123 ve a similar morphology, the overlying thick fibrous cap is intact, lined by endothelial cells, and d

124 However, plaque erosion with an intact fibrous cap is now responsible for about one third of AC

125 45 weeks, smooth muscle cell accumulation in fibrous caps is indistinguishable in the two groups.

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

127 rupture, which characteristically have thin fibrous caps, large lipid pools, and abundant foam cells

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

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

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

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

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

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

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

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

136 perlecan in the necrotic core as well as the fibrous cap of advanced human atherosclerotic lesions in

137 The fibrous cap of an atherosclerotic plaque may become thin

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

139 The fibrous cap of atherosclerotic plaques is composed predo

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

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

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

143 hin lesions as well as within the protective fibrous cap of the lesions.

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

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

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

147 ADAMTS7 expression was measured in fibrous caps of human carotid artery plaques.

148 t reduction of MIA3 protein in VSMCs in thin fibrous caps of late-stage atherosclerotic plaques compa

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

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

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

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

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

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

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

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

157 esions exceeds the protection exerted by the fibrous cap overlying the necrotic lipid core.

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

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

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

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

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

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

164 In ruptured lesions, maximal stress within fibrous cap (peak cap stress [PCS]: 174 67 vs. 52 42 kPa

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

166 We developed a fully automated method for fibrous cap quantification in IVOCT images, resulting in

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

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

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

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

171 Rupture of the fibrous cap (RFC) and erosion of an intact fibrous cap (

172 IFC, plaque erosion) and ACS due to ruptured fibrous cap (RFC, plaque rupture), facilitating the deve

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

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

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

176 vessels that may cause plaque hemorrhage and fibrous cap rupture.

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

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

179 immunohistochemistry, PCSK6 was localized to fibrous cap SMA+ cells and neovessels in plaques.

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

181 nockdown improved vessel wall morphology and fibrous cap stability.

182 reduced atherosclerotic burden, and promoted fibrous cap stability.

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

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

185 velocity (lipid-rich necrotic core content, fibrous cap structure, intraplaque hemorrhage), compleme

186 to have an associated threefold decrease in fibrous cap tensile stress compared to untreated control

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

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

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

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

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

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

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

194 =0.30), the number of continuous frames with fibrous cap thickness </=85 mum was higher in TCFA (6.5

195 TCFA was defined as a lesion with mean fibrous cap thickness <65 mum overlying a lipid arc >90

196 criteria: (1) lipid arc >=90(o), (2) minimum fibrous cap thickness <65 um, and (3) presence of either

197 rea <3.5 mm(2), Lipid arc >180 degrees , and fibrous cap thickness <75 um, similar to the CLIMA core

198 .4 kOmega vs. 7.2 +/- 1.0 kOmega, p = .019), fibrous cap thickness <=65 mum versus >65 mum (19.1 +/-

199 identified necrotic core area >=1.75 mm(2), fibrous cap thickness <=65 mum, and >=20 macrophages per

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

201 versus 12.5 degrees ) and increased minimum fibrous cap thickness (18.9 um versus 24.4 um).

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

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

204 on, lipid content reduction, and increase in fibrous cap thickness (ie, triple regression) are unknow

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

206 optical coherence tomography-derived minimal fibrous cap thickness (smaller values indicating thin-ca

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

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

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

210 Fibrous cap thickness and thin-cap fibroatheroma showed

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

212 rmore, our method showed a good agreement of fibrous cap thickness between two analysts with Bland-Al

213 volume by intravascular ultrasound, minimum fibrous cap thickness by optical coherence tomography, a

214 anges in percent atheroma volume and minimum fibrous cap thickness did not differ in relation to base

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

216 d that can detect lipidous plaque and assess fibrous cap thickness in IVOCT images.

217 den index within 4 mm reduction, and minimal fibrous cap thickness increase.

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

219 (1) a lipid arc at least 90 degrees , (2) a fibrous cap thickness less than 65 mum, and (3) either p

220 ssels (median area 1.53 mm(2)) with a median fibrous cap thickness of 62 mum.

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

222 o established vulnerability features such as fibrous cap thickness or macrophage infiltration.

223 lesional macrophage content while increasing fibrous cap thickness thus conferring plaque stability.

224 Mean change in minimal fibrous cap thickness was 62.67 mum with alirocumab vs 3

225 Fibrous cap thickness was not significantly different be

226 Fibrous cap thickness was significantly increased in Nog

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

228 terized by increased collagen deposition and fibrous cap thickness, along with a smaller necrotic cor

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

230 ding lumen area, lipid and calcium arcs, and fibrous cap thickness, and output segmented images and c

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

232 m), as well as a greater increase in minimum fibrous cap thickness, compared with placebo.

233 ified by morphometry and plaque stability by fibrous cap thickness, lipid accumulation, infiltration

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

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

236 h reduced plaque lipid content and increased fibrous cap thickness.

237 d by a larger necrotic core area and reduced fibrous cap thickness.

238 reduced oxidative stress, while maintaining fibrous cap thickness.

239 reduced oxidative stress, while maintaining fibrous cap thickness.

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

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

242 transcripts associated with inflammation and fibrous cap thinning and support further examination of

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

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

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

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

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

248 tomatically detected the outer border of the fibrous cap using a special dynamic programming algorith

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

250 Fibrous cap VSMCs exhibited markedly shorter telomeres c

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

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

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

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

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

256 cally, atherosclerotic plaque rupture of the fibrous cap was thought to be the main culprit in ACS.

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

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

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

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

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

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