ライフサイエンスコーパス: plaque rupture

1 Inflammation drives atherosclerotic plaque rupture.

2 ole for neovascularization in the process of plaque rupture.

3 ity (P=0.003) as an independent correlate to plaque rupture.

4 rosclerotic plaques, thereby contributing to plaque rupture.

5 gs may have implications for atherosclerotic plaque rupture.

6 n essential role in thrombus formation after plaque rupture.

7 clerotic plaques may help reduce the risk of plaque rupture.

8 od for detecting individuals at high risk of plaque rupture.

9 gh shear stress contributes significantly to plaque rupture.

10 There was no evidence of plaque rupture.

11 de have been shown to predict future risk of plaque rupture.

12 h normal vessels, where it may contribute to plaque rupture.

13 thrombosis and myocardial infarction without plaque rupture.

14 ptosis of macrophages limited to the site of plaque rupture.

15 s, contributing to arterial thrombosis after plaque rupture.

16 elated to exertion was associated with acute plaque rupture.

17 ation, and the acute coronary syndrome after plaque rupture.

18 processes associated with atherogenesis and plaque rupture.

19 re of tissue factor, such as during arterial plaque rupture.

20 d activity of MMP-9, an enzyme implicated in plaque rupture.

21 ation is considered one of the mechanisms of plaque rupture.

22 orphological characteristics associated with plaque rupture.

23 pathophysiologic triggers of atherosclerotic plaque rupture.

24 ysfunction promote thrombosis at the site of plaque rupture.

25 is of the natural history of atherosclerotic plaque rupture.

26 ry syndromes by altering the consequences of plaque rupture.

27 or coronary thrombogenicity in patients with plaque rupture.

28 s by these cells is thought to contribute to plaque rupture.

29 stabilize the plaque and reduce the risk for plaque rupture.

30 nd key morphological factors associated with plaque rupture.

31 with morphological features associated with plaque rupture.

32 laques is associated with increasing risk of plaque rupture.

33 xploit proteinases as therapeutic targets in plaque rupture.

34 with the potential to improve prediction of plaque rupture.

35 iple macrophage functions that could promote plaque rupture.

36 d to sufficient stress accumulation to cause plaque rupture.

37 feration and metastasis, and atherosclerotic plaque rupture.

38 isease, in particular aneurysm formation and plaque rupture.

39 owing percutaneous coronary interventions or plaque rupture.

40 f therapeutic strategies aimed at preventing plaque rupture.

41 tress pathways contribute to atherosclerotic plaque rupture.

42 rupture but also occurs in patients without plaque rupture.

43 fting the balance toward plaque stability vs plaque rupture.

44 p disruption, features associated with human plaque rupture.

45 crophages play a key role in atherosclerotic plaque rupture.

46 n 2 rodent models of vascular remodeling and plaque rupture.

47 ysfunction can result in apoptosis, favoring plaque rupture.

48 s through cell death is observed at sites of plaque rupture.

49 phage-mediated matrix degradation can induce plaque rupture.

50 ith plaque hemorrhage and may play a role in plaque rupture.

51 oci of macrophages and T cells compared with plaque ruptures.

52 ons have lesser degree of calcification than plaque ruptures.

53 Heart weight was higher in all cases of plaque rupture (519 +/- 109 g) than eroded plaque (381 +

54 Subclinical episodes of plaque rupture accelerate the progression of hemodynamic

55 cent luminal area stenosis was 78 +/- 12% in plaque rupture and 70 +/- 11% in superficial erosion (P

56 Considering the complex relationship between plaque rupture and acute coronary event risk suggested b

57 eir stable nature could mitigate the risk of plaque rupture and acute myocardial infarction.

58 ions leads to lesional necrosis and possibly plaque rupture and acute vascular occlusion.

59 ight into intrinsic features associated with plaque rupture and can enable the identification of high

60 tivation in humans may be causally linked to plaque rupture and cardiovascular events.

61 atherosclerosis is typically precipitated by plaque rupture and consequent thrombosis.

62 oronary atherosclerosis is the substrate for plaque rupture and coronary events.

63 coronary syndromes, which are usually due to plaque rupture and coronary thrombosis.

64 LVH is associated with plaque rupture and extent of disease in SCD in normotens

65 equent luminal obstruction include recurrent plaque rupture and healing and intraplaque neovasculariz

66 tion of new pathophysiologic determinants of plaque rupture and intracoronary thrombosis.

67 The probability of atherosclerotic plaque rupture and its thrombotic sequelae are thought t

68 Plaque rupture and platelet aggregation are pathogenetic

69 activity in lipid-rich atheroma may promote plaque rupture and precipitate acute coronary syndromes.

70 dicting an increased rate of atherosclerotic plaque rupture and restenosis after coronary/carotid int

71 le sensitivity and specificity for detecting plaque rupture and stroke.

72 ristics as a biomarker indicative of carotid plaque rupture and stroke.

73 tential as a diagnostic biomarker of carotid plaque rupture and stroke.

74 Atherosclerotic plaque rupture and subsequent acute events, such as myoc

75 ues suggests that VSMC apoptosis may promote plaque rupture and subsequent myocardial infarction.

76 atherosclerotic plaques, factors leading to plaque rupture and subsequent thrombosis, and their clin

77 (TF), molecules that probably contribute to plaque rupture and subsequent thrombus formation.

78 E06 measurements provide novel insights into plaque rupture and the potential atherogenicity of Lp(a)

79 intraplaque inflammation, a key mediator of plaque rupture and thromboembolism.

80 al circulation to the post-stenotic segment, plaque rupture and thrombosis at such sites may be clini

81 er than plaque size or stenosis severity, in plaque rupture and thrombosis have been recognized.

82 poptosis and autophagy play pivotal roles in plaque rupture and thrombosis of atherosclerotic lesions

83 Atherosclerotic plaque rupture and thrombosis underlie most myocardial i

84 rotic plaque deposition is distinct from MI (plaque rupture and thrombosis), and recent studies showe

85 atherosclerotic lesions are associated with plaque rupture and thrombosis, which are the most import

86 EP-1873, in an experimental animal model of plaque rupture and thrombosis.

87 are potentially relevant to atherosclerotic plaque rupture and thrombosis.

88 e coronary syndromes result from spontaneous plaque rupture and thrombosis.

89 be converted into an acute clinical event by plaque rupture and thrombosis.

90 evolving concepts in the pathophysiology of plaque rupture and thrombosis.

91 Areas of plaque rupture and thrombus are sites of predilection fo

92 Angioscopic plaque rupture and thrombus were independently associate

93 Nine rabbits (60%) developed plaque rupture and thrombus, including 25 thrombi visual

94 Plaque rupture and ulceration are common in women with m

95 cap of atherosclerotic plaques contribute to plaque rupture and, consequently, to thrombosis and myoc

96 e attenuated posterior capsule overlying the plaque ruptured and the lens nucleus subluxated into the

97 F uptake occurred at the site of all carotid plaque ruptures and was associated with histological evi

98 ined, closing the link between inflammation, plaque rupture, and blood thrombogenicity.

99 phages, closing the link among inflammation, plaque rupture, and blood thrombogenicity.

100 novel marker of plaque vulnerability, recent plaque rupture, and future cardiovascular risk.

101 often fatal complication of atherosclerotic plaque rupture, and recent evidence suggests that MCP-1

102 grading enzyme implicated in atherosclerotic plaque rupture, aneurysm formation, and other vascular s

103 d have shown that complex plaque anatomy and plaque rupture are more frequent in the presence of mark

104 The mechanisms of atherosclerotic plaque rupture are poorly understood.

105 asorum neovascularization, and mechanisms of plaque rupture are systematically evaluated.

106 t suggests that ACS patients are at risk for plaque rupture at multiple sites.

107 hemic myocardial injury on CMR may be due to plaque rupture but also occurs in patients without plaqu

108 that macrophages play a key role in inducing plaque rupture by secreting proteases that destroy the e

109 Flow-limiting plaque rupture can result in myocardial infarction, stro

110 The mean age at death was 53 +/- 10 years in plaque rupture cases versus 44 +/- 7 years in eroded pla

111 y thrombosis is dominated by atherosclerotic plaque rupture, complex pulsatile flows through stenotic

112 in vivo scenario permits an analysis of the plaque rupture consequences, eg, thrombosis.

113 nd necropsy studies suggest that the risk of plaque rupture correlates only weakly with the degree of

114 that HOCl-LDL exposed during atherosclerotic plaque rupture, coupled with low levels of primary agoni

115 difficult to quantify due to lack of in vivo plaque rupture data.

116 Sites of plaque rupture demonstrated a greater macrophage density

117 the clinical and angiographic correlates of plaque rupture detected by intravascular ultrasound (IVU

118 The frequency of plaque rupture/dissection was greater in culprit, noncul

119 onary occlusions to test our hypothesis that plaque ruptures do not occur uniformly throughout the co

120 n myocardial infarctions and atherosclerotic plaque rupture events in the coronary arteries has not b

121 Plaque rupture exposes thrombogenic components of the pl

122 sion, matrix metalloproteinase activity, and plaque rupture features in mice.

123 most common cause of coronary thrombosis is plaque rupture followed by plaque erosion, whereas calci

124 arized in five phases, from early lesions to plaque rupture, followed by plaque healing and fibrocalc

125 In the plaque-rupture group, 5 of 28 (18%) were women versus 11

126 Compared with control subjects, women with plaque ruptures had elevated TC (270 +/- 55 versus 194 +

127 Plaque rupture has dominated our thinking about ACS path

128 A number of triggers of plaque rupture have been identified.

129 Most plaque ruptures heal without causing symptoms, perhaps l

130 ed in mediating the tissue injury leading to plaque rupture; however, signals regulating their activa

131 tions that are implicated in atherosclerotic plaque rupture; however, the mechanisms that regulate fo

132 prit plaque in men dying during exertion was plaque rupture in 17 (68%) of 25 vs 27 (23%) of 116 men

133 eration and apoptosis that may contribute to plaque rupture in atherosclerosis.

134 tant role in atherosclerosis and its sequela plaque rupture in part by their secretion of matrix meta

135 Plaque rupture in this setting, if it occurs, is seconda

136 We report 300 plaque ruptures in 257 arteries in 254 patients.

137 We analyzed 80 plaque ruptures in 74 patients and compared culprit lesi

138 Independent predictors of culprit plaque ruptures in ACS patients were smaller minimum lum

139 tributes to MMP activation, and therefore to plaque rupture, in the artery wall.

140 Multiple factors influence plaque rupture, including the loss of vascular smooth mu

141 ol ratio (P=.002) were associated with acute plaque rupture, independent of age and other cardiac ris

142 In unstable coronary syndromes, plaque rupture initiates coagulation by exposing TF to b

143 menting coronary artery thrombosis caused by plaque rupture into cases with or without signs of conco

144 These data provide evidence that silent plaque rupture is a form of wound healing that results i

145 plaques lacking a superficial lipid core or plaque rupture is a frequent finding in sudden death due

146 Atherosclerotic plaque rupture is accompanied by an acute decrease in th

147 Persistent intracoronary thrombus after plaque rupture is associated with an increased risk of s

148 Plaque rupture is common.

149 These results may explain why plaque rupture is often apparent at sites with only mode

150 Although plaque rupture is responsible for most myocardial infarc

151 Atherosclerotic plaque rupture is the main cause of coronary thrombosis

152 While plaque rupture is the most frequent cause of coronary th

153 Plaque rupture is the precipitating pathophysiologic eve

154 ombosed lesion that most resembles the acute plaque rupture is the thin cap fibroatheroma (TCFA), whi

155 Carotid atherosclerotic plaque rupture is thought to cause transient ischemic at

156 The most important consequence of plaque rupture is thrombosis.

157 sudden coronary death, in particular, acute plaque rupture is unknown.

158 Atherosclerotic plaque rupture is usually a consequence of inflammatory

159 Although plaque rupture is usually hypothesized to be the predisp

160 lammation may play a role in coronary artery plaque rupture, it was hypothesized that NF-kappaB activ

161 Plaque rupture itself does not lead to symptoms.

162 It is not clear why some plaque ruptures lead to acute coronary syndromes (ACS) b

163 ly not causally related to the likelihood of plaque rupture leading to an acute coronary syndrome.

164 eved to result in cardiac arrhythmias and/or plaque rupture leading to death.

165 ents such as stenosis (leading to stroke) or plaque rupture (leading to myocardial infarction).

166 hic process is independently associated with plaque rupture, leading to coronary thrombosis.

167 The exposure of TF during plaque rupture likely induces acute thrombosis, leading

168 s that have previously been shown to predict plaque rupture locations accurately.

169 Percutaneous coronary intervention after plaque rupture may itself cause embolization and no-refl

170 in the men who died of acute thrombosis with plaque rupture (mean, 8.5+/-4.0) but only mildly elevate

171 Atherothrombi were classified as plaque ruptures (n=55) and plaque erosion (n=18); plaque

172 In the remaining 6 rabbits (control) without plaque rupture, no thrombus was observed on the MR image

173 Plaque ruptures occur with varying clinical presentation

174 Plaque rupture occurred not only in patients with unstab

175 Seven of 8 plaque ruptures occurred in women > 50 years of age vers

176 Plaque rupture of a fibrous cap with communication of th

177 ariate predictors of recurrent ischemia were plaque rupture on preprocedure angioscopy (p < 0.05, odd

178 h SMC damage, such as during atherosclerotic plaque rupture or balloon arterial injury.

179 Plaque rupture or erosion stimulates platelet activation

180 y of acute coronary syndromes often involves plaque rupture or fissure with platelet aggregation.

181 ease are primarily caused by atherosclerotic plaque rupture or fissuring and subsequent occlusive or

182 telet therapies in patients with spontaneous plaque rupture or intervention-associated plaque injury.

183 r macrophage apoptosis is essential to acute plaque rupture or is a response to the rupture itself re

184 ised lesions without macroscopic evidence of plaque rupture or thrombosis.

185 Plaque rupture or thrombus on preprocedure angioscopy or

186 Upon plaque rupture or vascular injury, tissue factor (TF) pr

187 vention of clinical sequelae associated with plaque rupture or vessel damage that exposes TF to blood

188 The search to find the location of future plaque ruptures or plaque erosions leading to myocardial

189 loproteinase-1, MMP-1) may determine whether plaques rupture or vessels develop stenosis.

190 effects on vascular function, plaque growth, plaque rupture, or thrombosis.

191 nd healed infarct (P = 0.03, OR 41), TC with plaque rupture (P = 0.02, OR 7), and hypertension with s

192 Angiographic ulceration was associated with plaque rupture (P=0.001), intraplaque hemorrhage (P=0.00

193 erogenesis and in the later stages of mature plaque rupture, particularly the transition of unstable

194 ct the earlier pathophysiologic processes of plaque rupture, platelet activation and resultant thromb

195 Plaque rupture/platelet aggregation precedes myocardial

196 It has been tacitly believed that plaque rupture (PR) is associated with angiographically

197 roma [TCFA]; n = 88), and disrupted plaques (plaque rupture [PR]; n = 102) from the hearts of 181 men

198 al cells (CEC) may provide a window into the plaque rupture process and identify a proximal biomarker

199 of molecular and cellular parameters driving plaque rupture-related events and the development of new

200 Macrophages, abundant at sites of plaque rupture, release proteinases that weaken plaques

201 The plaque rupture site contained the minimum lumen area (ML

202 Plaque rupture sites demonstrated a strong immunoreactiv

203 Furthermore, apoptosis at plaque rupture sites was more frequent than in areas of

204 In patients without plaque rupture, smooth muscle cells may be the thromboge

205 prototypical site of matrix degradation and plaque rupture, stained only weakly for TFPI-2 but inten

206 Intravascular ultrasound plaque rupture strongly correlated with complex angiogra

207 the plaque are independently correlated with plaque rupture, suggesting a contributory role for neova

208 the atherosclerotic plaque and contribute to plaque rupture, superimposed thrombosis, and acute coron

209 Development and use of a mouse model of plaque rupture that reflects the end stage of human athe

210 Plaque ruptures that expose larger areas of thrombogenic

211 n the vascular re-modelling events preceding plaque rupture (the most common cause of acute myocardia

212 ars in relating extracellular proteinases to plaque rupture, the cause of most myocardial infarctions

213 ammation is a determinant of atherosclerotic plaque rupture, the event leading to most myocardial inf

214 Atherosclerotic plaque rupture, the most important cause of acute cardio

215 In plaque ruptures, the fibrous cap was infiltrated by macr

216 lerotic plaque progression and contribute to plaque rupture, thereby interconnecting macroangiopathy

217 ew, animal models of spontaneous and induced plaque rupture, thrombosis, and hemorrhage and "vulnerab

218 cal analysis to predict acute events such as plaque rupture, to follow the progression of disease, an

219 was to assess whether diet-induced coronary plaque ruptures trigger atherothrombotic occlusions, res

220 rrent evidence suggests that a sole focus on plaque rupture vastly oversimplifies this complex collec

221 stics of coronary thrombosis associated with plaque rupture versus thrombosis in eroded plaques witho

222 The frequency and morphology of plaque rupture was compared in men dying at rest vs thos

223 Abrupt plaque rupture was excluded.

224 Plaque rupture was found in nearly 40% and late gadolini

225 Plaque rupture was then induced with the use of Russell'

226 Plaque rupture was triggered with Russell's viper venom

227 nflammatory response and proteolysis lead to plaque rupture, we have examined the role of cathepsin B

228 nflammatory factors associated with coronary plaque rupture, we hypothesized that obesity was associa

229 smoking) in addition to acute exertion with plaque rupture were determined.

230 characterized as thin-cap fibroatheromas or plaque rupture were more frequent in BMS (n = 7, 4%) tha

231 ve remodeling and calcified plaque with rare plaque ruptured were common in elderly people with acute

232 Plaque ruptures were detected during pre-intervention IV

233 on-ACS patients; both culprit and nonculprit plaque ruptures were studied in 6 of 54 ACS patients.

234 to thrombosis in stenotic arteries following plaque rupture, where local shear rates are extremely hi

235 cells, intimal thickening, angiogenesis and plaque rupture which are a result of atherosclerosis.

236 cated in the pathogenesis of atherosclerotic plaque rupture, which raises the possibility of the use

237 an acute clinical event by the induction of plaque rupture, which, in turn, leads to thrombosis.

238 a clinical syndrome consistent with existing plaque rupture who requires active therapy for the cardi

239 The association of plaque rupture with a smaller lumen area and/or thrombus

240 Most often, the culprit morphology is plaque rupture with exposure of highly thrombogenic, red

241 on of the lumen through gradual progression, plaque rupture with intraluminal thrombosis, or both.

242 Plaque rupture with subsequent thrombosis is recognized

243 Whether plaque rupture with thrombosis causes infarction, unstab

244 essels when matrix components are exposed by plaque rupture, with potentially disastrous results.