ライフサイエンスコーパス: plaque rupture

1 phage-mediated matrix degradation can induce plaque rupture.

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

3 een early, uncomplicated atherosclerosis and plaque rupture.

4 ole for neovascularization in the process of plaque rupture.

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

6 rosclerotic plaques, thereby contributing to plaque rupture.

7 gs may have implications for atherosclerotic plaque rupture.

8 n essential role in thrombus formation after plaque rupture.

9 ich than the fibrinous clots precipitated by plaque rupture.

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

11 Inflammation drives atherosclerotic plaque rupture.

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

13 gh shear stress contributes significantly to plaque rupture.

14 orphological characteristics associated with plaque rupture.

15 There was no evidence of plaque rupture.

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

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

18 thrombosis and myocardial infarction without plaque rupture.

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

20 s, contributing to arterial thrombosis after plaque rupture.

21 elated to exertion was associated with acute plaque rupture.

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

23 processes associated with atherogenesis and plaque rupture.

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

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

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

27 pathophysiologic triggers of atherosclerotic plaque rupture.

28 ysfunction promote thrombosis at the site of plaque rupture.

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

30 ry syndromes by altering the consequences of plaque rupture.

31 or coronary thrombogenicity in patients with plaque rupture.

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

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

34 ty that has been involved in atherosclerotic plaque rupture.

35 /- mice was studied in an inducible model of plaque rupture.

36 sis increases the risk of an atherosclerotic plaque rupture.

37 arily targeted at the prevention of coronary plaque rupture.

38 heroma (TCFA) is a prominent risk factor for plaque rupture.

39 is of the natural history of atherosclerotic plaque rupture.

40 nd key morphological factors associated with plaque rupture.

41 with morphological features associated with plaque rupture.

42 laques is associated with increasing risk of plaque rupture.

43 xploit proteinases as therapeutic targets in plaque rupture.

44 with the potential to improve prediction of plaque rupture.

45 iple macrophage functions that could promote plaque rupture.

46 d to sufficient stress accumulation to cause plaque rupture.

47 feration and metastasis, and atherosclerotic plaque rupture.

48 isease, in particular aneurysm formation and plaque rupture.

49 owing percutaneous coronary interventions or plaque rupture.

50 f therapeutic strategies aimed at preventing plaque rupture.

51 tress pathways contribute to atherosclerotic plaque rupture.

52 rupture but also occurs in patients without plaque rupture.

53 fting the balance toward plaque stability vs plaque rupture.

54 p disruption, features associated with human plaque rupture.

55 crophages play a key role in atherosclerotic plaque rupture.

56 ysfunction can result in apoptosis, favoring plaque rupture.

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

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

59 ons have lesser degree of calcification than plaque ruptures.

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

61 Subclinical episodes of plaque rupture accelerate the progression of hemodynamic

62 ute coronary syndromes (ACS), after coronary plaque rupture, accounting for approximately one-third o

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

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

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

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

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

68 in human endarterectomies is associated with plaque rupture and cardiovascular events.

69 osclerotic plaques, implying a lower risk of plaque rupture and cardiovascular events.

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

71 crophages predominate in the pathogenesis of plaque rupture and consequent thrombosis, but polymorpho

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

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

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

75 peripheral revascularization which involves plaque rupture and endothelial disruption confers very h

76 Although plaque rupture and erosion both initiate platelet activa

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

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

79 al pathways through which proteolysis causes plaque rupture and identify substrates that are cleaved

80 proaches in mouse models of protease-induced plaque rupture and in ruptured human plaques, we aimed t

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

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

83 Plaque rupture and platelet aggregation are pathogenetic

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

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

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

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

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

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

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

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

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

93 is primarily due to coronary atherosclerotic plaque rupture and subsequent thrombus formation.

94 flammatory vascular disorder, complicated by plaque rupture and subsequently atherothrombosis.

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

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

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

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

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

100 Atherosclerotic plaque rupture and thrombosis underlie most myocardial i

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

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

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

104 are potentially relevant to atherosclerotic plaque rupture and thrombosis.

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

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

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

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

109 Angioscopic plaque rupture and thrombus were independently associate

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

111 Plaque rupture and ulceration are common in women with m

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

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

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

115 flammation (an indicator of vulnerability to plaque rupture) and fibrosis (an indicator of plaque sta

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

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

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

119 major factor in the risk of atherosclerotic plaque rupture, and its evaluation remains challenging w

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

121 l, which can cause blood flow impairment, or plaque rupture, and ultimately lead to myocardial ischem

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

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

124 The mechanisms of atherosclerotic plaque rupture are poorly understood.

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

126 r, the molecular mechanisms that precipitate plaque rupture are unknown.

127 stress concentrations excellently predicted plaque rupture (area under the curve: 0.940 for PCS, 0.9

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

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

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

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

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

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

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

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

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

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

138 Sites of plaque rupture demonstrated a greater macrophage density

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

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

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

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

143 Plaque rupture exposes thrombogenic components of the pl

144 n) and ACS due to ruptured fibrous cap (RFC, plaque rupture), facilitating the development of potenti

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

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

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

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

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

150 Plaque rupture has dominated our thinking about ACS path

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

152 Thin-cap fibroatheroma (TCFA) and plaque rupture have been recognized as the most frequent

153 a cause of coronary thrombosis distinct from plaque rupture, have garnered recent interest.

154 Most plaque ruptures heal without causing symptoms, perhaps l

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

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

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

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

159 h-risk atherosclerotic features that portend plaque rupture in human coronary artery disease and may

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

161 plaque biomechanics, which in turn predicts plaque rupture in patients.

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

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

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

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

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

167 ify mechanisms that connect proteolysis with plaque rupture, including inflammation, basement-membran

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

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

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

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

172 6.2% (67/145) of participants, most commonly plaque rupture, intraplaque cavity, or layered plaque.

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

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

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

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

177 Plaque rupture is common.

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

179 Atherosclerotic plaque rupture is responsible for a majority of acute va

180 Although plaque rupture is responsible for most myocardial infarc

181 Atherosclerotic plaque rupture is the etiology of ischemic stroke and my

182 Atherosclerotic plaque rupture is the main cause of coronary thrombosis

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

184 Plaque rupture is the precipitating pathophysiologic eve

185 Plaque rupture is the proximate cause of most myocardial

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

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

188 The most important consequence of plaque rupture is thrombosis.

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

190 Atherosclerotic plaque rupture is usually a consequence of inflammatory

191 Although plaque rupture is usually hypothesized to be the predisp

192 The likelihood of a plaque rupturing is thought to be associated with its co

193 ocardial infarction (T1MI), which arises via plaque rupture, is essential, because treatment differs

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

195 Plaque rupture itself does not lead to symptoms.

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

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

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

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

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

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

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

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

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

205 , brachiocephalic, and carotid arteries with plaque rupture, MI, and stroke.

206 Accordingly, an inducible plaque rupture model of ApoE-/-Irf5-/- mice had signific

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

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

209 Plaque ruptures occur with varying clinical presentation

210 Plaque rupture occurred not only in patients with unstab

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

212 Atherosclerotic plaque rupture occurs at increased frequency in the earl

213 Plaque rupture occurs if stress within coronary lesions

214 Plaque rupture of a fibrous cap with communication of th

215 Historically, atherosclerotic plaque rupture of the fibrous cap was thought to be the

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

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

218 o acute clinical events upon atherosclerotic plaque rupture or erosion and arterial thrombus formatio

219 or myocardial infarction are atherosclerotic plaque rupture or erosion and, to a lesser extent, erupt

220 Plaque rupture or erosion stimulates platelet activation

221 laque histology was classified as either (i) plaque rupture or erosion, (ii) intraplaque haemorrhage,

222 e coronary syndromes (ACS) arise from either plaque rupture or erosion, but other mechanisms, includi

223 d plaque inflammation, and predisposition to plaque rupture or erosion.

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

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

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

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

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

229 Plaque rupture or thrombus on preprocedure angioscopy or

230 p thickness less than 65 mum, and (3) either plaque rupture or thrombus presence.

231 thickness <65 um, and (3) presence of either plaque rupture or thrombus.

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

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

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

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

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

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

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

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

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

241 Plaque rupture/platelet aggregation precedes myocardial

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

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

244 In human carotid atherosclerotic plaques, ruptures predominantly occurred in the proximal

245 The pathogenesis of plaque rupture probably does not pertain to superficial

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

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

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

249 and two mechanisms of MI, plaque erosion and plaque rupture, remain unclear.

250 Coronary plaque rupture remains the prominent mechanism of myocar

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

252 Plaque rupture sites demonstrated a strong immunoreactiv

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

254 d significantly lower frequencies of carotid plaque ruptures, smaller necrotic cores, and less CD11c+

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

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

257 Intravascular ultrasound plaque rupture strongly correlated with complex angiogra

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

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

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

261 Plaque ruptures that expose larger areas of thrombogenic

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

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

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

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

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

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

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

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

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

271 Atherosclerotic plaque ruptures, triggered by blood flow-associated biom

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

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

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

275 Abrupt plaque rupture was excluded.

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

277 Principal component analysis confirmed plaque rupture was responsible for the greatest percenta

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

279 Plaque rupture was triggered with Russell's viper venom

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

281 thrombus formation stage on atherosclerotic plaque rupture, we hypothesized that factor V Leiden may

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

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

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

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

286 Plaque ruptures were detected during pre-intervention IV

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

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

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

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

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

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

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

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

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

296 Moreover, they do not undergo spontaneous plaque rupture with MI and stroke or do so at such a low

297 cardiovascular events, including spontaneous plaque rupture with MI and stroke.

298 Plaque rupture with subsequent thrombosis is recognized

299 Whether plaque rupture with thrombosis causes infarction, unstab

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