ライフサイエンスコーパス: myocardial fibrosis

1 erized by increased lipid levels and diffuse myocardial fibrosis.

2 s-linking by LOX, the BAPN treatment reduced myocardial fibrosis.

3 congestive heart failure, hypertension, and myocardial fibrosis.

4 frequently demonstrate multiple patterns of myocardial fibrosis.

5 and exercise capacity that may be related to myocardial fibrosis.

6 T1 mapping was applied to assess diffuse myocardial fibrosis.

7 ium enhancement) and diffuse (by T1 mapping) myocardial fibrosis.

8 at have the potential to assess interstitial myocardial fibrosis.

9 rast enhancement was used to detect areas of myocardial fibrosis.

10 c magnetic resonance imaging is a marker for myocardial fibrosis.

11 T1 mapping are sensitive to the presence of myocardial fibrosis.

12 th factor-beta (TGF-beta), a key mediator of myocardial fibrosis.

13 of the LV myocardium as an index of diffuse myocardial fibrosis.

14 /-26 g/m(2); P=0.01), but the same degree of myocardial fibrosis.

15 cyte hypertrophy and disarray, and increased myocardial fibrosis.

16 stigated the molecular and cellular bases of myocardial fibrosis.

17 , increased ejection fraction, and decreased myocardial fibrosis.

18 en shown to be a surrogate marker of diffuse myocardial fibrosis.

19 ement MRI was acquired for identification of myocardial fibrosis.

20 tients, and is more pronounced in those with myocardial fibrosis.

21 n, a known contributor to the development of myocardial fibrosis.

22 n blood pressure, systemic inflammation, and myocardial fibrosis.

23 itium provides a noninvasive way to quantify myocardial fibrosis.

24 tricular (LV) volume, increased LV mass, and myocardial fibrosis.

25 ly constricted coronary arterioles and focal myocardial fibrosis.

26 integrin protein in the heart and displayed myocardial fibrosis.

27 IX levels in mice with thrombosis as well as myocardial fibrosis.

28 information beyond LV EF and the presence of myocardial fibrosis.

29 terized by myocyte hypertrophy and extensive myocardial fibrosis.

30 ell as diastolic dysfunction with increasing myocardial fibrosis.

31 increase in myocyte cross-sectional area and myocardial fibrosis.

32 riable results associated with the degree of myocardial fibrosis.

33 in disease the perforin+ mice develop severe myocardial fibrosis.

34 ased, in association with the development of myocardial fibrosis.

35 < .0001), indicating the presence of diffuse myocardial fibrosis.

36 1/ECV measures and variables associated with myocardial fibrosis.

37 may potentially reflect diffuse interstitial myocardial fibrosis.

38 not associated with the development of focal myocardial fibrosis.

39 scular effects, including the development of myocardial fibrosis.

40 ystolic dysfunction, cardiac hypertrophy and myocardial fibrosis.

41 rs of systemic and vascular inflammation and myocardial fibrosis.

42 s early transcriptional effects that lead to myocardial fibrosis.

43 n cardiac edema and a subsequent increase in myocardial fibrosis.

44 stigated the role of premature senescence in myocardial fibrosis.

45 echanism and potential therapeutic target in myocardial fibrosis.

46 to determine its pathophysiological role in myocardial fibrosis.

47 use of left ventricular (LV) dysfunction and myocardial fibrosis.

48 siderosis, myocardial perfusion, and diffuse myocardial fibrosis.

49 collagen regulation and thereby age-related myocardial fibrosis.

50 m enhancement images were acquired to detect myocardial fibrosis.

51 ngiotensin II (AngII)-mediated, hypertensive myocardial fibrosis.

52 and this was associated with a reduction in myocardial fibrosis (2.36+/-0.87 versus control 3.89+/-1

53 ischemia group had a significant increase in myocardial fibrosis (24+/-1.8% versus 14+/-1.1%, P<0.001

54 olume index (-5.8%, P=0.017), and noninfarct myocardial fibrosis (-5.6%, P=0.026) in comparison with

55 ation (68%), systolic dysfunction (46%), and myocardial fibrosis (67%); inferolateral negative T wave

56 isk of sudden death include the detection of myocardial fibrosis (a substrate for ventricular arrhyth

57 sy is the gold standard for the diagnosis of myocardial fibrosis, a number of circulating biomarkers

58 In patients with increased diffuse myocardial fibrosis, abnormal passive ventricular stiffn

59 d by 4-chamber dilation and in some patients myocardial fibrosis, abnormal perfusion reserve, diastol

60 In the absence of myocardial fibrosis, alphavbeta3 expression correlated s

61 nt (LGE) has emerged as an in vivo marker of myocardial fibrosis, although its role in stratifying su

62 At 1 year, the ICH group showed increased myocardial fibrosis and accelerated coronary vasculopath

63 Mechanical factors, myocardial fibrosis and alterations in cardiac myocyte p

64 bnormalities may reflect increase in diffuse myocardial fibrosis and are associated with diastolic LV

65 rocytes) are important to the development of myocardial fibrosis and are suggested to migrate to the

66 (progressive myocyte hypertrophy, increased myocardial fibrosis and attenuated responsiveness to bet

67 lar hypertrophy, cardiomyocyte disarray, and myocardial fibrosis and attenuates hypertrophic and prof

68 nd determine the association between diffuse myocardial fibrosis and diastolic dysfunction.

69 ociated miR-133a downregulation and improved myocardial fibrosis and diastolic function without affec

70 recent data examining the genetic aspects of myocardial fibrosis and further clarifies potential card

71 robust regenerative response with decreased myocardial fibrosis and improvement of left ventricular

72 TGF/CCN2 using a specific antibody decreases myocardial fibrosis and improves the left ventricular dy

73 nd pericardium, may explain the high rate of myocardial fibrosis and increased cardiac dysfunction in

74 to explore the relationship between diffuse myocardial fibrosis and indexes of diastolic performance

75 Evidence of diffuse myocardial fibrosis and is already present in children a

76 factor (CTGF/CCN2) expression to mediate the myocardial fibrosis and left ventricular dysfunction.

77 ormalities including diastolic dysfunctions, myocardial fibrosis and metabolic could be suppressed by

78 red neurogenesis in the brain and occasional myocardial fibrosis and minimized thymus development.

79 Low FT3 level is associated with myocardial fibrosis and perfusion/metabolism abnormaliti

80 semiquantitative histological assessment of myocardial fibrosis and positively correlated with nucle

81 erative left ventricular (LV) remodeling and myocardial fibrosis and postoperative remodeling and sym

82 ECG strain is a specific marker of midwall myocardial fibrosis and predicts adverse clinical outcom

83 ST2 and Gal-3 are promising biomarkers of myocardial fibrosis and remodeling in HF.

84 levels of galectin-3, a protein involved in myocardial fibrosis and remodeling, have been associated

85 roblast state and play a fundamental role in myocardial fibrosis and remodeling.

86 pathy (DCM) that is characterized by diffuse myocardial fibrosis and sudden death.

87 stopathological changes include interstitial myocardial fibrosis and the appearance of vacuolated car

88 ese findings are important to the biology of myocardial fibrosis and tissue repair.

89 correlates with histologic quantification of myocardial fibrosis and with ECV derived by using equili

90 Intramyocardial lipid levels, myocardial fibrosis, and cardiac function (measured on t

91 including myocardial aging, ischemic injury, myocardial fibrosis, and cardiomyocyte proliferation.

92 g to the development of cardiac hypertrophy, myocardial fibrosis, and congestive heart failure.

93 art appear similar; ventricular hypertrophy, myocardial fibrosis, and impairments in ventricular func

94 ity, augments circulating NP levels, reduces myocardial fibrosis, and improves LV function in the set

95 Systemic HTN induces LV hypertrophy, myocardial fibrosis, and isolated diastolic dysfunction

96 ations show an association between ischemia, myocardial fibrosis, and LV remodeling, providing suppor

97 enchymal rejection, neointimal vasculopathy, myocardial fibrosis, and macrophage infiltration.

98 , increased aortic stiffness correlates with myocardial fibrosis, and may represent another potential

99 nce (n=41), such as ventricular hypertrophy, myocardial fibrosis, and minor coronary artery disease,

100 y for the determination of cardiac function, myocardial fibrosis, and myocardial lipid content.

101 educed left ventricular longitudinal strain, myocardial fibrosis, and pulmonary hypertension.

102 erse left ventricular remodeling, noninfarct myocardial fibrosis, and serum biomarkers of systemic in

103 ed a novel locus for cardiomyopathy, diffuse myocardial fibrosis, and sudden death to chromosome 10q2

104 cular sections, microvascular density (MVD), myocardial fibrosis, and their relationship were quantif

105 ation by mononuclear cells, mild to moderate myocardial fibrosis, and various vascular changes rangin

106 f cardiac function, myocardial inflammation, myocardial fibrosis, aortic stiffness, and pericardial f

107 Left ventricular dilation and myocardial fibrosis are associated with increased blood

108 trate that patients with PA exhibit frequent myocardial fibrosis as demonstrated by late gadolinium e

109 1 mapping can noninvasively quantify diffuse myocardial fibrosis as extracellular volume fraction (EC

110 In patients with HCM, myocardial fibrosis as measured by late gadolinium enhan

111 Diffuse myocardial fibrosis, assessed by CMR-derived T1 mapping,

112 Diffuse myocardial fibrosis, assessed by post-contrast myocardia

113 th asymptomatic MR demonstrate a spectrum of myocardial fibrosis associated with reduced myocardial d

114 f mdx mice as young as 1 month, and detected myocardial fibrosis at 6 months.

115 Myocardial fibrosis at baseline was an independent indic

116 rker actually reflects histologically proven myocardial fibrosis before it is applied clinically.

117 to severely affected dystrophic dogs reduced myocardial fibrosis, blocked increased serum cardiac tro

118 cular volumes, function, and the presence of myocardial fibrosis by cardiac magnetic resonance imagin

119 Our objective was to ameliorate age-related myocardial fibrosis by disrupting collagen cross-linking

120 Myocardial fibrosis by late gadolinium enhancement was d

121 g macrophages are critical to AngII-mediated myocardial fibrosis by preventing the development of fib

122 lysin or phosphodiesterase 9 inhibition, and myocardial fibrosis by spironolactone.

123 Myocardial fibrosis can be visualized by late gadolinium

124 which can reduce ventricular hypertrophy and myocardial fibrosis, can improve diastolic function to a

125 Myocardial fibrosis caused by maladaptive extracellular

126 ge HCM cohort with no or only mild symptoms, myocardial fibrosis detected by CMR was associated with

127 Our aim was to determine whether myocardial fibrosis, detected by cardiovascular magnetic

128 In hypertrophic cardiomyopathy (HCM) myocardial fibrosis, detected by late gadolinium enhance

129 In conclusion, diffuse myocardial fibrosis, determined by ECV, is a common and

130 is factor (MHCsTNF mice) develop progressive myocardial fibrosis, diastolic dysfunction, and adverse

131 Myocardial fibrosis did not occur.

132 Yet, myocardial fibrosis does not seem to be detectable at a

133 -17A-deficient mice had reduced interstitial myocardial fibrosis, downregulated expression of matrix

134 6 versus 63+/-5%; P<0.05) and an increase in myocardial fibrosis (extracellular volume of 0.34+/-0.03

135 vessel number (55.3 vs 15.9%; P < 0.05), and myocardial fibrosis (grade 3.29 vs 1.8; P < 0.05).

136 Increased myocardial fibrosis has been detected in the endomyocard

137 Myocardial fibrosis has been shown to be reversible and

138 rent levels of lifelong physical activity on myocardial fibrosis has not been evaluated.

139 LV diastolic dysfunction in the presence of myocardial fibrosis has not previously been established.

140 cardiomyopathy (HCM), both with and without myocardial fibrosis, have altered aortic stiffness as as

141 g Ang II administration revealed progressive myocardial fibrosis, hypertrophy, and dysfunction in WT

142 udy was to evaluate the relationship between myocardial fibrosis identified by cardiac magnetic reson

143 tion of elderly patients, is correlated with myocardial fibrosis (ie, deposition of excess extracellu

144 s speckle-tracking echocardiography, diffuse myocardial fibrosis imaging, and absolute myocardial per

145 Myocardial fibrosis impairs cardiac function, in additio

146 ction (ECV) to discover and quantify diffuse myocardial fibrosis in 25 individuals with SCA (mean age

147 -enhanced MRI identified increased levels of myocardial fibrosis in 6, 9 and 12-month-old mdx mice, t

148 However, the relationship to myocardial fibrosis in a community-based population is u

149 n cardiac function, and a high prevalence of myocardial fibrosis in a contemporary group of asymptoma

150 for the presence of 6 distinct pattern(s) of myocardial fibrosis in addition to signal threshold-base

151 n of ET-1 biosynthesis significantly reduced myocardial fibrosis in allografts.

152 ECV may help characterize the development of myocardial fibrosis in HCM and ultimately assist in deve

153 Myocardial fibrosis in HCM is a progressive and fast phe

154 We assessed the presence and amount of myocardial fibrosis in HCM patients and prospectively fo

155 The prevalence of myocardial fibrosis in HCM was 70%.

156 relationship between peripheral markers and myocardial fibrosis in HCM.

157 the origin of collagen in the progression of myocardial fibrosis in human adult transplanted hearts.

158 Myocardial fibrosis in hypertensive heart disease remain

159 ross-talk is required for the development of myocardial fibrosis in inflammatory cardiomyopathy.

160 as been shown to quantify the full extent of myocardial fibrosis in noninfarcted myocardium.

161 can provide noninvasive evidence of diffuse myocardial fibrosis in patients referred for evaluation

162 , pattern, and prognostic significance of LV myocardial fibrosis in patients with AF.

163 4+/-8.0%) and diffuse (T1 time, 478+/-79 ms) myocardial fibrosis in patients with HCM, peripheral lev

164 ate the yet unknown clinical significance of myocardial fibrosis in patients with non-ischemic cardio

165 c dysfunction is associated with microscopic myocardial fibrosis in SCA mice, but the cause of diasto

166 Similarly, myocardial fibrosis in the absence of myocarditis or lef

167 nderlying mechanisms that drive the aberrant myocardial fibrosis in the models in which GSK-3beta is

168 The role of myocardial fibrosis in the prediction of sudden death an

169 wever, periostin peptide treatment increased myocardial fibrosis in the remote region at one week and

170 owed late gadolinium enhancement, indicating myocardial fibrosis, in 71% of subjects with overt hyper

171 Myocardial fibrosis increased with decreasing MVD in con

172 ltaPDZ nNOS expression significantly reduced myocardial fibrosis, inflammation and apoptosis.

173 Myocardial fibrosis is a common feature of many cardiomy

174 Myocardial fibrosis is a feature of many cardiac disease

175 Diffuse myocardial fibrosis is a hallmark of cardiomyopathy.

176 Myocardial fibrosis is a hallmark of hypertrophic cardio

177 Myocardial fibrosis is a hallmark of hypertrophic cardio

178 Myocardial fibrosis is a hallmark of hypertrophic cardio

179 Diffuse myocardial fibrosis is a novel mechanism that appears to

180 Myocardial fibrosis is a significant global health probl

181 hemic cardiomyopathy without history of CHF, myocardial fibrosis is a strong and independent predicto

182 Myocardial fibrosis is common in patients with chronic a

183 Myocardial fibrosis is identified frequently in HCM; how

184 Myocardial fibrosis is linked with adverse clinical outc

185 es offer noninvasive approaches to detecting myocardial fibrosis, ischemia, hypertrophy, and disorder

186 rized by progressive cardiac dysfunction and myocardial fibrosis late in the disease process.

187 dary endpoints included change in noninfarct myocardial fibrosis, left ventricular ejection fraction,

188 posttransplant cardiomyocyte hypertrophy and myocardial fibrosis likely contributes to these derangem

189 iecho short-axis spin-echo acquisition), and myocardial fibrosis (Look-Locker gradient echo).

190 as no association between blood pressure and myocardial fibrosis, LV mass was independently associate

191 ients; the reasons for this are unclear, but myocardial fibrosis may be important.

192 The reduction in myocardial fibrosis may be primarily responsible for the

193 AD), coronary microvascular rarefaction, and myocardial fibrosis may contribute to HFpEF pathophysiol

194 study was to evaluate whether biomarkers of myocardial fibrosis measurements 1 month after MI may pr

195 Although noninvasively detected myocardial fibrosis (MF) has clinical implications in hy

196 t ventricular function on the progression of myocardial fibrosis (MF) identified on cardiovascular ma

197 To investigate whether myocardial fibrosis (MF) is similarly prevalent both in

198 Quantifying myocardial fibrosis (MF) with myocardial extracellular v

199 ombosis and/or thromboembolism, but also for myocardial fibrosis mimicking human myocardial infarctio

200 EPL also decreased myocardial fibrosis, myocyte apoptosis, and the ratio of

201 LGE CMR suggestive of myocardial fibrosis occurs in the systemic RV of patient

202 ver 6 years of cardiomyocyte hypertrophy and myocardial fibrosis of the cardiac allograft in transpla

203 urpose of this study was to evaluate diffuse myocardial fibrosis of the left ventricle (LV) in patien

204 iabetic patients have increased interstitial myocardial fibrosis on histological examination.

205 d normally, without histological evidence of myocardial fibrosis or hypertrophy.

206 n ACI rats receiving 7 days of CsA exhibited myocardial fibrosis, perivascular inflammation, and inti

207 Assessment of myocardial fibrosis predicts both risk of sudden cardiac

208 Myocardial fibrosis, predominantly at the subepicardium

209 Myocardial fibrosis, predominantly in the basal inferola

210 are related to both replacement and diffuse myocardial fibrosis processes.

211 ly attenuated chronic alcohol intake-induced myocardial fibrosis, protein carbonyl formation, apoptos

212 Fatty infiltration and myocardial fibrosis provide limited value in children an

213 Myocardial fibrosis quantified by extracellular volume (

214 Ablating CCR2 signaling did confer myocardial fibrosis reductions, but these benefits were

215 mice demonstrated significant reductions in myocardial fibrosis relative to wild type, but this was

216 However, the mechanisms of Ang II-induced myocardial fibrosis remain to be clarified.

217 rdiomyopathy, its role on the development of myocardial fibrosis remains unclear.

218 ived from aged PAI-1-deficient mice revealed myocardial fibrosis resulting from excessive accumulatio

219 rofound post-MI pericardial inflammation and myocardial fibrosis, resulting in cardiomyopathy and dea

220 gradually increases over time, while percent myocardial fibrosis rises early and remains in a modestl

221 accounting for demographics (including age), myocardial fibrosis risk factors, and left ventricular e

222 Percent myocardial fibrosis rose early (1 to 2 months) posttrans

223 l delayed enhancement (MDE) (an indicator of myocardial fibrosis) sequences.

224 CAD, coronary microvascular rarefaction, and myocardial fibrosis than controls.

225 eased aortic stiffness) in HCM patients with myocardial fibrosis than in those without (9.66 +/- 6.43

226 induces PH with biventricular remodeling and myocardial fibrosis that can be detected and monitored u

227 03/+) mice developed neither hypertrophy nor myocardial fibrosis, the pathologic manifestations of HC

228 Myocardial fibrosis, total collagen, and the collagen ty

229 Myocardial fibrosis turnover after MI is associated with

230 natriuretic peptide as well as biomarkers of myocardial fibrosis (type 1 collagen telopeptide, aminot

231 cardioCEST MRI enables in vivo imaging of myocardial fibrosis using endogenous contrast mechanisms

232 onic volume overload in MR is a stimulus for myocardial fibrosis using T1-mapping cardiac MRI.

233 for early hypertension treatment to minimize myocardial fibrosis, ventricular hypertrophy, and arrhyt

234 es increased, consistent with the changes in myocardial fibrosis verified by pathology.

235 ium was harvested for analysis of perfusion, myocardial fibrosis, vessel function, protein expression

236 ognized as a potential therapeutic target in myocardial fibrosis via interactions with fibroblasts.

237 Median myocardial fibrosis was 8.5% (interquartile range, 5.7-1

238 In addition, myocardial fibrosis was also significantly greater (P<0.

239 Myocardial fibrosis was assessed from magnetic resonance

240 In this cohort of late Fontan survivors, myocardial fibrosis was common and associated with adver

241 actility in the ischemic territory, although myocardial fibrosis was decreased in both HCW and HCV.

242 Myocardial fibrosis was detected by late gadolinium enha

243 Myocardial fibrosis was detected to a significantly lowe

244 Myocardial fibrosis was determined with late gadolinium

245 iation between LA left atrium parameters and myocardial fibrosis was evaluated with the Student t tes

246 rdiac magnetic resonance; noninfarct related myocardial fibrosis was identified by a diffuse pattern

247 lation between either ARD or BRD and percent myocardial fibrosis was noted (r=0.37 and -0.39, respect

248 Myocardial fibrosis was present in 55 patients (72%) and

249 Histologically, loss of beta cells and myocardial fibrosis was present in the transgenic group

250 y intravascular ultrasound, and interstitial myocardial fibrosis was quantified at 1 year.

251 year, MMPs were evaluated, and interstitial myocardial fibrosis was quantified.

252 Myocardial fibrosis was related to conduction abnormalit

253 Any pattern of myocardial fibrosis was seen in 248 patients (78%) with

254 ent (TBPC), reflecting the degree of diffuse myocardial fibrosis, was calculated as a function of the

255 Age-adjusted ECV, a marker of myocardial fibrosis, was elevated in anthracycline-treat

256 ine a possible mechanism for the increase in myocardial fibrosis, we also measured levels of TGF-beta

257 Because DMD patients show myocardial fibrosis well before functional impairment, w

258 Pericardial effusions and myocardial fibrosis were 3 and 4x more common, respectiv

259 low at rest and during hyperemia (hMBF), and myocardial fibrosis were assessed with magnetic resonanc

260 function, response to dobutamine stress and myocardial fibrosis were assessed.

261 MR parameters that have been associated with myocardial fibrosis were related to older age in the MES

262 n (Ecc) and T1 time, a surrogate for diffuse myocardial fibrosis, were assessed with multivariable li

263 osclerosis, associated with perivascular and myocardial fibrosis, whereas none of the apoE-KO mice di

264 Cardiovascular magnetic resonance detects myocardial fibrosis, which appears as LGE after contrast

265 ardiomyopathy) is characterized by increased myocardial fibrosis, which impairs left ventricular rela

266 ent emergence of GSK-3beta as a regulator of myocardial fibrosis will also be discussed.

267 ere is severe pathology, particularly severe myocardial fibrosis with ventricular dilation, reminisce