ライフサイエンスコーパス: myocardial fibrosis

1 not associated with the development of focal myocardial fibrosis.

2 scular effects, including the development of myocardial fibrosis.

3 ystolic dysfunction, cardiac hypertrophy and myocardial fibrosis.

4 rs of systemic and vascular inflammation and myocardial fibrosis.

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

6 stigated the role of premature senescence in myocardial fibrosis.

7 echanism and potential therapeutic target in myocardial fibrosis.

8 to determine its pathophysiological role in myocardial fibrosis.

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

10 collagen regulation and thereby age-related myocardial fibrosis.

11 m enhancement images were acquired to detect myocardial fibrosis.

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

13 erized by increased lipid levels and diffuse myocardial fibrosis.

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

15 congestive heart failure, hypertension, and myocardial fibrosis.

16 frequently demonstrate multiple patterns of myocardial fibrosis.

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

18 T1 mapping was applied to assess diffuse myocardial fibrosis.

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

20 at have the potential to assess interstitial myocardial fibrosis.

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

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

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

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

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

26 cyte hypertrophy and disarray, and increased myocardial fibrosis.

27 stigated the molecular and cellular bases of myocardial fibrosis.

28 , increased ejection fraction, and decreased myocardial fibrosis.

29 ement MRI was acquired for identification of myocardial fibrosis.

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

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

32 ation may be a promising strategy to inhibit myocardial fibrosis.

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

34 itium provides a noninvasive way to quantify myocardial fibrosis.

35 acellular matrix remodeling and interstitial myocardial fibrosis.

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

37 ly constricted coronary arterioles and focal myocardial fibrosis.

38 integrin protein in the heart and displayed myocardial fibrosis.

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

40 ial ischemia, while chimpanzees are prone to myocardial fibrosis.

41 type-specific manner to control pathological myocardial fibrosis.

42 s early transcriptional effects that lead to myocardial fibrosis.

43 siderosis, myocardial perfusion, and diffuse myocardial fibrosis.

44 ation of myocardial NO and the occurrence of myocardial fibrosis.

45 /-26 g/m(2); P=0.01), but the same degree of myocardial fibrosis.

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

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

48 < .0001), indicating the presence of diffuse myocardial fibrosis.

49 1/ECV measures and variables associated with myocardial fibrosis.

50 may potentially reflect diffuse interstitial myocardial fibrosis.

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

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

53 lammatory effect was associated with reduced myocardial fibrosis 28 days post-myocardial ischemia-rep

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 ibroblast might attenuate the development of myocardial fibrosis, a pathophysiological hallmark of HF

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

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

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

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

63 l fibrosis and analyzed associations between myocardial fibrosis and a composite end point of all-cau

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

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

66 etermined the prevalence and the patterns of myocardial fibrosis and analyzed associations between my

67 administration showed a marked reduction in myocardial fibrosis and apoptosis in the injured hearts,

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

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

70 eased prevalence of coronary artery disease, myocardial fibrosis and arrhythmias.

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

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

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

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

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

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

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

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

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

80 ume (ECV) by CMR is a marker of interstitial myocardial fibrosis and is associated with diastolic dys

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

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

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

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

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

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

87 ischemia assessed by CMR is associated with myocardial fibrosis and reduced exercise capacity in HCM

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

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

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

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

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

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

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

95 exercise-induced cardiac biomarker release, myocardial fibrosis, and atrial fibrillation.

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

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

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

99 chimpanzees, particularly those affected by myocardial fibrosis, and could influence the risk of car

100 stically, DAPA suppressed ER stress, reduced myocardial fibrosis, and improved overall function.

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

102 ts in inducible AF, left atrial enlargement, myocardial fibrosis, and inflammation.

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

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

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

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

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

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

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

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

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

112 f boron supplementation on cardiac function, myocardial fibrosis, apoptosis and regeneration in a rat

113 e/TP53 pathway in the heart and induction of myocardial fibrosis, apoptosis, cardiac dysfunction, and

114 Expression of LMNA(D300N) led to severe myocardial fibrosis, apoptosis, cardiac dysfunction, and

115 Deletion of Tp53 partially rescued myocardial fibrosis, apoptosis, proliferation of nonmyoc

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

117 Both the presence and the extent of myocardial fibrosis are independently associated with th

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

119 1 mapping can noninvasively quantify diffuse myocardial fibrosis as extracellular volume fraction (EC

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

121 as regional left ventricular hypertrophy and myocardial fibrosis, as well as structurally abnormal el

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

123 Diffuse myocardial fibrosis, assessed by post-contrast myocardia

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

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

126 Myocardial fibrosis at baseline was an independent indic

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

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

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

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

131 Myocardial fibrosis by late gadolinium enhancement was d

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

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

134 Myocardial fibrosis can be visualized by late gadolinium

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

136 Development of myocardial fibrosis, cardiac myocyte atrophy and loss of

137 ably modulated molecular pathways regulating myocardial fibrosis, cardiomyocyte apoptosis, angiogenes

138 ccurately assess the relation between CV and myocardial fibrosis density on late gadolinium-enhanced

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

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

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

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

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

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

145 -17A-deficient mice had reduced interstitial myocardial fibrosis, downregulated expression of matrix

146 rdiac function and reduce the progression of myocardial fibrosis during heart failure development aft

147 non-HIV-infected women) exhibited increased myocardial fibrosis (extracellular volume fraction, 0.34

148 6 versus 63+/-5%; P<0.05) and an increase in myocardial fibrosis (extracellular volume of 0.34+/-0.03

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

150 Increased myocardial fibrosis has been detected in the endomyocard

151 Myocardial fibrosis has been shown to be reversible and

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

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

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

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

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

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

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

159 Myocardial fibrosis impairs cardiac function, in additio

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

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

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

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

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

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

166 Myocardial fibrosis in HCM is a progressive and fast phe

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

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

169 relationship between peripheral markers and myocardial fibrosis in HCM.

170 Whether myocardial fibrosis in heart transplant recipients is in

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

172 Myocardial fibrosis in hypertensive heart disease remain

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

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

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

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

177 Few data exist on the degree of interstitial myocardial fibrosis in patients with classical low-flow,

178 4+/-8.0%) and diffuse (T1 time, 478+/-79 ms) myocardial fibrosis in patients with HCM, peripheral lev

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

180 n show improved cardiac function and reduced myocardial fibrosis in response to pressure overload or

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

182 on between LA function, RV hypertension, and myocardial fibrosis in SCA.

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

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

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

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

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

188 Myocardial fibrosis increased with decreasing MVD in con

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

190 Myocardial fibrosis is a common feature of many cardiomy

191 Myocardial fibrosis is a feature of many cardiac disease

192 Myocardial fibrosis is a hallmark of cardiac remodeling

193 Diffuse myocardial fibrosis is a hallmark of cardiomyopathy.

194 Myocardial fibrosis is a hallmark of hypertrophic cardio

195 Myocardial fibrosis is a hallmark of hypertrophic cardio

196 Myocardial fibrosis is a hallmark of hypertrophic cardio

197 Myocardial fibrosis is a major determinant of clinical o

198 Diffuse myocardial fibrosis is a novel mechanism that appears to

199 Myocardial fibrosis is a significant global health probl

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

201 Myocardial fibrosis is a well-described histopathologic

202 Myocardial fibrosis is an important pathophysiological m

203 Myocardial fibrosis is common in patients with chronic a

204 Study of the molecular basis of myocardial fibrosis is hampered by limited access to tis

205 Myocardial fibrosis is identified frequently in HCM; how

206 Myocardial fibrosis is key for atrial fibrillation maint

207 Myocardial fibrosis is linked with adverse clinical outc

208 In heart transplant recipients, myocardial fibrosis is seen on late gadolinium enhanceme

209 rdiovascular diseases, especially idiopathic myocardial fibrosis, is one of the most significant caus

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

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

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

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

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

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

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

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

218 Myocardial fibrosis may contribute to the pathophysiolog

219 These findings suggest that diffuse myocardial fibrosis may not be the main factor responsib

220 Results Interstitial myocardial fibrosis measured by iECV was higher in patie

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

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

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

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

225 Quantifying myocardial fibrosis (MF) with myocardial extracellular v

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

227 In the myocardial fibrosis model for mice, PYSNO exhibited a po

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

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

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

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

232 We sought to determine whether myocardial fibrosis on late gadolinium enhancement cardi

233 nic PDE9a inhibition, with no differences in myocardial fibrosis or cardiac morphometry.

234 Assessment of myocardial fibrosis predicts both risk of sudden cardiac

235 Myocardial fibrosis, predominantly at the subepicardium

236 Myocardial fibrosis, predominantly in the basal inferola

237 All hearts affected by marked myocardial fibrosis presented with bone or cartilage for

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

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

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

241 Myocardial fibrosis quantified by extracellular volume (

242 monocyte CCR2 expression related directly to myocardial fibrosis (r = 0.48; P = .04) and inversely to

243 g WHIV, soluble CD163 levels correlated with myocardial fibrosis (r = 0.53; P = .02), while circulati

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

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

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

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

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

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

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

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

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

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

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

255 s during adverse cardiac remodeling leads to myocardial fibrosis that can compromise cardiac function

256 03/+) mice developed neither hypertrophy nor myocardial fibrosis, the pathologic manifestations of HC

257 In addition to detecting myocardial fibrosis through late gadolinium enhancement

258 Myocardial fibrosis, total collagen, and the collagen ty

259 Myocardial fibrosis turnover after MI is associated with

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

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

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

263 es) which were either healthy or affected by myocardial fibrosis using X-ray microtomography.

264 The addition of myocardial fibrosis variables to models with cardiac all

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

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

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

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

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

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

271 Myocardial fibrosis was assessed from magnetic resonance

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

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

274 Myocardial fibrosis was detected by late gadolinium enha

275 Myocardial fibrosis was detected to a significantly lowe

276 Myocardial fibrosis was determined with late gadolinium

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

278 The prevalence of primary myocardial fibrosis was higher among women (5.2%, n=64)

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

280 Every 1% increase in myocardial fibrosis was independently associated with a

281 With a median follow-up of 2.6 years, myocardial fibrosis was independently associated with al

282 Myocardial fibrosis was present in 18% (37% infarct patt

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

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

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

286 Myocardial fibrosis was related to conduction abnormalit

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

288 , among patients with LFLG-AS, the degree of myocardial fibrosis was similar in patients with versus

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

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

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

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

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

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

295 ECV measures of diffuse myocardial fibrosis were associated with HF outcomes, de

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

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

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

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

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