ライフサイエンスコーパス: dilated cardiomyopathy

1 scle cell leads to myocyte instability and a dilated cardiomyopathy.

2 he most common type of genetic alteration in dilated cardiomyopathy.

3 , and leiomodin-2-knockout mice present with dilated cardiomyopathy.

4 venting progression of inflammation-mediated dilated cardiomyopathy.

5 to identify novel mutations causing familial dilated cardiomyopathy.

6 al and adjuvant epicardial CA in nonischemic dilated cardiomyopathy.

7 to one that leads to chronic remodeling and dilated cardiomyopathy.

8 children who are transplanted for idiopathic dilated cardiomyopathy.

9 heart failure than children with idiopathic dilated cardiomyopathy.

10 on that ultimately results in a severe fatal dilated cardiomyopathy.

11 patients, and those with either ischemic or dilated cardiomyopathy.

12 many cardiac genes, and loss of RBM20 causes dilated cardiomyopathy.

13 the structural alterations in patients with dilated cardiomyopathy.

14 al human disease phenotypes, hypertrophic or dilated cardiomyopathy.

15 recover spontaneously, some develop chronic dilated cardiomyopathy.

16 patients with heart failure due to ischaemic dilated cardiomyopathy.

17 evated in left ventricles from patients with dilated cardiomyopathy.

18 ises heart function and structure, producing dilated cardiomyopathy.

19 metabolic remodelling and has a key role in dilated cardiomyopathy.

20 nts with ischemic dilated cardiomyopathy and dilated cardiomyopathy.

21 as a therapeutic target for the treatment of dilated cardiomyopathy.

22 o known as MLIP) is reduced in patients with dilated cardiomyopathy.

23 apy in a canine model of tachypacing-induced dilated cardiomyopathy.

24 nderlies the Python mouse model of monogenic dilated cardiomyopathy.

25 elevated COUP-TFII levels on development of dilated cardiomyopathy.

26 tricular chamber enlargement consistent with dilated cardiomyopathy.

27 nd of unknown pathogenesis in a patient with dilated cardiomyopathy.

28 as/sudden death in patients with nonischemic dilated cardiomyopathy.

29 ation (Id cDKOs), which develops adult-onset dilated cardiomyopathy.

30 utes up to 40% of patients with non-ischemic dilated cardiomyopathy.

31 rhythmic events in patients with nonischemic dilated cardiomyopathy.

32 h genes and postnatal development of a fatal dilated cardiomyopathy.

33 ith SPEG mutations additionally present with dilated cardiomyopathy.

34 n cardiac death in patients with nonischemic dilated cardiomyopathy.

35 induced hypertrophy and in human hearts with dilated cardiomyopathy.

36 ion beyond LVEF in patients with nonischemic dilated cardiomyopathy.

37 s of PPCM patients, but not in patients with dilated cardiomyopathy.

38 ient mice were protected from progression to dilated cardiomyopathy.

39 nce, and long-term survival in patients with dilated cardiomyopathy.

40 s performed in 220 probands with adult-onset dilated cardiomyopathy.

41 eft ventricular outflow tract obstruction or dilated cardiomyopathy.

42 transplantation in patients with nonischemic dilated cardiomyopathy.

43 ence is available specifically on idiopathic dilated cardiomyopathy.

44 The majority (85%) carried the diagnosis of dilated cardiomyopathy.

45 xamines long-term outcomes for children with dilated cardiomyopathy.

46 there was an unexpectedly high prevalence of dilated cardiomyopathy.

47 ted, can lead to contractile dysfunction and dilated cardiomyopathy.

48 in-deficient Drosophila heart tubes, causing dilated cardiomyopathy.

49 ular arrhythmias in patients with idiopathic dilated cardiomyopathy.

50 t ventricle (LV) ultimately transitions to a dilated cardiomyopathy.

51 ative relatives, and 9 with noncompaction or dilated cardiomyopathy.

52 g heart rate of children with chronic HF and dilated cardiomyopathy.

53 COX and copper deficiency that resulted in a dilated cardiomyopathy.

54 ponin protein stoichiometry in patients with dilated cardiomyopathy.

55 sease remodelling in patients suffering from dilated cardiomyopathy.

56 c insert are linked to heart disease such as dilated cardiomyopathies.

57 ple mechanistic pathways to hypertrophic and dilated cardiomyopathies.

58 re detected in about one-third of idiopathic dilated cardiomyopathies.

59 Twenty-seven patients (8 dilated cardiomyopathy, 10 normal ejection fraction, and

60 who had undergone heart transplantation for dilated cardiomyopathy 11 months prior to presentation o

61 Brugada syndrome (7), long QT syndromes (5), dilated cardiomyopathy (2), and hypertrophic cardiomyopa

62 Of the 40 patients with dilated cardiomyopathy, 20 were randomized to receive in

63 d by coronary artery abnormalities (5, 14%), dilated cardiomyopathy (3, 8%), myocarditis related (3,

64 ethnicity (18% vs. 2%), and have idiopathic-dilated cardiomyopathy (62% vs. 9%) (all p < 0.0001).

65 frequently fulfilled diagnostic criteria for dilated cardiomyopathy (64% versus 36%), associated with

66 arrhythmias (69% and 52%, respectively), and dilated cardiomyopathy (74% and 14%, respectively).

67 ts without congenital heart disease, 53% had dilated cardiomyopathy, 91% of patients received milrino

68 In patients with dilated cardiomyopathy, a more longitudinal orientation

69 ion using RNA-sequencing in 97 patients with dilated cardiomyopathy and 108 non-diseased controls.

70 .5 years; 64 patients (65.9%) had idiopathic dilated cardiomyopathy and 21 patients (21.6%) had ische

71 the 69 children with mixed hypertrophic and dilated cardiomyopathy and 38% (95% CI 25-51) at 2 years

72 wall LGE identifies a group of patients with dilated cardiomyopathy and an LVEF >/=40% at increased r

73 aborted SCD among consecutive referrals with dilated cardiomyopathy and an LVEF >/=40% to our center

74 Here, we studied a family with dilated cardiomyopathy and associated conduction system

75 Mutation in DnaJC19 results in dilated cardiomyopathy and ataxia syndrome, whereas expr

76 tem cells were used to examine a family with dilated cardiomyopathy and atrial and ventricular arrhyt

77 d with lamin A/C deletion resulted in severe dilated cardiomyopathy and cardiac dysfunction in the ab

78 we link a subset of 517 epigenetic loci with dilated cardiomyopathy and cardiac gene expression.

79 compared with subjects with noninflammatory dilated cardiomyopathy and controls.

80 myocardial tissue and blood of patients with dilated cardiomyopathy and controls.

81 he left ventricles of patients with ischemic dilated cardiomyopathy and dilated cardiomyopathy.

82 tein U (hnRNP U) in the heart develop lethal dilated cardiomyopathy and display numerous defects in c

83 obal developmental delay, failure to thrive, dilated cardiomyopathy and epilepsy, ultimately leading

84 l mutations within HSPB7 are associated with dilated cardiomyopathy and heart failure in human patien

85 ocytes, notably in ageing hearts, leading to dilated cardiomyopathy and heart failure in LGM2B patien

86 knockout mice spontaneously developed lethal dilated cardiomyopathy and heart failure with an early i

87 (2)(+) responsiveness in a model of familial dilated cardiomyopathy and improve cardiac function and

88 nd inflammation in patients with nonischemic dilated cardiomyopathy and inflammatory cardiomyopathy (

89 lled 60 patients (median age, 57 years) with dilated cardiomyopathy and left ventricular ejection fra

90 f Titin truncation variants in patients with dilated cardiomyopathy and population controls.

91 -defibrillator implantation to patients with dilated cardiomyopathy and severely reduced LV function

92 the giant sarcomeric protein Titin result in dilated cardiomyopathy and skeletal myopathy.

93 nstrated significant improvement in cases of dilated cardiomyopathy and structural heart disease in i

94 se of ivabradine in paediatric patients with dilated cardiomyopathy and symptomatic chronic heart fai

95 relationship of ivabradine in children with dilated cardiomyopathy and symptomatic chronic HF.

96 intracoronary CD34+ cell transplantation in dilated cardiomyopathy and the relationship between intr

97 In patients with nonischemic dilated cardiomyopathy and VT, endocardial and adjuvant

98 No CEs occurred in patients without dilated cardiomyopathy and/or LGE.

99 is patients, 11 ischemic heart disease, nine dilated cardiomyopathy, and 11 nonfailing donors.

100 n of function occurs in 20% of children with dilated cardiomyopathy, and 40% die or undergo transplan

101 pathogenesis of hypertrophic cardiomyopathy, dilated cardiomyopathy, and arrhythmogenic right ventric

102 growth retardation, hypoglycemia, myopathy, dilated cardiomyopathy, and cardiac arrest.

103 the regulation of development, ischemic and dilated cardiomyopathy, and myocardial infarction.

104 ed increased myocyte apoptosis and fibrosis, dilated cardiomyopathy, and premature death.

105 e cardiac Jak2-deleted mice had hypertrophy, dilated cardiomyopathy, and severe left ventricular dysf

106 ach for some patients with Brugada syndrome, dilated cardiomyopathy, and sick sinus syndrome in the f

107 channelopathies, including Brugada syndrome, dilated cardiomyopathy, and sick sinus syndrome; however

108 are hypersensitive to Ca(2+) activation, and dilated cardiomyopathies are hyposensitive.

109 ed cardiomyopathies allowed establishment of dilated cardiomyopathy as mostly cytoskeleton, force tra

110 osin heavy chain (MHC) cause hypertrophic or dilated cardiomyopathy as these mutations should not dir

111 nd Becker muscular dystrophy (BMD), X-linked dilated cardiomyopathy, as well as DMD and BMD female ca

112 t for either sex in a setting of more severe dilated cardiomyopathy associated with atrial fibrillati

113 arched for fish homologues of 51 known human dilated cardiomyopathy-associated genes.

114 on could not reliably identify patients with dilated cardiomyopathy at risk of fatal ventricular tach

115 n D1275N associated with sick sinus syndrome/dilated cardiomyopathy/atrial arrhythmias.

116 these circRNAs are dynamically regulated in dilated cardiomyopathy but not in hypertrophic cardiomyo

117 day 6.5-9.5 developed a phenotype similar to dilated cardiomyopathy by 1 year of age.

118 may be a viable approach to the treatment of dilated cardiomyopathy by not only preventing maladaptiv

119 achycardia (VT) in patients with nonischemic dilated cardiomyopathy can be challenging because of the

120 age-dependent cardiac phenotypes, including dilated cardiomyopathy, cardiac conduction disturbance,

121 cted probands, including two with documented dilated cardiomyopathy, carrying homozygous or compound-

122 ncation mutation information from 1714 human dilated cardiomyopathy cases and >69 000 controls and fo

123 E1356K, R1382W, E1555K, and R1768K) and one dilated cardiomyopathy-causing (R1500W) tail mutations o

124 elanocortin-4 receptor (MC4R) in mice causes dilated cardiomyopathy, characterized by reduced contrac

125 d changes in prognosis of a large idiopathic dilated cardiomyopathy cohort systematically followed du

126 In pediatric patients with dilated cardiomyopathy, compared with dimension and area

127 rdiac development and the pathophysiology of dilated cardiomyopathy, congenital heart failure and/or

128 ith homozygous MYBPC3-null mutations develop dilated cardiomyopathy, coupled with myocyte hyperplasia

129 otential of silencing miR-34a in settings of dilated cardiomyopathy (DCM) and atrial fibrillation (AF

130 mains debilitating heart conditions, such as dilated cardiomyopathy (DCM) and hypertrophic cardiomyop

131 ompared them with samples from patients with dilated cardiomyopathy (DCM) and inflammatory cardiomyop

132 R) to disease progression in mouse models of dilated cardiomyopathy (DCM) and pressure overload hyper

133 phospholamban (PLN) gene are associated with dilated cardiomyopathy (DCM) and severe heart failure.

134 rect targets of FXR1 in human left ventricle dilated cardiomyopathy (DCM) biopsy samples and mouse mo

135 ABSTRACT: Dilated cardiomyopathy (DCM) can be caused by mutations

136 Childhood dilated cardiomyopathy (DCM) carries high morbidity and

137 c metabolite quantification in patients with dilated cardiomyopathy (DCM) compared with that at 3 T.

138 Dilated cardiomyopathy (DCM) due to mutations in RBM20,

139 Improved understanding of dilated cardiomyopathy (DCM) due to titin truncation (TT

140 Non-ischemic dilated cardiomyopathy (DCM) has been recognized as a he

141 Studies of children with dilated cardiomyopathy (DCM) have suggested that improve

142 Here, we determined that dilated cardiomyopathy (DCM) in fibrillin 1-deficient mi

143 esidue 9 in PLN to cysteine (R9C) results in dilated cardiomyopathy (DCM) in humans and transgenic mi

144 Dilated cardiomyopathy (DCM) is a common form of cardiom

145 Dilated cardiomyopathy (DCM) is a condition of abnormal

146 Familial dilated cardiomyopathy (DCM) is a genetically heterogene

147 Dilated cardiomyopathy (DCM) is a highly heterogeneous t

148 Dilated cardiomyopathy (DCM) is a leading cause of heart

149 Dilated cardiomyopathy (DCM) is an important cause of he

150 Dilated cardiomyopathy (DCM) is best understood as the f

151 The cause of idiopathic dilated cardiomyopathy (DCM) is unknown by definition, b

152 The multifactorial pathogenesis leading to dilated cardiomyopathy (DCM) makes stratification diffic

153 Patients with nonischemic dilated cardiomyopathy (DCM) may be at lower risk for ve

154 ix hypertrophic cardiomyopathy (HCM) and two dilated cardiomyopathy (DCM) mutants were studied by bio

155 Nonischemic dilated cardiomyopathy (DCM) often has a genetic pathoge

156 tudies reveal reduced force generation and a dilated cardiomyopathy (DCM) phenotype.

157 Peripartum cardiomyopathy (PPCM) and dilated cardiomyopathy (DCM) show similarities in clinic

158 g heart and in the heart of a mouse model of dilated cardiomyopathy (DCM) triggered by Serum Response

159 periments indicate that mutations that cause dilated cardiomyopathy (DCM) uncouple this modulation, b

160 We addressed this question in patients with dilated cardiomyopathy (DCM) using a dual approach.

161 tive incidence of SCD at 15 years was 5% for dilated cardiomyopathy (DCM), 6% for hypertrophic cardio

162 mode of inheritance, are important causes of dilated cardiomyopathy (DCM), a disease characterized by

163 inding protein RBM20 have been implicated in dilated cardiomyopathy (DCM), a major cause of chronic h

164 Ntvs)] are the most common genetic cause for dilated cardiomyopathy (DCM), a major cause of heart fai

165 rotein, is often associated with arrhythmia, dilated cardiomyopathy (DCM), and heart failure.

166 ogies for familial atrial fibrillation (AF), dilated cardiomyopathy (DCM), and mixed cardiac phenotyp

167 rtality) suggest that for many patients with dilated cardiomyopathy (DCM), implantable cardioverter-d

168 disease (CCD) and, after six months of age, dilated cardiomyopathy (DCM), most noticeably in the mal

169 fraction are strong predictors of outcome in dilated cardiomyopathy (DCM), there are limited data reg

170 tes have been identified in certain cases of dilated cardiomyopathy (DCM), traditionally labeled idio

171 mice count among the first mouse models for dilated cardiomyopathy (DCM), yet the exact role of MLP

172 human healthy hearts and failing hearts with dilated cardiomyopathy (DCM).

173 with a range of cardiac diseases, including dilated cardiomyopathy (DCM).

174 phic function among children with idiopathic dilated cardiomyopathy (DCM).

175 reifuss muscular dystrophy (EDMD) as well as dilated cardiomyopathy (DCM).

176 n-truncating variants (TTNtv) commonly cause dilated cardiomyopathy (DCM).

177 tions of CPET with outcomes in children with dilated cardiomyopathy (DCM).

178 ing variants (TTNtvs) are the major cause of dilated cardiomyopathy (DCM); however, allelic heterogen

179 patients with aortic stenosis (AS, n=9) and dilated cardiomyopathy (DCM, n=6).

180 otypes (hypertrophic cardiomyopathy, HCM and dilated cardiomyopathy, DCM) associated with mutations i

181 Inflammatory dilated cardiomyopathy (DCMi) is a major cause of heart

182 Patients with myocarditis or dilated cardiomyopathy develop autoantibodies to SERCA2a

183 in quality control, we used a mouse model of dilated cardiomyopathy driven by cardiac restricted over

184 show multiple disease phenotypes, including dilated cardiomyopathy, exercise intolerance, and hepato

185 loci that are significantly associated with dilated cardiomyopathy (false discovery corrected P</=0.

186 aring the survival of children with familial dilated cardiomyopathy (FDCM) to that of children with i

187 cardioverter defibrillator in patients with dilated cardiomyopathy for the primary prevention of sud

188 Main etiologies of HF in LA are idiopathic dilated cardiomyopathy (from 1.3% to 37%), C'D (from 1.3

189 d controls, affecting known as well as novel dilated cardiomyopathy genes.

190 und that eQTL variants are also enriched for dilated cardiomyopathy genome-wide association signals i

191 lume Variability) in pediatric patients with dilated cardiomyopathy has reported reproducibility of s

192 Most known genes for human dilated cardiomyopathy have a corresponding zebrafish or

193 eased c-Cbl expression in human ischemic and dilated cardiomyopathy hearts and in response to patholo

194 white race, female sex, diagnosis other than dilated cardiomyopathy, higher blood urea nitrogen, and

195 T syndrome, hypertrophic cardiomyopathy, and dilated cardiomyopathy hiPSC-CMs by immunostaining and s

196 Young adult L/L and L/+ mice have dilated cardiomyopathy, hypertension, and increased plas

197 uel starvation, ischemia, pressure overload, dilated cardiomyopathy, hypertrophy, and heart failure.

198 ts that cause hypertrophic, restrictive, and dilated cardiomyopathy (I79N, DeltaE96, and DeltaK210, r

199 tients (n = 154) with documented chronic and dilated cardiomyopathy (ICM, n = 61; NICM, n = 93) requi

200 ailure therapies to children with idiopathic dilated cardiomyopathy (IDC), prognosis remains poor.

201 y (FDCM) to that of children with idiopathic dilated cardiomyopathy (IDCM) has produced conflicting r

202 nction and myocardial injuries in idiopathic dilated cardiomyopathy (IDCM) using cardiac magnetic res

203 orse for patients with ACM versus idiopathic dilated cardiomyopathy (IDCM) with continued exposure.

204 ension development predicts hypertrophic and dilated cardiomyopathies in mice associated with essenti

205 ommon cause of heart failure was nonischemic dilated cardiomyopathy in 27.5% (whites, 19.9%; P<0.001)

206 t has been previously associated with severe dilated cardiomyopathy in a mouse model.

207 cal and functional changes characteristic of dilated cardiomyopathy in CSN8(CKO) mice.

208 and metabolic compromise in the etiology of dilated cardiomyopathy in DMD and identify a window of o

209 Moreover, dilated cardiomyopathy in humans was associated with inc

210 ainstay of breast cancer chemotherapy, cause dilated cardiomyopathy in many patients.

211 iated with features of both hypertrophic and dilated cardiomyopathy in mice.

212 th deregulated energy homeostasis leading to dilated cardiomyopathy in mice.

213 ns presented with severe hypertrophic and/or dilated cardiomyopathy in utero, at birth, or in early c

214 m will facilitate systems biology studies of dilated cardiomyopathy in zebrafish.

215 c cardiomyopathy, ischemic heart disease, or dilated cardiomyopathy, in comparison to nonfailing hear

216 Health Organization criteria for idiopathic dilated cardiomyopathy, including negative coronary angi

217 Dilated cardiomyopathy is a leading cause of congestive

218 Because a common finding in dilated cardiomyopathy is a reduction in the myofilament

219 Up to 40% of dilated cardiomyopathy is associated with inflammation o

220 involved in viral RNA replication.IMPORTANCE Dilated cardiomyopathy is the most common indication for

221 tes into the spectrum of hypertrophic versus dilated cardiomyopathy is unknown.

222 tant mice die at 13 wk as a result of severe dilated cardiomyopathy leading to heart failure.

223 Forty-seven patients with idiopathic dilated cardiomyopathy (left ventricular ejection fracti

224 We treated a dilated cardiomyopathy-linked mouse model expressing a m

225 Despite disparate causes for dilated cardiomyopathy, maladaptive cardiac remodeling a

226 ing to heart failure in the Python monogenic dilated cardiomyopathy model.

227 y bowel disease, infections, cerebral palsy, dilated cardiomyopathy, muscular dystrophy, and schizoph

228 to mitigate the effects of hypertrophic and dilated cardiomyopathy mutations at their sources, leadi

229 In patients with dilated cardiomyopathy, myocardial Gal-3 expression corr

230 tional mutant mice developed signs of severe dilated cardiomyopathy, myocardial infarctions, and prem

231 emaining cardiac diagnosis groups, including dilated cardiomyopathy, myocarditis, and ischemic and no

232 was examined in human explanted hearts with dilated cardiomyopathy (n = 25).

233 Dilated cardiomyopathy (n=27), myocarditis or sarcoidosi

234 findings, patients were classified as having dilated cardiomyopathy (n=40) or iCMP (n=75).

235 schemic cardiomyopathy [ICM], 13 nonischemic dilated cardiomyopathy [NICM], 15 arrhythmogenic right v

236 achycardia (VT) in patients with nonischemic dilated cardiomyopathy (NIDCM) are insufficient.

237 lar tachycardia (VT) ablation in nonischemic dilated cardiomyopathy (NIDCM) are insufficient.

238 ere obtained in 20 patients with nonischemic dilated cardiomyopathy (NIDCM), 20 patients with hypertr

239 tic information in patients with nonischemic dilated cardiomyopathy (NIDCM).

240 hy, few studies exist in chronic nonischemic dilated cardiomyopathy (NIDCM).

241 usal variant in a large family with familial dilated cardiomyopathy of unknown pathogenesis.

242 ividuals with either the most severe form of dilated cardiomyopathy or whose mutations demonstrated c

243 confidence interval [CI] 1.03-3.48; P=0.04), dilated cardiomyopathy (OR 1.93, 95% CI 1.03-3.57; P=0.0

244 We enrolled 409 consecutive ischemic and dilated cardiomyopathy patients (mean age: 64+/-12 years

245 nces of gene expression and splicing between dilated cardiomyopathy patients and controls, affecting

246 T syndrome, hypertrophic cardiomyopathy, and dilated cardiomyopathy patients at the single cell level

247 ) in ischemic cardiomyopathy and nonischemic dilated cardiomyopathy patients evaluated for primary pr

248 The most severely affected dilated cardiomyopathy patients harbor Titin truncations

249 Of 110 dilated cardiomyopathy patients, 55 were randomized to r

250 ssion are each important determinants of the dilated cardiomyopathy phenotype and are controlled by g

251 d that the knockout strategy ameliorates the dilated cardiomyopathy phenotype in vitro.

252 humanized" telomere lengths, the devastating dilated cardiomyopathy phenotype seen in patients with D

253 Focusing on the dilated cardiomyopathy phenotype we found that eQTL vari

254 her compensated-concentric POH (POH-CLVH) or dilated cardiomyopathy (POH-DCM); they were compared to

255 jection Delivery Effects on Neomyogenesis in Dilated Cardiomyopathy [PoseidonDCM]; NCT01392625).

256 en with myocarditis and 1249 with idiopathic dilated cardiomyopathy received HT.

257 ive, longitudinal study of 472 patients with dilated cardiomyopathy referred to a UK center for CMR i

258 iling revealed that >95% of the hypertrophic/dilated cardiomyopathy-related genes that were significa

259 during cardiac contraction in patients with dilated cardiomyopathy relative to controls.

260 etween diastole and systole in patients with dilated cardiomyopathy relative to healthy controls usin

261 ole of LGE-CMR in the risk stratification of dilated cardiomyopathy requires further investigation.

262 d reduced ejection fraction due to ischaemic dilated cardiomyopathy resulted in a significant reducti

263 tions associated with muscular dystrophy and dilated cardiomyopathy resulted in more deformable nucle

264 Myocarditis can cause dilated cardiomyopathy resulting in end-stage heart fail

265 ids from hearts explanted from patients with dilated cardiomyopathy revealed elevated polyunsaturated

266 signatures and myocardium from subjects with dilated cardiomyopathy showed excessive Parkin and CHOP

267 if concentric hypertrophy does progress to a dilated cardiomyopathy, such a transition would occur ov

268 ted from a patient suffering from idiopathic dilated cardiomyopathy, suggesting that such mutant viru

269 ffective in females in a setting of moderate dilated cardiomyopathy than in males.

270 BCL2-associated athanogene 3 (BAG3) develop dilated cardiomyopathy that is associated with a destabi

271 Approximately 20% of boys will die of dilated cardiomyopathy that is associated with cytoskele

272 isease are those classes of hypertrophic and dilated cardiomyopathy that result from single amino-aci

273 r envelope gene SYNE1 in a child with severe dilated cardiomyopathy that underwent transplant, as wel

274 164 ischemic cardiomyopathy, 150 nonischemic dilated cardiomyopathy), the mean left ventricular eject

275 In patients with idiopathic dilated cardiomyopathy, the absence of LGE at baseline i

276 In idiopathic dilated cardiomyopathy, there are scarce data on the inf

277 ers produce reverse-remodeling in idiopathic dilated cardiomyopathy, they partially reverse changes i

278 tified in other congenital heart defects and dilated cardiomyopathy, this study reveals compound hete

279 the cMyBP-C((t/t)) hearts undergoing severe dilated cardiomyopathy, though this does not seem to pre

280 In patients with dilated cardiomyopathy, transendocardial CD34(+) cell tr

281 ere pathologies, such as aseptic meningitis, dilated cardiomyopathy, type I diabetes, paralysis, and

282 with ischemic cardiomyopathy or nonischemic dilated cardiomyopathy undergoing cardiovascular magneti

283 -nine patients with ischemic or non-ischemic dilated cardiomyopathy undergoing prophylactic ICD impla

284 Sixty-nine patients with idiopathic dilated cardiomyopathy underwent implantable cardioverte

285 hundred fifty-eight patients with idiopathic dilated cardiomyopathy underwent programmed ventricular

286 y shows that different gene mutations induce dilated cardiomyopathy via diverse cellular pathways.

287 CD34+ transplantation in dilated cardiomyopathy was associated with short-term im

288 rge family with autosomal dominant, familial dilated cardiomyopathy was identified.

289 Ang II levels in explanted human hearts with dilated cardiomyopathy were elevated despite ACE inhibit

290 ve cardiac fibrosis, all features present in dilated cardiomyopathy, were observed in the aged sFRP-1

291 n of enlarged hollow donut mitochondria with dilated cardiomyopathy, which could be rescued by cardio

292 t be an ideal candidate for the treatment of dilated cardiomyopathy, which displays modest microvascu

293 mutant IDH2 expression in adults resulted in dilated cardiomyopathy, white matter abnormalities throu

294 d 59+/-15 years, 80% males) with nonischemic dilated cardiomyopathy who underwent CA.

295 en with myocarditis and 1583 with idiopathic dilated cardiomyopathy who were <18 years old and listed

296 V symptomatic heart failure due to ischaemic dilated cardiomyopathy, who had left ventricular ejectio

297 in the mouse heart for the first time during dilated cardiomyopathy with heart failure.

298 on of the Speg gene locus in mice leads to a dilated cardiomyopathy with immature-appearing cardiomyo

299 n occurred in 26% of patients with childhood dilated cardiomyopathy within 1 year of diagnosis and ~1

300 magnetic resonance identified patients with dilated cardiomyopathy without severe LV systolic dysfun