ライフサイエンスコーパス: dilated cardiomyopathy

1 (TTNtv) are the most common genetic cause of dilated cardiomyopathy.

2 duced myocyte complex N-glycosylation causes dilated cardiomyopathy.

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

4 hmogenic right ventricular cardiomyopathy or dilated cardiomyopathy.

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

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

7 (TTNtv) are the commonest cause of heritable dilated cardiomyopathy.

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

9 se-specific considerations were required for dilated cardiomyopathy.

10 induced hypertrophy and in human hearts with dilated cardiomyopathy.

11 ular arrhythmias in patients with idiopathic dilated cardiomyopathy.

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

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

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

15 ponin protein stoichiometry in patients with dilated cardiomyopathy.

16 sease remodelling in patients suffering from dilated cardiomyopathy.

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

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

19 venting progression of inflammation-mediated dilated cardiomyopathy.

20 to identify novel mutations causing familial dilated cardiomyopathy.

21 al and adjuvant epicardial CA in nonischemic dilated cardiomyopathy.

22 children who are transplanted for idiopathic dilated cardiomyopathy.

23 heart failure than children with idiopathic dilated cardiomyopathy.

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

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

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

27 the structural alterations in patients with dilated cardiomyopathy.

28 al human disease phenotypes, hypertrophic or dilated cardiomyopathy.

29 recover spontaneously, some develop chronic dilated cardiomyopathy.

30 patients with heart failure due to ischaemic dilated cardiomyopathy.

31 evated in left ventricles from patients with dilated cardiomyopathy.

32 ises heart function and structure, producing dilated cardiomyopathy.

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

34 dilation, and a fourth-degree relative with dilated cardiomyopathy.

35 understanding of the genetic architecture of dilated cardiomyopathy.

36 d on the uncharacterized lncRNA GATA6-AS1 in dilated cardiomyopathy.

37 alterations of signaling pathways leading to dilated cardiomyopathy.

38 respiratory failure, and in the older cases, dilated cardiomyopathy.

39 nd in heart tissue from patients with MI and dilated cardiomyopathy.

40 TTN) are the leading known cause of familial dilated cardiomyopathy.

41 lly induced trophic signaling and eventually dilated cardiomyopathy.

42 s with regard to monitoring for (late-onset) dilated cardiomyopathy.

43 viral proteinase 2A in cases of unexplained dilated cardiomyopathy.

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

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

46 rtrophic cardiomyopathy (1/500 individuals), dilated cardiomyopathy (1/250) and arrhythmogenic right

47 ard ratios were 1.15 (95% CI, 1.14-1.17) for dilated cardiomyopathy, 1.09 (95% CI, 1.06-1.12) for hyp

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

49 Of these, 481 were diagnosed with dilated cardiomyopathy, 246 had hypertrophic cardiomyopa

50 ARVC, 9 (25%) of 36; LQTS, 48 (20%) of 238; dilated cardiomyopathy, 5 (9%) of 58; and HCM, 28 (8%) o

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

52 In patients with dilated cardiomyopathy, a more longitudinal orientation

53 this critical overlap region associated with dilated cardiomyopathy, A277V, will alter Tpm binding an

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

55 .5 years; 64 patients (65.9%) had idiopathic dilated cardiomyopathy and 21 patients (21.6%) had ische

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

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

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

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

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

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

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

63 A subgroup of dilated cardiomyopathy and control subjects underwent ca

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

65 compared with subjects with noninflammatory dilated cardiomyopathy and controls.

66 a pair of siblings with rapidly progressive dilated cardiomyopathy and death in early infancy.

67 CaMKII overexpression (mtCaMKII) have severe dilated cardiomyopathy and decreased ATP that causes ele

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

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

70 members) with ASD combined with a late-onset dilated cardiomyopathy and further characterize the cons

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

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

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

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

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

76 Here the authors focus on genetics of dilated cardiomyopathy and provide a roadmap for impleme

77 Patients with ischemic or dilated cardiomyopathy and reduced left ventricular ejec

78 characterized by fibrosis: human and murine dilated cardiomyopathy and repaired tetralogy of Fallot.

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

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

81 ubunit-encoding Kcne2 (Kcne2(CS-/-) ) causes dilated cardiomyopathy and terminal HF (median longevity

82 the titin and sarcomere variants that cause dilated cardiomyopathy and the desmosomal variants that

83 istry than in large cohorts of patients with dilated cardiomyopathy and TTNtv cardiomyopathy and not

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

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

86 earts of transplant recipients (ischemic and dilated cardiomyopathy), and from nonused donor hearts.

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

88 ble cases by cardiac MRI, 3 were found to be dilated cardiomyopathy, and 2 were found to be end-stage

89 120 patients with ischemic, 60 patients with dilated cardiomyopathy, and 30 patients with normal LVEF

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

91 uctive cardiomyopathy, 131 genes/17 ncRNA in dilated cardiomyopathy, and 51 genes/5 ncRNA in ischemic

92 ertrophic obstructive cardiomyopathy, 151 in dilated cardiomyopathy, and 55 in ischemic cardiomyopath

93 ive cardiomyopathy, ischemic cardiomyopathy, dilated cardiomyopathy, and 9 control patients with nonf

94 nalysis of fibrotic scarring in non-ischemic dilated cardiomyopathy, and its relationship to electric

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

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

97 ntified in a pediatric patient with sporadic dilated cardiomyopathy, and we determined a molecular me

98 Moreover, TTNtv associated with dilated cardiomyopathy are estimated to be present in 0.

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

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

101 ecellularized ECM resulting from ischemic or dilated cardiomyopathy, as well as from mouse infarcted

102 in the hearts of individuals with idiopathic dilated cardiomyopathy, as well as the hearts of patient

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

104 ause an autosomal dominant inherited form of dilated cardiomyopathy associated with cardiac conductio

105 sed cardiac microtissue contraction, whereas dilated cardiomyopathy-associated variants decreased con

106 sed cardiac microtissue contraction, whereas dilated cardiomyopathy-associated variants decreased con

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

108 are frequent causes of acute myocarditis and dilated cardiomyopathy, but an effective antiviral thera

109 gene mutations are a known cause of familial dilated cardiomyopathy, but the precise mechanisms trigg

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

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

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

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

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

115 scular dystrophy (DMD) develop a progressive dilated cardiomyopathy characterized by inflammatory cel

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

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

118 of cardiovascular mortality compared with a dilated cardiomyopathy control group (odds ratio, 1.10 [

119 nd how TNNT2 variants cause hypertrophic and dilated cardiomyopathies could improve heart failure ris

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

121 vestigate the frequency and genetic basis of dilated cardiomyopathy (DCM) among relatives of index pa

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

123 ) is an established therapy in patients with dilated cardiomyopathy (DCM) and conduction disorders.

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

125 in striated muscle tropomyosin are linked to dilated cardiomyopathy (DCM) and hypertrophic cardiomyop

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

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

128 Genotype-phenotype correlations in dilated cardiomyopathy (DCM) and, in particular, the eff

129 c disease identified an Iranian patient with dilated cardiomyopathy (DCM) as a carrier of a novel, ho

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

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

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

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

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

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

136 own to be associated with the development of dilated cardiomyopathy (DCM) in Doberman Pinchers (DPs).

137 exploring the molecular basis of congenital dilated cardiomyopathy (DCM) in genome-edited pigs homoz

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

139 Dilated cardiomyopathy (DCM) is a clinical diagnosis cha

140 Dilated cardiomyopathy (DCM) is a common condition, whic

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

142 Dilated cardiomyopathy (DCM) is a condition of abnormal

143 Dilated cardiomyopathy (DCM) is a genetically heterogene

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

145 Dilated cardiomyopathy (DCM) is a leading cause of morbi

146 Familial dilated cardiomyopathy (DCM) is a leading cause of sudde

147 Dilated cardiomyopathy (DCM) is a major cause of mortali

148 Dilated cardiomyopathy (DCM) is a major co-existing form

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

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

151 Dilated cardiomyopathy (DCM) is associated with mutation

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

153 Dilated cardiomyopathy (DCM) is genetically heterogeneou

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

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

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

157 We investigated a dilated cardiomyopathy (DCM) mutation (F764L) in human b

158 rdiomyocytes (iPSC-CMs) from patients with a dilated cardiomyopathy (DCM) mutation, troponin T (TnT)-

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

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

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

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

163 hythmogenic right ventricular cardiomyopathy/dilated cardiomyopathy (DCM) with an initial focus on PL

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

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

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

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

168 a frequency of 6% among Danish patients with dilated cardiomyopathy (DCM), it was the aim to investig

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

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

171 s) are common in individuals with idiopathic dilated cardiomyopathy (DCM).

172 on and systolic dysfunction resembling human dilated cardiomyopathy (DCM).

173 ost frequently mutated genes associated with dilated cardiomyopathy (DCM).

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

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

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

177 common inciting stressors, a syndrome called dilated cardiomyopathy (DCM).

178 Genetic analysis is a first-tier test in dilated cardiomyopathy (DCM).

179 CCM), hypertrophic cardiomyopathy (HCM), and dilated cardiomyopathy (DCM).

180 cause a diverse array of diseases, including dilated cardiomyopathy (DCM).

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

182 rlying structural heart disease consisted of dilated cardiomyopathy (DCM, 49%), arrhythmogenic right

183 chanically Assisted Circulatory Support with dilated cardiomyopathy (DCM, n=19 921), nonamyloid restr

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

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

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

187 involvement is characterized by progressive dilated cardiomyopathy, decreased fractional shortening

188 Patients with myocarditis or dilated cardiomyopathy develop autoantibodies to SERCA2a

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

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

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

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

193 Ntv) are the most prevalent genetic cause of dilated cardiomyopathy, found in <=25% of familial cases

194 he decedents with an antemortem diagnosis of dilated cardiomyopathy fulfilled definite 2010 Task Forc

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

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

197 opathy Precision Medicine Study is that most dilated cardiomyopathy has a genetic basis.

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

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

200 is the major cause of death and manifests as dilated cardiomyopathy, heart failure, arrhythmias, and

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

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

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

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 ified in association with ASD and late-onset dilated cardiomyopathy in a large, multi-generational fa

207 verse cardiovascular events in patients with dilated cardiomyopathy in a multicenter setting as part

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

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

210 and clinically relevant treatment to rescue dilated cardiomyopathy in patients with DMD.

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

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

213 isease models of myocardial infarction (MI), dilated cardiomyopathy induced via aortic banding, and s

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

215 Dilated cardiomyopathy is associated with increased risk

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

217 Heart failure due to dilated cardiomyopathy is frequently caused by myocardit

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

219 ual myocardial injury whereas others develop dilated cardiomyopathy is unclear.

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

221 an be a precursor of chronic myocarditis and dilated cardiomyopathy, leading causes of heart transpla

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

223 ult cardiac vasculature and thereby prevents dilated cardiomyopathy-like defects.

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

225 005) and of patients with end-stage ischemic-dilated cardiomyopathy (mean difference, 0.13 [95% CI, 0

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

227 Compared with other forms of dilated cardiomyopathy, mutations in LMNA are responsibl

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

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

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

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

232 ular cardiomyopathy (ARVC) (n = 9 [8%]), and dilated cardiomyopathy (n = 5 [4%]).

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

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

235 hese, 15 (7%) were diagnosed antemortem with dilated cardiomyopathy (n=8) or ACM (n=7).

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

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

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

239 atio, 1.08 [95% CI, 1.05-1.11]; P<0.001) and dilated cardiomyopathy (odds ratio, 1.04 [95% CI, 1.01-1

240 LN R14del mutation are at risk of developing dilated cardiomyopathy or arrhythmogenic right ventricul

241 tes myocardial inflammation with established dilated cardiomyopathy or hypokinetic nondilated phenoty

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

243 heart failure instead of the commonly taught dilated cardiomyopathy pathway.

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 with cardiac ribosome occupancy levels of 30 dilated cardiomyopathy patients demonstrates that these

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

248 Methods Thirty-four dilated cardiomyopathy patients, 30 ischemic cardiomyopa

249 idence of heart failure hospitalization than dilated cardiomyopathy patients.

250 milar cardiovascular risk when compared with dilated cardiomyopathy patients.

251 arrhythmias in LVNC patients were similar to dilated cardiomyopathy patients.

252 an tissues, and upregulated in the hearts of dilated cardiomyopathy patients.

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

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

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

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

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

258 The hypothesis of the Dilated Cardiomyopathy Precision Medicine Study is that

259 ere calculated in parents of 128 present-day dilated cardiomyopathy probands with TTNtv using the rev

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

261 ntractions are known to trigger a reversible dilated cardiomyopathy referred as arrhythmia-induced ca

262 Consecutive patients with dilated cardiomyopathy referred for cardiac magnetic res

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

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

265 ral functions involved in the development of dilated cardiomyopathy remain unclear.

266 in gene are associated with hypertrophic and dilated cardiomyopathy, respectively.

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

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

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

270 with a subsequent cardiomyopathy, especially dilated cardiomyopathy, starting already at mildly eleva

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

272 ome occupancy in the hearts of patients with dilated cardiomyopathy suggested the same posttranscript

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

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

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

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

277 164 ischemic cardiomyopathy, 150 nonischemic dilated cardiomyopathy), the mean left ventricular eject

278 s large multinational study of patients with dilated cardiomyopathy, the presence of LGE showed stron

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

280 with ischemic cardiomyopathy or nonischemic dilated cardiomyopathy undergoing cardiovascular magneti

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

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

283 tal RNA from cardiac tissue of patients with dilated cardiomyopathy was extracted, and sequences corr

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

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

286 se in risk with higher BMI, particularly for dilated cardiomyopathy, where a hazard ratio of 4.71 (95

287 NT2 variants are a cause of hypertrophic and dilated cardiomyopathies, which promote heart failure by

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

289 Mutations in A-type nuclear lamins cause dilated cardiomyopathy, which is postulated to result fr

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

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

292 ailure medications in patients with previous dilated cardiomyopathy who were now asymptomatic, whose

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

294 Patients with dilated cardiomyopathy whose symptoms and cardiac functi

295 Many patients deemed to have recovered from dilated cardiomyopathy will relapse following treatment

296 iffered considerably: loss of titin leads to dilated cardiomyopathy with combined systolic and diasto

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

298 The primary endpoint was a relapse of dilated cardiomyopathy within 6 months, defined by a red

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

300 that often presents as heart failure due to dilated cardiomyopathy years after anthracycline exposur