ライフサイエンスコーパス: DCM

1 right ventricular cardiomyopathy (n = 111), DCM (n = 95), hypertrophic cardiomyopathy (n = 40) and p

2 nalyzed rare variants from 6112 HCM and 1315 DCM patients and 33,370 ExAC controls.

3 Twenty-six subjects (14 DCM and 12 normal) underwent cardiac magnetic resonance

4 CMR was performed in 19 control subjects, 19 DCM, and 13 HCM patients.

5 idues (expected 23%; HCM 54%, p=2.6x10(-19); DCM 26%, p=0.66; controls 20%, p=0.23).

6 In addition, DCM has been identified as a predictor of positive respo

7 s to decipher allelic heterogeneity in adult DCM.

8 Myr exerts cardioprotective effects against DCM through the blockage of inflammation, oxidative stre

9 used as a natural and safe treatment against DCM via Nrf2 activation.

10 Although DCM samples showed reexpression of EH-myomesin, an isofo

11 However, although DCM patients do not recover and slowly deteriorate furth

12 tive, genotype-phenotype study of ambulatory DCM patients, we show that prognostic factors for all-ca

13 ferent populations responsible for anaerobic DCM and CM metabolism, and further imply that the DCM an

14 Fpassive-cardiomyocytes was higher in AS and DCM at shorter muscle lengths, whereas Fpassive-collagen

15 n donor and to lower than baseline in AS and DCM.

16 further upward in donor and upward in AS and DCM.

17 ugmentation) is a possible remedy at CF- and DCM-contaminated sites without CT, which strongly inhibi

18 omponents were unaltered between control and DCM iPSC-CMs, we found that phosphodiesterases (PDEs) 2A

19 ythmia, conduction system disease (CSD), and DCM vulnerability.

20 que in hypertrophic cardiomyopathy (HCM) and DCM.

21 HCM mutants were hypersensitive and DCM mutants were hyposensitive to Ca(2+) in regulated ac

22 f cardiomyocytes in heart tissue of PPCM and DCM patients and compared these with nonfailing controls

23 e molecular designs of the DCM-Cys probe and DCM reporter.

24 ly inhibited CF organohalide respiration and DCM organohalide fermentation.

25 impairment was observed in ISHD samples, and DCM samples showed an intermediate response.

26 tial therapeutic targets for RAF1-associated DCM and further expand the clinical spectrum of RAF1-rel

27 ting active removal of peroxide compounds at DCM.

28 pigenetic modifications of PDE genes in both DCM iPSC-CMs and patient tissue.

29 f NAD(+) in the murine failing heart of both DCM and transverse aorta constriction mice that was acco

30 Diabetic cardiomyopathy (DCM) has been increasingly considered as a main cause of

31 Diabetic cardiomyopathy (DCM) is the leading cause of morbidity and mortality amo

32 2 (Nrf2) to prevent diabetic cardiomyopathy (DCM), male db/db and age-matched wild-type (WT) mice wer

33 injuries caused by diabetic cardiomyopathy (DCM).

34 R-34a in settings of dilated cardiomyopathy (DCM) and atrial fibrillation (AF) has not been assessed

35 conditions, such as dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM), which are of

36 s from patients with dilated cardiomyopathy (DCM) and inflammatory cardiomyopathy (ICM).

37 are associated with dilated cardiomyopathy (DCM) and severe heart failure.

38 human left ventricle dilated cardiomyopathy (DCM) biopsy samples and mouse models of DCM through BioI

39 ABSTRACT: Dilated cardiomyopathy (DCM) can be caused by mutations in sarcomeric and non-sa

40 ion in patients with dilated cardiomyopathy (DCM) compared with that at 3 T.

41 Dilated cardiomyopathy (DCM) due to mutations in RBM20, a gene encoding an RNA-b

42 ved understanding of dilated cardiomyopathy (DCM) due to titin truncation (TTNtv) may help guide pati

43 Non-ischemic dilated cardiomyopathy (DCM) has been recognized as a heritable disorder for ove

44 ies of children with dilated cardiomyopathy (DCM) have suggested that improved survival has been prim

45 , we determined that dilated cardiomyopathy (DCM) in fibrillin 1-deficient mice is a primary manifest

46 ine (R9C) results in dilated cardiomyopathy (DCM) in humans and transgenic mice, but the downstream s

47 Dilated cardiomyopathy (DCM) is a common form of cardiomyopathy causing systolic

48 Dilated cardiomyopathy (DCM) is a condition of abnormal myocardium with unknown

49 Dilated cardiomyopathy (DCM) is a highly heterogeneous trait with sarcomeric gen

50 Dilated cardiomyopathy (DCM) is a leading cause of heart failure.

51 Dilated cardiomyopathy (DCM) is an important cause of heart failure.

52 Dilated cardiomyopathy (DCM) is best understood as the final common response of

53 cause of idiopathic dilated cardiomyopathy (DCM) is unknown by definition, but its familial subtype

54 hogenesis leading to dilated cardiomyopathy (DCM) makes stratification difficult.

55 nts with nonischemic dilated cardiomyopathy (DCM) may be at lower risk for ventricular arrhythmias co

56 opathy (HCM) and two dilated cardiomyopathy (DCM) mutants were studied by biochemical approaches.

57 Nonischemic dilated cardiomyopathy (DCM) often has a genetic pathogenesis.

58 rce generation and a dilated cardiomyopathy (DCM) phenotype.

59 omyopathy (PPCM) and dilated cardiomyopathy (DCM) show similarities in clinical presentation.

60 of a mouse model of dilated cardiomyopathy (DCM) triggered by Serum Response Factor transcription fa

61 mutations that cause dilated cardiomyopathy (DCM) uncouple this modulation, but this has not been dem

62 ion in patients with dilated cardiomyopathy (DCM) using a dual approach.

63 15 years was 5% for dilated cardiomyopathy (DCM), 6% for hypertrophic cardiomyopathy (HCM), 12% for

64 important causes of dilated cardiomyopathy (DCM), a disease characterized by enlarged ventricular di

65 on genetic cause for dilated cardiomyopathy (DCM), a major cause of heart failure and premature death

66 ted with arrhythmia, dilated cardiomyopathy (DCM), and heart failure.

67 l fibrillation (AF), dilated cardiomyopathy (DCM), and mixed cardiac phenotype syndromes, yet the mol

68 r many patients with dilated cardiomyopathy (DCM), implantable cardioverter-defibrillators do not inc

69 r six months of age, dilated cardiomyopathy (DCM), most noticeably in the males.

70 in certain cases of dilated cardiomyopathy (DCM), traditionally labeled idiopathic (iDCM), where the

71 rst mouse models for dilated cardiomyopathy (DCM), yet the exact role of MLP in cardiac signalling pr

72 failing hearts with dilated cardiomyopathy (DCM).

73 diseases, including dilated cardiomyopathy (DCM).

74 TNtv) commonly cause dilated cardiomyopathy (DCM).

75 hy (EDMD) as well as dilated cardiomyopathy (DCM).

76 mes in children with dilated cardiomyopathy (DCM).

77 e the major cause of dilated cardiomyopathy (DCM); however, allelic heterogeneity (TTNtvs in differen

78 enosis (AS, n=9) and dilated cardiomyopathy (DCM, n=6).

79 diomyopathy, HCM and dilated cardiomyopathy, DCM) associated with mutations in the beta-myosin heavy

80 In Catheter-DCM, patients were randomized to either ixmyelocel-T or

81 e show that prognostic factors for all-cause DCM also predict outcome in TTNtv DCM, and that TTNtv DC

82 findings indicate that titin mutations cause DCM by disrupting critical linkages between sarcomerogen

83 runcations in the A-band domain of TTN cause DCM, whereas truncations in the I band are better tolera

84 Yet, the majority of variants causing DCM remain to be identified.

85 ro-2-propanol (HFIP) and methylene chloride (DCM) is described.

86 Detection of pre-clinical DCM could substantially reduce morbidity and mortality b

87 include CM phenotype, family history of CM (DCM), severity of systolic dysfunction (DCM), and extent

88 rol and demonstrate the utility of combining DCM with causal manipulations to test and refine models

89 Conversely, DCM associated with abnormal AT1R and FAK signaling was

90 PELP1-cyto DCM induced robust HMEC migration, which was reduced in

91 fer from chronic, progressively debilitating DCM that ultimately leads to cardiac failure and death,

92 diac dysfunction, such as conduction defect, DCM, and heart failure, remains unclear.

93 that the culture lost the ability to degrade DCM.

94 omplete heart block, but no longer developed DCM or the other phenotypes, including sex bias.

95 with those in chloroform or dichloromethane (DCM).

96 mixed culture RM grows with dichloromethane (DCM) as the sole energy source generating acetate, metha

97 ariants cause hypertrophic (HCM) or dilated (DCM) cardiomyopathy by disrupting sarcomere contraction

98 frican family with severe autosomal dominant DCM.

99 In families with autosomal-dominant DCM, heterozygous missense mutations were identified in

100 H2 generated during DCM degradation is consumed by the hydrogenotrophic CM d

101 omethane (CM) was not an intermediate during DCM utilization consistent with the observation that CM

102 CM (DCM), severity of systolic dysfunction (DCM), and extent of LV hypertrophy (HCM).

103 We randomly assigned (1:1) clinics to either DCM (involving training for physicians in use of treatme

104 rmation flow within the previously estimated DCM.

105 there is little compelling reason to exclude DCM compounds from screening decks in favor of previousl

106 Experimentally, DCM laser dye has been embedded into lamellar metal/diel

107 toskeleton, have been implicated in familial DCM to date.

108 used to describe the prevalence of familial DCM among idiopathic DCM cases and the genetic architect

109 ly, we established an iPSC model of familial DCM from patients with a mutation in TNNT2, a sarcomeric

110 p, we established a new paradigm of familial DCM pathogenesis as a developmental disorder that is pat

111 CM than in patients with genetic or familial DCM (40% vs. 25%; p = 0.04).

112 nstrated in 35 (16%) and genetic or familial DCM in 70 (33%) patients, including 16 (8%) patients wit

113 Genetic or familial DCM per se was of no prognostic significance, but when i

114 esis, this study demonstrates RBM20 familial DCM is a developmental disorder initiated by molecular d

115 ndeed, hiPSC-CMs recapitulate RBM20 familial DCM phenotype in a dish and establish a tool to dissect

116 ures the first hiPSC model of RBM20 familial DCM.

117 r molecule is a charge-transfer fluorophore, DCM, which is strongly fluorescent in its pristine state

118 patients, underscoring the ongoing need for DCM gene discovery.

119 microbubble destruction (UTMD) technique for DCM prevention.

120 has shown promise as a molecular therapy for DCM, but its delivery is inefficient and non-specific.

121 ional Human Genome Research Institute-funded DCM Precision Medicine Study, which aims to enroll 1300

122 robust formylation with an in situ generated DCM anion has been developed for the asymmetric construc

123 ses in rate pressure product in both groups (DCM, 76+/-15% and normal, 79+/-9%; P=0.84).

124 alysed in human non-ischemic dilated hearts (DCM).

125 prevalence of familial DCM among idiopathic DCM cases and the genetic architecture of idiopathic DCM

126 et rigorous clinical criteria for idiopathic DCM along with 2600 of their relatives.

127 Most children in both cohorts had idiopathic DCM (64% vs. 63%, respectively).

128 We hypothesize that most idiopathic DCM, whether familial or nonfamilial, has a genetic basi

129 s and the genetic architecture of idiopathic DCM in multiple ethnicity-ancestry groups.

130 the cause of approximately 6% of idiopathic DCM, commonly underpins more aggressive management becau

131 this study will demonstrate that idiopathic DCM has a genetic basis and guide best practices for a g

132 function initially, children with idiopathic DCM can recover normal LV size and function, particularl

133 disease, and all individuals with idiopathic DCM will undergo exome sequencing to identify relevant v

134 t concentrations exceeding 3000 ppmv impeded DCM degradation.

135 Implementing DCM in different health care systems should become an ac

136 In DCM, E2A was similar to control subjects in diastole, bu

137 In DCM, increased FXR1 expression appears to play an import

138 Sheetlet function was abnormal in DCM with altered systolic conformation and reduced mobil

139 ot accompanied by increased NOS1 activity in DCM, partly due to the elevated PIN levels and not becau

140 higher in AS at longer muscle lengths and in DCM at shorter and longer muscle lengths.

141 We found that alphaSKA is augmented in DCM compared with healthy controls, 43.1 +/- 0.9% versus

142 SC-CMs) but that this pathway was blunted in DCM iPSC-CMs.

143 The MOGE(S) classification in DCM is applicable, and each attribute or the gene-enviro

144 f global cardiac performance, is elevated in DCM; however, its prognostic implications have not been

145 iance structure, the S:D ratio was higher in DCM patients (-0.425 [0.072]; P<0.001) because of shorte

146 erentiation but never directly implicated in DCM before, was a prominently perturbed pathway.

147 t variants in genes previously implicated in DCM.

148 Obtaining more realistic V0 information in DCM can improve the identifiability of the system and wo

149 ilitates the aggregation of these modules in DCM-d2 solution, through halogen bonding, forming oligom

150 ignificance of FXR1 upregulation observed in DCM.

151 genotype, cardiac phenotype, and outcomes in DCM.

152 microvascular dysfunction and oxygenation in DCM, suggesting that the impairment of perfusion is not

153 MPRI was significantly reduced in DCM (1.51+/-0.11 versus normal 1.86+/-0.10; P=0.03).

154 Resting PCr/ATP was reduced in DCM (1.66+/-0.07 versus normal 2.12+/-0.06; P=0.002).

155 robust HMEC migration, which was reduced in DCM from PELP1-cyto HMECs expressing IKK shRNA.

156 t of heart failure in mice, more robustly in DCM, and partially after transverse aorta constriction,

157 ce in oxygenation between groups: SIDelta in DCM 17+/-3% versus normal 20+/-2% (P=0.38).

158 ases (PDEs) 2A and PDE3A were upregulated in DCM iPSC-CMs and that PDE2A was also upregulated in DCM

159 C-CMs and that PDE2A was also upregulated in DCM patient tissue.

160 y shows that different gene mutations induce DCM via diverse cellular pathways.

161 g to investigate how the V0 value influences DCM.

162 -50% of DCM cases and up to 25% of inherited DCM has been attributed to truncating mutations in the s

163 improves symptoms in patients with ischemic DCM but not in patients with nonischemic DCM.

164 To the best of our knowledge, ixCELL-DCM is the largest cell therapy study done in patients w

165 d, placebo-controlled phase 2B trial (ixCELL-DCM), patients from 31 sites in North America with New Y

166 Dementia care management (DCM) can increase the quality of care for people with de

167 llaborative-care depression care management (DCM) intervention could improve outcomes for Chinese adu

168 Dark chemical matter (DCM) compounds, which have been tested and found to be i

169 m the oligotrophic deep chlorophyll maximum (DCM) of the South China Sea.

170 Double conditioned medium (DCM) from the activated THP-1 cells was then applied to

171 assessed using a Distance Constraint Model (DCM).

172 Here, we introduce dynamic causal modeling (DCM) for optogenetic fMRI experiments-which uniquely all

173 Previously, dynamic causal modeling (DCM) indicated that mid LPFC integrates abstract, rostra

174 Using dynamic causal modeling (DCM) of cross-spectral densities, we quantify the putati

175 Moreover, dynamic causal modeling (DCM) was performed to identify the most likely functiona

176 s studies involving dynamic causal modeling (DCM) which embodies the hemodynamic model to invert the

177 using (stochastic) dynamic causal modeling (DCM).

178 males and females in (1) a model of moderate DCM and (2) a model of severe DCM with AF.

179 ients with degenerative cervical myelopathy (DCM) are felt to have lower recovery potential following

180 -wide basal ganglia-thalamocortical network, DCM accurately reproduced the empirically observed time

181 n in patients with nongenetic or nonfamilial DCM than in patients with genetic or familial DCM (40% v

182 mic DCM but not in patients with nonischemic DCM.

183 mber of the F-Box protein family, as a novel DCM-causing locus.

184 have been proposed to account for 25-50% of DCM cases and up to 25% of inherited DCM has been attrib

185 The results show that the ability of DCM analysis to reveal information about brain causality

186 mentioned characteristics and the ability of DCM-Cys to provide selective, nanomolar-level in vitro c

187 echlorinated CF to stoichiometric amounts of DCM.

188 d the molecular mechanisms of these cases of DCM; this strategy has been central to understanding Alz

189 associated mutations and may be causative of DCM.

190 of heart failure, notably in the context of DCM, a disease with few therapeutic options.

191 teria of TCM, 79 patients had a diagnosis of DCM, and 91 had a diagnosis of ICM.

192 to be in line with the expected fraction of DCM calculated based on a probability analysis.

193 Understanding of the genetics of DCM and how specific mutations affect arrhythmic risk is

194 ier displayed histopathological hallmarks of DCM and reduced TNNI3K protein staining with unique amor

195 utic effects of bFGF-NP/UTMD on the heart of DCM rats were studied by measuring LV systolic and diast

196 iew will address diagnosis and management of DCM, including the role of genetic evaluation.

197 rt tissue in a transgenic R9C mouse model of DCM compared with wild-type littermates.

198 thy (DCM) biopsy samples and mouse models of DCM through BioID proximity assay and RNA immunoprecipit

199 issue samples from human and mouse models of DCM via Western blot analysis.

200 The observed large number of DCM compounds in the BI screening deck is found to be in

201 omplex may contribute to the pathogenesis of DCM.

202 utation is implicated in the pathogenesis of DCM.

203 A significant proportion of DCM cases have an underlying genetic or inflammatory bas

204 To test the effectiveness and safety of DCM in the treatment and care of people with dementia li

205 ed the impaired beta-adrenergic signaling of DCM iPSC-CMs, suggesting therapeutic potential.

206 g cardiovascular activity in early stages of DCM.

207 l adjunct to help further refine subtypes of DCM, especially where arrhythmia risk is increased, and

208 ntial therapeutic agent for the treatment of DCM.

209 Children <18 years of age with some type of DCM enrolled in the Pediatric Cardiomyopathy Registry we

210 The cause of a substantial percentage of DCMs remains unknown, and no gene-specific therapy is av

211 Methodologically rigorous clinical trials on DCM are lacking.

212 of RAF1 mutations was ~9% in childhood-onset DCM cases in these three cohorts.

213 Optimizing DCMs of theta and gamma frequency range responses, model

214 Our DCM results suggested that the precision of predictabili

215 trum of ribosomopathies to include pediatric DCM.

216 are links between pKa(LAC) and pKa(THF), pKa(DCM), pKa(MeCN) for neutral and cationic acids.

217 amples compared with controls, whereas PPCM, DCM, and ISHD samples all showed increased myofilament C

218 nd gas, on the removal efficiency of 500 ppm DCM was investigated.

219 lts indicated that BSE at high dose prevents DCM in a manner congruent with SFN treatment.

220 Herein is described a new probe, DCM-Cys, that preferentially reacts with cysteine to for

221 critical for the translation of a promising DCM prevention strategy.

222 2-methyl-6-p-(dimethylamino)styryl-4H-pyran (DCM) laser dye in deuterated dimethyl sulfoxide and its

223 ysteine to form a dicyanomethylene-4H-pyran (DCM) reporter whose red-energy fluorescence can be stimu

224 Interestingly, cultures that received DCM and CM together degraded both compounds concomitantl

225 Patients with dementia receiving DCM had an increased chance of receiving antidementia dr

226 in family presenting with a severe recessive DCM and LVNC.

227 th the observation that CM could not replace DCM as a growth substrate.

228 E1 gene (nesprin-1) were identified in seven DCM patients by mutation screening.

229 el of moderate DCM and (2) a model of severe DCM with AF.

230 ence of significant protection in the severe DCM and AF model in either sex.

231 ilst the primary molecular mechanism of some DCM-associated mutations in the contractile apparatus ha

232 In end-stage DCM, PKCalpha is concentrated at the intercalated disc o

233 his prospective, observational cohort study, DCM patients underwent clinical evaluation, late gadolin

234 sembly in both toluene-d8 and, surprisingly, DCM-d2 into dimers, with significant stabilities, throug

235 tion of each of four starter cultures: Texel DCM-1, Texel LM-30, Biostar Sprint, and SM-181.

236 The analysis suggests not only that DCM compounds have the chance to occasionally provide va

237 The DCM is an ensemble based statistical mechanical approach

238 The DCM sensor can also be used as an economical spray kit t

239 The DCM/HCM-associated mutants of vinculin occur in the 68-r

240 e stiffness was reduced about 38% in all the DCM mutant samples.

241 gene sequences dominated the culture and the DCM-degrader Candidatus Dichloromethanomonas elyunquensi

242 Growth of the CF-respiring and the DCM-degrading Dehalobacter populations and detoxificatio

243 e PIP2 Unlike vinculin, wild-type MV and the DCM/HCM-associated R975W mutant bind PIP2 in their inact

244 A similar strategy was implemented for the DCM formylation reaction.

245 ursor is increased, to a higher level in the DCM (40-fold) than in transverse aorta constriction (4-f

246 after 4 hours of oxygen via facemask in the DCM group.

247 hogenic role for elevated CELF1 level in the DCM heart.

248 n of miR-34a provides more protection in the DCM model in females than males.

249 rdiac functions and tissue morphology in the DCM rats were observed in bFGF-NP/UTMD group.

250 Moreover, the DCM-causing mutation ACTC E361G blunts this phosphorylat

251 trolled, thus preventing overaddition of the DCM anion and rendering the process reproducible.

252 1 expression is also a shared feature of the DCM heart.

253 = 640 nm) are red-shifted from those of the DCM-Cys probe (lambdaabs(probe) = 440 nm, lambdaemis(pro

254 e attributed to the molecular designs of the DCM-Cys probe and DCM reporter.

255 fragments (VL to Fab), and subsequently, the DCM was combined with molecular dynamics (MD) simulation

256 nd CM metabolism, and further imply that the DCM and CM degradation pathways are mechanistically dist

257 We have previously established that the DCM can be robustly applied across a series of antibody

258 We randomly assigned eight clinics to the DCM intervention (164 patients enrolled) and eight prima

259 Attachment of an acryl moiety to the DCM reporter via a self-eliminating, electron-withdrawin

260 Such crystalline phase originates from THF, DCM, or the irreversible desolvation of entrapped benzen

261 y we defined the pathogenic effects of three DCM-causing mutations: the sarcomeric mutations in genes

262 e 12 months, patients in clinics assigned to DCM had a significantly greater reduction in HAMD score

263 ge number of genes and alleles attributed to DCM, comprehensive genetic testing encompasses ever-incr

264 overview distinct genetic pathways linked to DCM and their pathogenetic mechanisms.

265 crocosms that received 6% (v/v) of the CF-to-DCM-dechlorinating culture Dhb-CF to achieve an initial

266 isease prevention in LNA-antimiR-34a treated DCM female mice was characterized by attenuated heart en

267 ce of receiving antidementia drug treatment (DCM, 114 of 291 [39.2%] vs care as usual, 31 of 116 [26.

268 all-cause DCM also predict outcome in TTNtv DCM, and that TTNtv DCM does not appear to be associated

269 predict outcome in TTNtv DCM, and that TTNtv DCM does not appear to be associated with worse medium-t

270 improved when their primary care clinic used DCM.

271 However, patients over 65 with DCM still achieve functionally significant improvement a

272 out titin were significantly associated with DCM.

273 0 serial echocardiograms of 48 children with DCM (7.0+/-6.0 years) and 25 controls.

274 xercise testing is feasible in children with DCM and is useful to predict outcomes.

275 Children with DCM have improved survival in the more recent era.

276 We examined 52 children with DCM who underwent CPET at median age 12.6 years (interqu

277 enter, retrospective review of children with DCM who underwent CPET.

278 Sample preparation involved extraction with DCM/methanol, a cleanup step with silica, and conversion

279 3 ppmv was observed in cultures growing with DCM, and the addition of exogenous H2 at concentrations

280 ness was a common feature in all hearts with DCM-associated mutations and may be causative of DCM.

281 Cx43 level was detected in mouse models with DCM, including myotonic dystrophy type 1 and CELF1 overe

282 The association of PLEKHM2 mutation with DCM and LVNC supports the importance of autophagy for no

283 egistry data suggest that many patients with DCM and an out-of-hospital cardiac arrest do not have a

284 MR spectroscopy is feasible in patients with DCM and gives higher signal-to-noise ratios and more pre

285 atients with TCM compared with patients with DCM and ICM.

286 a key criterion for selecting patients with DCM for an implantable cardioverter-defibrillator for pr

287 e approach to the selection of patients with DCM for implantable cardioverter-defibrillator implantat

288 ort study of 5,307 consecutive patients with DCM or ICM, no history of sustained ventricular arrhythm

289 ATP was significantly lower in patients with DCM than in control subjects at 7 T, which is consistent

290 A total of 213 consecutive patients with DCM were included: organ involvement was demonstrated in

291 A total of 479 patients with DCM were prospectively enrolled in the CSM-International

292 ed to increased risk of SCD in patients with DCM, and a higher posterior wall thickness Z-score was t

293 o 0.92; p = 0.005), whereas in patients with DCM, no such difference was observed (hazard ratio: 0.92

294 In patients with DCM, TTNtv throughout titin were significantly associate

295 performed at 3 T and 7 T in 25 patients with DCM.

296 dictor of functional status in patients with DCM.

297 the MOGE(S) classification in patients with DCM.

298 8(+) macrophages compared with patients with DCM.

299 failure with indications for CRT, those with DCM may not benefit from additional primary prevention i

300 hose with ICM but in only 0.4% of those with DCM.