ライフサイエンスコーパス: DCM

1 DCM is the leading cause of death in laminopathies.

2 DCM related to mutations in LMNA is a common inherited c

3 vity formation with 34.20% in non-DCM, 9.09% DCM, and 8 % in CNS (P <0.001).

4 linical investigations were performed in 109 DCM index patients and 445 of their relatives.

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

6 ne (DCM-total) extract used in TPHd; and (3) DCM extract with hydrocarbons isolated by silica gel cle

7 A total of 487 DCM patients were analyzed by next-generation sequencing

8 the molecular and cellular consequences of a DCM mutation in troponin-T, DeltaK210.

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

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

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

12 tations in the tail of MYH7 (p < 0.001), and DCM without NCCM in relatives (p < 0.001).

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

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

15 y hypomethylated genome-wide in controls and DCM hearts, but overall CpG methylation was increased in

16 que in hypertrophic cardiomyopathy (HCM) and DCM.

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

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

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

20 Although tSCI and DCM have different aetiologies, they show similar degree

21 Review describes the insights into tSCI and DCM that have been revealed by neuroimaging and outlines

22 ast, no association between hiPSI TTNtvs and DCM was discerned among individuals of African ancestry.

23 acroscale shape and microscale architecture, DCMs can be engineered with the necessary design freedom

24 As DCM eventually leads to impaired contractility, standard

25 etic investigations of 76 disease-associated DCM genes.

26 performed in 5 control and 5 LMNA-associated DCM hearts.

27 LADs are redistributed in LMNA-associated DCM in association with markedly altered CpG methylation

28 horter event-free survival than asymptomatic DCM relatives (P<0.001).

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

30 enes cose-gregate in individuals affected by DCM.

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

32 and genetic basis of dilated cardiomyopathy (DCM) among relatives of index patients with unexplained

33 apy in patients with dilated cardiomyopathy (DCM) and conduction disorders.

34 myosin are linked to dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM), respectively

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

36 type correlations in dilated cardiomyopathy (DCM) and, in particular, the effects of gene variants on

37 Iranian patient with dilated cardiomyopathy (DCM) as a carrier of a novel, homozygous single nucleoti

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

39 h the development of dilated cardiomyopathy (DCM) in Doberman Pinchers (DPs).

40 basis of congenital dilated cardiomyopathy (DCM) in genome-edited pigs homozygous for an RBM20 allel

41 Dilated cardiomyopathy (DCM) is a clinical diagnosis characterized by left ventr

42 Dilated cardiomyopathy (DCM) is a common condition, which carries significant mo

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

44 Dilated cardiomyopathy (DCM) is a genetically heterogeneous cardiac disease char

45 Dilated cardiomyopathy (DCM) is a leading cause of morbidity and mortality world

46 Familial dilated cardiomyopathy (DCM) is a leading cause of sudden cardiac death and a ma

47 Dilated cardiomyopathy (DCM) is a major cause of mortality and morbidity in lami

48 Dilated cardiomyopathy (DCM) is a major co-existing form of heart failure (HF) w

49 Dilated cardiomyopathy (DCM) is an important cause of heart failure and the lead

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

51 Dilated cardiomyopathy (DCM) is associated with mutations in cardiomyocyte sarco

52 Dilated cardiomyopathy (DCM) is genetically heterogeneous, with >100 purported d

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

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

55 We investigated a dilated cardiomyopathy (DCM) mutation (F764L) in human beta-cardiac myosin by de

56 from patients with a dilated cardiomyopathy (DCM) mutation, troponin T (TnT)-R173W, display sarcomere

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 cular cardiomyopathy/dilated cardiomyopathy (DCM) with an initial focus on PLN and development of eff

61 Danish patients with dilated cardiomyopathy (DCM), it was the aim to investigate the associated disea

62 omyopathy (HCM), and dilated cardiomyopathy (DCM).

63 diseases, including dilated cardiomyopathy (DCM).

64 uals with idiopathic dilated cardiomyopathy (DCM).

65 ion resembling human dilated cardiomyopathy (DCM).

66 enes associated with dilated cardiomyopathy (DCM).

67 TNtv) commonly cause dilated cardiomyopathy (DCM).

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

69 s, a syndrome called dilated cardiomyopathy (DCM).

70 a first-tier test in dilated cardiomyopathy (DCM).

71 disease consisted of dilated cardiomyopathy (DCM, 49%), arrhythmogenic right ventricular dysplasia (A

72 ulatory Support with dilated cardiomyopathy (DCM, n=19 921), nonamyloid restrictive cardiomyopathy (R

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

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

75 Mutations in several genes can cause DCM, including genes encoding structural components of t

76 plex N-glycosylation are sufficient to cause DCM and early death.

77 We suggest that the K15N mutation causes DCM by altering Ca(2+)-dependent thin-filament regulatio

78 tinct from a set of previously characterized DCM mutations.

79 (13 kDa Mw) dissolved in methylene chloride (DCM) was spray-dried before washing the microspheres in

80 hydrocarbons isolated by silica gel cleanup (DCM-SGC).

81 e percent and 56% of patients in the non-CNS DCM and CNS groups, respectively, developed disseminatio

82 ystem (CNS) disseminated coccidioidomycosis (DCM) has not been previously characterized.

83 isease, and disseminated coccidioidomycosis (DCM).

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

85 Fully connected DCM models were specified for each treatment condition t

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

87 that the culture lost the ability to degrade DCM.

88 id-phase extract (HLB); (2) dichloromethane (DCM-total) extract used in TPHd; and (3) DCM extract wit

89 ng piperidine as a base and dichloromethane (DCM) and N,N-dimethylformamide (DMF) as solvents) and re

90 In dichloromethane (DCM-d(2)), nonalkylated BINAM-derived bisurea catalyst e

91 g electrochemically "inert" dichloromethane (DCM) as a diluent in concentrated ethyl acetate (EA)-bas

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

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

94 M, NCCM with left ventricular (LV) dilation (DCM), and NCCM with LV hypertrophy (HCM).

95 While these mechanisms can drive DCM formation, they do not account for top-down controls

96 ght-dependent grazing is sufficient to drive DCM formation.

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

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

99 he greatest upregulation, with HLB exceeding DCM-total, and no upregulation in the hydrocarbon fracti

100 clinical investigations identified familial DCM in a total of 32% (n=35).

101 clinical investigations to identify familial DCM.

102 y pathogenic variants identified in familial DCM provides a firm basis for offering genetic investiga

103 ry Support profile 1 (30.4% versus 17.9% for DCM and 21.0% for nonamyloid RCM, P=0.04) at device impl

104 ial involvement as a genetic risk factor for DCM in this family.

105 Here, we propose a new mechanism for DCM formation: Light-dependent grazing by microzooplankt

106 nse/TP53 axis as a responsible mechanism for DCM in laminopathies and as a potential intervention tar

107 years [interquartile range, 49-66 years] for DCM and 55 years [interquartile range, 46-62 years] for

108 no upregulation in the hydrocarbon fraction (DCM-SGC).

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

110 Genetic DCM is characterized by a profile of electrical phenotyp

111 Genetic DCM was independently associated with electrical phenoty

112 Electrical phenotypes are common in genetic DCM, but their exact contribution to the clinical course

113 associated electrical phenotypes of genetic DCM (P<0.001).

114 One-fifth of all relatives (n=95) had DCM of whom 60% (n=57) had symptoms of heart failure at

115 identified only 34% (n=12/35) of hereditary DCM, whereas systematic clinical screening identified th

116 y cardiomyocyte genes as causes of heritable DCM, including mutations in LMNA, which encodes the nucl

117 ividuals of African ancestry, despite a high DCM prevalence (odds ratio, 1.8 [0.2-13.7]; P=0.57).

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

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

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

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

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

123 c variation and environmental factors impact DCM heritability remains unclear.

124 t concentrations exceeding 3000 ppmv impeded DCM degradation.

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

126 otein, SOS1 (Son of sevenless homolog 1), in DCM pathogenesis.

127 across the groups: 0.65% in non-DCM, 25% in DCM, and 88% in CNS (P<0.001).

128 les observed in 39.61% in non-DCM, 13.64% in DCM, and 20% in CNS (P<0.001).

129 ew toward multiparametric risk assessment in DCM with the hope of creating parametric risk models to

130 ignment as well as impaired contractility in DCM TnT-R173W iPSC-CMs.

131 nes in cis, were differentially expressed in DCM.

132 MR data characterizing the species formed in DCM-d(2) when reacting a bisurea catalyst with tetra-n-b

133 t variants in genes previously implicated in DCM.

134 h 12 genes, highlighting their importance in DCM and translating into high interpretability in diagno

135 serum response factor (SRF), is increased in DCM porcine and patient cardiac tissues and plays a cruc

136 but overall CpG methylation was increased in DCM.

137 ysregulates local sarcomeric microdomains in DCM iPSC-CMs.

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

139 ignificance of FXR1 upregulation observed in DCM.

140 genotype, cardiac phenotype, and outcomes in DCM.

141 determine pathogenic role of TP53 pathway in DCM, Tp53 gene was conditionally deleted in cardiac myoc

142 l investigations were routinely performed in DCM index-patients and their relatives.

143 re able to provide useful rick prediction in DCM.

144 re-organization and contractile recovery in DCM.

145 LADs were redistributed in DCM as evidenced by a gain of 520 and loss of 149 genomi

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

147 have limited value in diagnostic testing in DCM at present.

148 visage a broader role for genetic testing in DCM.

149 lic volume strongly associates with incident DCM in the general population.

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

151 iants can interact combinatorially to induce DCM, particularly when influenced by other disease-provo

152 -50% of DCM cases and up to 25% of inherited DCM has been attributed to truncating mutations in the s

153 coplasmic reticulum, are linked to inherited DCM.

154 nanospheres in the liquid-liquid interface (DCM-water bilayer) for the very first time, transmuting

155 in SOS1 as a contributing factor to isolated DCM.

156 In addition, >=76 recognized and likely DCM-genes were investigated.

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

158 Deep Chlorophyll Maxima (DCMs) are subsurface peaks in chlorophyll-a concentratio

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

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

161 rts to determine their validity as Mendelian DCM genes but have limited value in diagnostic testing i

162 alled directionally compliant metamaterials (DCMs) because they manifest prescribed compliant directi

163 in the EA solvent were surrounded by mobile DCM diluent.

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

165 We used spectral dynamic causal modeling (DCM) for resting-state fMRI data.

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

167 Dynamic causal modelling (DCM) combined with Canonical Variance Analysis (CVA) rev

168 Here we assess dynamic causal models (DCM) of cortical network responses, as generative models

169 robustly associated with dominant monogenic DCM.

170 f which is degenerative cervical myelopathy (DCM) - have provided important insights into the pathoph

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

172 as non-disseminated coccidioidomycosis (non-DCM, 462 patients), DCM (44 patients), and CNS (25 patie

173 pulmonary nodules observed in 39.61% in non-DCM, 13.64% in DCM, and 20% in CNS (P<0.001).

174 ly different across the groups: 0.65% in non-DCM, 25% in DCM, and 88% in CNS (P<0.001).

175 ences in cavity formation with 34.20% in non-DCM, 9.09% DCM, and 8 % in CNS (P <0.001).

176 g from 36% in familial to 13% in nonfamilial DCM.

177 d in genetic versus patients with nongenetic DCM (P=0.01).

178 ening identified the remaining 66% (n=23) of DCM families.

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

180 OCD levels in the endomyocardial biopsies of DCM patients associated with renal failure compared to D

181 associated mutations and may be causative of DCM.

182 addition, identifying the probable cause of DCM helps tailor specific therapies to improve prognosis

183 variant carrier status in a large cohort of DCM patients.

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

185 as an important factor in the development of DCM.

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

187 the variable penetrance and expressivity of DCM-associated genetic variants in vivo.

188 anges in the heart are a defining feature of DCM, we report a genome-wide association study of cardia

189 Nongenetic forms of DCM can result from different aetiologies, including inf

190 ntributing primarily to early-onset forms of DCM.

191 ts contribute to the complex heritability of DCM.

192 A family history of DCM identified only 34% (n=12/35) of hereditary DCM, whe

193 A family history of DCM occurred in 11% (n=12) while clinical investigations

194 dy helps characterize the natural history of DCM, provides insight into the host immunologic response

195 c data from a large family with a history of DCM, we discovered that heterozygous sequence variants i

196 CI, Auguste et al. generate a mouse model of DCM in which they delete Lmna in cardiomyocytes and disc

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

198 TTNtv was associated with increased odds of DCM in individuals of European ancestry (odds ratio [95%

199 lterations contribute to the pathogenesis of DCM in laminopathies.

200 rat sarcoma signaling in the pathogenesis of DCM, we assessed functional impact of each variant on th

201 genetic polymorphisms in the pathogenesis of DCM.

202 phenotype and ultimately the pathogenesis of DCM.

203 ays a crucial role in the pathophysiology of DCM.

204 gnment of sarcomeric proteins in presence of DCM TnT-R173W.

205 neous aetiology and clinical presentation of DCM make a correct and timely diagnosis challenging.

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

207 nd LMNA gene variants identify the subset of DCM patients who are at greatest risk for SCD and life-t

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

209 ntial therapeutic agent for the treatment of DCM.

210 cohort enriched in familial and early-onset DCM.

211 t in a pedigree with aggressive, early-onset DCM.

212 on 412 probands and family members from our DCM cohort, identifying several SOS1 variants with poten

213 coccidioidomycosis (non-DCM, 462 patients), DCM (44 patients), and CNS (25 patients).

214 s resulting in autosomal recessive pediatric DCM due to presumptive JPH2 truncation.

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

216 e the burden of rare variants in 56 putative DCM genes in 1040 patients with DCM and 912 healthy volu

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

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

219 tributes to the pathogenesis of LMNA-related DCM and point to PDGF receptor-beta (PDGFRB) as a potent

220 Here we modelled the LMNA-related DCM in vitro using patient-specific induced pluripotent

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

222 ding, encapsulation efficiency, and residual DCM and water content.

223 In the largest sequenced DCM cohort yet described, we observe robust disease asso

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

225 c variant of whom 36% (n=27/74) had sporadic DCM, whereas 60% (21/35) were familial cases.

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

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

228 g of biogeochemical cycling at and above the DCM.

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

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

231 re, biochemistry, and function caused by the DCM-linked mutation, M8R, which is located at the overla

232 hanisms, light-dependent grazing deepens the DCM, improving the fit of a global model with observatio

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

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

235 alyzed the expression levels of MYOCD in the DCM patients with and without renal diseases.

236 sudden cardiac death and pump failure in the DCM population.

237 ey have been tested less specifically in the DCM setting.

238 = 640 nm) are red-shifted from those of the DCM-Cys probe (lambdaabs(probe) = 440 nm, lambdaemis(pro

239 MYOCD has shown to be partially rescuing the DCM phenotype in porcine model.

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

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

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

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

244 Thus, DCMs show promise as irregularly shaped flexure bearings

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

246 ts associated with renal failure compared to DCM alone.

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

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

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

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

251 Work on the mechanisms underlying DCM formation has historically focused on phytoplankton

252 thogenic gene variants in a large unselected DCM population and determined the role of electrical phe

253 ple extraction of the desired products using DCM or ethyl acetate, followed by subjecting the recover

254 dentified 73 relatives with NCCM and 34 with DCM or HCM without NCCM.

255 ng 244 individuals of European ancestry with DCM in PennMedicine BioBank, hiPSI TTNtv carriers had lo

256 variants in TTN and DSP were associated with DCM in all comparisons.

257 hiPSI TTNtvs were not associated with DCM in individuals of African ancestry, despite a high D

258 LMNA(D300N) mutation is associated with DCM in progeroid syndromes.

259 e genetic variants have been associated with DCM, but common variant studies of the disease have yiel

260 c expression of LMNA(D300N), associated with DCM, led to pathogenic activation of the E2F/DNA damage

261 out titin were significantly associated with DCM.

262 hown to have robust disease association with DCM.

263 Thirty percent of RBM20-carriers with DCM died suddenly or experienced severe ventricular arrh

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

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

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

267 3 ppmv was observed in cultures growing with DCM, and the addition of exogenous H2 at concentrations

268 RNA sequencing of human hearts with DCM associated with defined LMNA pathogenic variants cor

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

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

271 NCCM with DCM (53%) was associated with LV systolic dysfunction (p

272 on of a pathogenic variant in a patient with DCM, familial segregation was performed.

273 ency of rare variation in 2538 patients with DCM across protein-coding regions of 56 commonly tested

274 senting a broad range of adult patients with DCM and 26% of cases in the diagnostic referral cohort e

275 56 putative DCM genes in 1040 patients with DCM and 912 healthy volunteers processed with identical

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

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

278 1.3% versus 6.7% and 19.4% for patients with DCM and nonamyloid RCM, respectively, P=0.014).

279 programmed cardiomyocytes from patients with DCM carrying the R636S allele.

280 ailure in gene-edited pigs and patients with DCM caused by RBM20 mutation.

281 Still, one-third of the patients with DCM do not respond to CRT.

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

283 This study included 689 patients with DCM from the Maastricht Cardiomyopathy Registry, undergo

284 Compared with patients with DCM or nonamyloid RCM who received durable MCS, those wi

285 ther aggregated data from 1498 patients with DCM sequenced in diagnostic laboratories and the Exome A

286 esses of nonresponse to CRT in patients with DCM using endomyocardial biopsies.

287 wed familial disease in 46% of patients with DCM who were initially deemed nonfamilial by history.

288 ht and Innsbruck registries of patients with DCM, 99 patients underwent endomyocardial biopsies befor

289 to clinical care will benefit patients with DCM, as will new diagnostic tools, such as serum biomark

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

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

292 e the first-line treatment for patients with DCM.

293 with a poor response to CRT in patients with DCM.

294 8(+) macrophages compared with patients with DCM.

295 quency of <1:10.000, and (3) segregated with DCM in >=7 affected individuals.

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

297 for patients with ACM relative to those with DCM or nonamyloid RCM (P<0.001) but did not differ signi

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

299 red superior to that observed for those with DCM.

300 subanalyses for individuals with and without DCM diagnoses.