ライフサイエンスコーパス: cardiomyopathy

1 ion of lipids and glucose is central to T2DM cardiomyopathy.

2 rs that are unique to pediatric hypertrophic cardiomyopathy.

3 ons of the epicardium to heart formation and cardiomyopathy.

4 crucial need to rule out light chain amyloid cardiomyopathy.

5 r disease outcomes in patients with ischemic cardiomyopathy.

6 ges to predict VAs in patients with ischemic cardiomyopathy.

7 a safe, preventative therapy for associated cardiomyopathy.

8 ous outcome, followed by clinical history of cardiomyopathy.

9 , estimating ejection fraction and assessing cardiomyopathy.

10 right ventricular cardiomyopathy or dilated cardiomyopathy.

11 are the commonest cause of heritable dilated cardiomyopathy.

12 lopment of obesity/diabetes mellitus-induced cardiomyopathy.

13 ised of an HLHS proband and relative(s) with cardiomyopathy.

14 or implantation in patients with nonischemic cardiomyopathy.

15 fic considerations were required for dilated cardiomyopathy.

16 n procedure data from patients with ischemic cardiomyopathy.

17 henotypes for long-term outcomes in ischemic cardiomyopathy.

18 performed on this model to study MFS related cardiomyopathy.

19 2 fourth-degree relatives with hypertrophic cardiomyopathy.

20 strategy to treat NS-associated hypertrophic cardiomyopathy.

21 s, related lethality, and the development of cardiomyopathy.

22 These alterations precede development of the cardiomyopathy.

23 activated during the formation of the atrial cardiomyopathy.

24 us in patients with obstructive hypertrophic cardiomyopathy.

25 iological role in the development of hepatic cardiomyopathy.

26 the 5 families with TNNI3 p.Arg21Cys-related cardiomyopathy.

27 f2) may either ameliorate or worsen diabetic cardiomyopathy.

28 n, and a fourth-degree relative with dilated cardiomyopathy.

29 nding of the genetic architecture of dilated cardiomyopathy.

30 jor ventricular gap junction protein, in DMD cardiomyopathy.

31 uncharacterized lncRNA GATA6-AS1 in dilated cardiomyopathy.

32 hereby worsening the progression of diabetic cardiomyopathy.

33 volved in cardiac hypertrophy, fibrosis, and cardiomyopathy.

34 cytes from patients with doxorubicin-induced cardiomyopathy.

35 chronic disease associated with hypertensive cardiomyopathy.

36 ionship between cocaine and heart failure or cardiomyopathy.

37 have been implicated in the pathogenicity of cardiomyopathy.

38 for the treatment and prevention of diabetic cardiomyopathy.

39 of a cumulative and progressively developing cardiomyopathy.

40 matory mediators in the pathology of hepatic cardiomyopathy.

41 tor, in symptomatic obstructive hypertrophic cardiomyopathy.

42 rognostic role in patients with hypertrophic cardiomyopathy.

43 f MYL4 (myosin light chain 4)-related atrial cardiomyopathy.

44 s in cardiomyocyte proliferation defects and cardiomyopathy.

45 ffectively discriminate CA from hypertrophic cardiomyopathy.

46 spectively reviewed for clinical features of cardiomyopathy.

47 derlying cardiac disease is termed cirrhotic cardiomyopathy.

48 point to a critical role of obesity in T2DM cardiomyopathy.

49 nostic criteria had poor sensitivity for DSP cardiomyopathy.

50 hanisms and early interventions for diabetic cardiomyopathy.

51 g those with rs6689879*C and CTCAE grade 2-4 cardiomyopathy.

52 cardiomyopathy, termed diabetic or lipotoxic cardiomyopathy.

53 ast one patient for inherited arrhythmias or cardiomyopathies.

54 cardiomyopathy (1/500 individuals), dilated cardiomyopathy (1/250) and arrhythmogenic right ventricu

55 (1/250) and arrhythmogenic right ventricular cardiomyopathy (1/5,000) are probably conservative given

56 The global estimates for hypertrophic cardiomyopathy (1/500 individuals), dilated cardiomyopat

57 congenital heart disease (2%), hypertrophic cardiomyopathy (2%), and others (5%).

58 Additionally, 28 patients with hypertrophic cardiomyopathy, 30 with chronic myocardial infarction an

59 (25%) of 36; LQTS, 48 (20%) of 238; dilated cardiomyopathy, 5 (9%) of 58; and HCM, 28 (8%) of 354.

60 vation (FD 58.2+/-5.0 ms versus hypertrophic cardiomyopathy 55.6+/-4.3 ms, chronic myocardial infarct

61 Hepatic cardiomyopathy, a special type of heart failure, develop

62 tical overlap region associated with dilated cardiomyopathy, A277V, will alter Tpm binding and thin f

63 In hypertrophic cardiomyopathy, after a primary prevention implant, ICD

64 etween body weight in adolescence and future cardiomyopathy among men was recently identified.

65 d in those <24 years of age, 30 (77%) of 39; cardiomyopathies and BrS predominated in those >24 years

66 ich is known as cardiac trabeculation, cause cardiomyopathies and embryonic lethality, yet how tissue

67 on of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association st

68 Cardiomyopathies and neuronal disorders are associated w

69 - 12 years, 83% were males, 52% had ischemic cardiomyopathy and 54% were destination therapy.

70 percent of these patients had acute ischemic cardiomyopathy and 66% underwent cardiopulmonary resusci

71 dred eighty-three patients with hypertrophic cardiomyopathy and a low- or intermediate 5-year risk of

72 progressive childhood retinal degeneration, cardiomyopathy and almost undetectable plasma taurine le

73 Partial nephrectomy induced cardiomyopathy and anemia in the mice, introducing oxida

74 ene mutations account for 3% of hypertrophic cardiomyopathy and carriers have a heterogeneous phenoty

75 rial content and function, leading to severe cardiomyopathy and death.

76 verexpression (mtCaMKII) have severe dilated cardiomyopathy and decreased ATP that causes elevated cy

77 prognostic usefulness of MRI in hypertrophic cardiomyopathy and Fabry disease.

78 h wild-type or variant transthyretin amyloid cardiomyopathy and heart failure (mean age, 74.5 years)

79 ng therapeutic strategy for aging-associated cardiomyopathy and heart failure.

80 tion leads to an infiltrative or restrictive cardiomyopathy and is the major contributor to poor prog

81 Patients with hypertrophic cardiomyopathy and MYBPC3 variants were identified from

82 diac or renal stressor, would mimic diabetic cardiomyopathy and nephropathy, respectively.

83 ciated with arrhythmogenic right ventricular cardiomyopathy and of an endomyocardial biopsy showing f

84 ays involved in the pathogenesis of diabetic cardiomyopathy and potential cardioprotective strategies

85 Patients with ischemic or dilated cardiomyopathy and reduced left ventricular ejection fra

86 upA) murine model recapitulates hypertrophic cardiomyopathy and skeletal muscle weakness of human IOP

87 in and sarcomere variants that cause dilated cardiomyopathy and the desmosomal variants that cause ei

88 identify individuals at risk for PVC-induced cardiomyopathy and to identify preventative and therapeu

89 milial amyloidosis, 0.15% for PRKAG2-related cardiomyopathy, and 1 patient with Noonan syndrome.

90 astole and systole in 20 CA, 11 hypertrophic cardiomyopathy, and 10 control subjects with calculation

91 enosis and associated secondary hypertrophic cardiomyopathy, and 15 controls) in identical midventric

92 All 4 patients had nonischemic cardiomyopathy, and 3 had left ventricular assist device

93 ents with ischemic, 60 patients with dilated cardiomyopathy, and 30 patients with normal LVEF.

94 thophysiological abnormality in hypertrophic cardiomyopathy, and a major determinant of dynamic left

95 ed 5 weeks after Px with the aim of inducing cardiomyopathy, and cardiac function and remodeling was

96 ucing ACC2 deletion prevents obesity-induced cardiomyopathy, and if so, to elucidate the underlying m

97 ile range, 58-75) years, 40% had an ischemic cardiomyopathy, and median HF duration was 2.8 years (0.

98 ejection fraction was 20%, 81% had ischemic cardiomyopathy, and PAINESD score was 18+/-5.

99 associated with progressive muscle weakness, cardiomyopathy, and respiratory failure.

100 The clinical features of diabetic cardiomyopathy are cardiac hypertrophy and diastolic dys

101 ges of arrhythmogenic right ventricular (RV) cardiomyopathy are limited.

102 ommendations for AM and chronic inflammatory cardiomyopathy are mainly based on expert opinion given

103 ogenic (P/LP) variants associated with MCVD (cardiomyopathies, arrhythmias, connective tissue disorde

104 = 9 [8%]), arrhythmogenic right ventricular cardiomyopathy (ARVC) (n = 9 [8%]), and dilated cardiomy

105 Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited cardiomyopathy, wh

106 Arrhythmogenic right ventricular cardiomyopathy (ARVC), with skin manifestations, has bee

107 cessive form of NS with massive hypertrophic cardiomyopathy as clinically the most prevalent symptom

108 tients aged less than 70 years with ischemic cardiomyopathy as indicated using logistic regression ad

109 rized ECM resulting from ischemic or dilated cardiomyopathy, as well as from mouse infarcted tissue,

110 to include mild adult forms with or without cardiomyopathy, associate ASC-1 depletion with isolated

111 sphorylation of Ser(16) was disrupted by the cardiomyopathy-associated DeltaArg(14) mutation, implyin

112 and case-control cohorts revealed defects in cardiomyopathy-associated genes in patients with HLHS, w

113 set of TTNtv-positive children evaluated for cardiomyopathy at Texas Children's Hospital was retrospe

114 rated aging, these mice develop hypertrophic cardiomyopathy at ~13 months of age, presumably due to o

115 d for the diagnosis of transthyretin amyloid cardiomyopathy (ATTR-CM).

116 MD cohort (n=81), and a cohort of all other cardiomyopathies, called cardiomyopathy-unmatched (n=41

117 tion, evaluation for a familial component of cardiomyopathy can lead to increased identification of p

118 Cardiomyopathy cases were identified by linking the Medi

119 c transplantation as a result of restrictive cardiomyopathy caused by a heterozygous R406W-desmin mut

120 Investigating the effects of cardiomyopathy-causing mutations could help clarify TNT1

121 Cirrhotic cardiomyopathy (CCM) is cardiac dysfunction in patients

122 nd outcome of patients with Danon disease in cardiomyopathy centers throughout Europe.

123 hronic inflammatory process that can lead to cardiomyopathy (Chagas disease).

124 PRKAG2 syndrome is a progressive cardiomyopathy characterized by high rates of atrial fib

125 Inflammatory cardiomyopathy, characterized by inflammatory cell infil

126 This executive summary of the hypertrophic cardiomyopathy clinical practice guideline provides reco

127 m This executive summary of the hypertrophic cardiomyopathy clinical practice guideline provides reco

128 he ATTR-ACT trial (Transthyretin Amyloidosis Cardiomyopathy Clinical Trial), published literature, US

129 and relatively small genotyped hypertrophic cardiomyopathy cohorts have precluded detailed genotype-

130 s lower in cardiac tissue from patients with cardiomyopathy compared to controls.

131 Despite extensive research, inflammatory cardiomyopathy complicated by left ventricular dysfuncti

132 nal Research, Cardiac Failure & Myocarditis, Cardiomyopathies/Congenital & Genetics, Cardio-Oncology,

133 NNT2 variants cause hypertrophic and dilated cardiomyopathies could improve heart failure risk determ

134 Diabetic cardiomyopathy (DbCM) is a major complication in type-1

135 e the frequency and genetic basis of dilated cardiomyopathy (DCM) among relatives of index patients w

136 established therapy in patients with dilated cardiomyopathy (DCM) and conduction disorders.

137 Dilated cardiomyopathy (DCM) is a common condition, which carrie

138 Dilated cardiomyopathy (DCM) is a genetically heterogeneous card

139 Dilated cardiomyopathy (DCM) is an important cause of heart fail

140 Dilated cardiomyopathy (DCM) is genetically heterogeneous, with

141 ytes (iPSC-CMs) from patients with a dilated cardiomyopathy (DCM) mutation, troponin T (TnT)-R173W, d

142 nciting stressors, a syndrome called dilated cardiomyopathy (DCM).

143 tic analysis is a first-tier test in dilated cardiomyopathy (DCM).

144 tructural heart disease consisted of dilated cardiomyopathy (DCM, 49%), arrhythmogenic right ventricu

145 ly Assisted Circulatory Support with dilated cardiomyopathy (DCM, n=19 921), nonamyloid restrictive c

146 riteria for arrhythmogenic right ventricular cardiomyopathy diagnosis and data regarding this phenoty

147 ce Criteria arrhythmogenic right ventricular cardiomyopathy diagnosis was reached only in 11/25 patie

148 Arrhythmogenic right ventricular cardiomyopathy diagnostic criteria had poor sensitivity

149 n the growing field of iPSC-based sarcomeric cardiomyopathy disease models.

150 Early pathogenesis of diabetic cardiomyopathy (DMCM) may involve lipotoxicity of cardio

151 overt Duchenne muscular dystrophy-associated cardiomyopathy (DMDAC) may direct clinical management to

152 fficult to predict in patients with ischemic cardiomyopathy either by clinical tools or by attempting

153 We sequenced 29 families with hypertrophic cardiomyopathy enriched for pediatric-onset disease and

154 In 12 patients with EMB-proven cardiomyopathy, EVM identified pathological areas that h

155 Cardiomyopathy features, heart failure and arrhythmia, a

156 ential therapeutic target in LMNA-associated cardiomyopathy, for which there is no specific effective

157 To further investigate HLHS-cardiomyopathy gene associations in cases versus control

158 e compared for rare variant burden across 56 cardiomyopathy genes utilizing a weighted burden test ap

159 esearch and increased clinical experience in cardiomyopathy genetics, an improved understanding of th

160 Although cardiomyopathy has emerged as a leading cause of death i

161 h attention this phenomenon, termed diabetic cardiomyopathy, has received over several decades, under

162 he incidence and prevalence of the inherited cardiomyopathies have been derived from screening studie

163 Clinical correlates of DSP cardiomyopathy have been limited to small case series.

164 thogenesis and clinical features of diabetic cardiomyopathy have been well-studied in the past decade

165 relates of LVT regression were a nonischemic cardiomyopathy (hazard ratio [HR]: 2.74; 95% confidence

166 s a hallmark of hypertrophic and restrictive cardiomyopathies (HCM and RCM).

167 syndrome (LQTS) (n = 48 [42%]), hypertrophic cardiomyopathy (HCM) (n = 28 [24%]), Brugada syndrome (B

168 g of relatives of patients with hypertrophic cardiomyopathy (HCM) caused by sarcomere protein (SP) ge

169 sex on phenotypic expression in hypertrophic cardiomyopathy (HCM) has not been well characterized in

170 tribution of MYBPC3(Delta25) to hypertrophic cardiomyopathy (HCM) in a large patient cohort.

171 ess the genetic architecture of hypertrophic cardiomyopathy (HCM) in patients of predominantly Chines

172 Hypertrophic cardiomyopathy (HCM) is an uncommon but important cause

173 Hypertrophic cardiomyopathy (HCM) occurs as a spontaneous disease in

174 tage" has been used to describe hypertrophic cardiomyopathy (HCM) with left ventricular systolic dysf

175 ominant phenocopy of sarcomeric hypertrophic cardiomyopathy (HCM), characterized by ventricular pre-e

176 often structurally abnormal in hypertrophic cardiomyopathy (HCM).

177 7) represent a leading cause of hypertrophic cardiomyopathy (HCM).

178 iation therapy exposures and late effects of cardiomyopathy, hearing loss, stroke, thyroid disorders,

179 cedent cardiac conditions (ie, heart failure/cardiomyopathy, hypertension, myocardial infarction, atr

180 tion velocity (CV) in patients with ischemic cardiomyopathy (ICM) and ventricular tachycardia (VT) is

181 rdiovascular events in patients with dilated cardiomyopathy in a multicenter setting as part of an em

182 eport the early onset of severe hypertrophic cardiomyopathy in a novel murine IOPD model generated ut

183 inicians to diagnose and manage hypertrophic cardiomyopathy in adult and pediatric patients as well a

184 inicians to diagnose and manage hypertrophic cardiomyopathy in adult and pediatric patients as well a

185 se cardiac dysfunction, but protects against cardiomyopathy in chronically obese mice.

186 tudies that investigate heart failure and/or cardiomyopathy in cocaine users for mechanisms independe

187 This cardiomyopathy, similar to cirrhotic cardiomyopathy in humans, is characterized by systemic h

188 dipocytes controls the development of uremic cardiomyopathy in mice subjected to partial nephrectomy.

189 wever, there is no reliable model of hepatic cardiomyopathy in mice.

190 February 2020, including initial reports of cardiomyopathy in one-third of the patients.

191 ng 4756 genotyped patients with hypertrophic cardiomyopathy in Sarcomeric Human Cardiomyopathy Regist

192 sts) may delay or prevent the development of cardiomyopathy in severe liver disease.

193 o early onset and accelerated development of cardiomyopathy in T1D, and CR-Atg5KO-induced adverse phe

194 led to distinctive improvements on reducing cardiomyopathy, including inhibition in lipo-toxicity by

195 In contrast, chronic inflammatory cardiomyopathy indicates myocardial inflammation with es

196 into the mouse model of experimental uremic cardiomyopathy, intraperitoneally.

197 Cardiomyopathy is a common complication among muscular d

198 Peripartum cardiomyopathy is a form of systolic heart failure affec

199 Childhood-onset cardiomyopathy is a heterogeneous group of conditions th

200 art mitochondrial subpopulations in diabetic cardiomyopathy is associated with obesity; however, many

201 The term diabetic cardiomyopathy is defined as the presence of abnormaliti

202 Although the pathogenesis of the cardiomyopathy is multifactorial, diabetic dyslipidaemia

203 Inflammatory cardiomyopathy is predominantly mediated by viral infect

204 Hypertrophic cardiomyopathy is the leading cause of sudden cardiac de

205 positive patients with isolated hypertrophic cardiomyopathy <18 years of age at diagnosis were eligib

206 TNNI3 p.Arg21Cys-related cardiomyopathy manifested a malignant phenotype-SCD occu

207 nd inotropic support at transplant to form a cardiomyopathy-matched cohort (n=162).

208 In total, we identified 1699 cases of cardiomyopathy (mean age at diagnosis, 46.2 [SD 9.1] yea

209 that reduced glucose utilization in diabetic cardiomyopathy might defend against glucotoxicity and ca

210 escued the abnormal phenotypes in the atrial cardiomyopathy models.

211 In hypertrophic cardiomyopathy, multimodality imaging is crucial to conf

212 PRKAG2 cardiomyopathy must be considered in patients with HCM a

213 nd the pathophysiological effects of genetic cardiomyopathy mutations.

214 e X-linked Danon disease manifests by severe cardiomyopathy, myopathy, and neuropsychiatric problems.

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

216 ongenital heart disease (n = 72, 23.5%), and cardiomyopathy (n = 72, 23.5%).

217 rillation, congenital heart disease, various cardiomyopathies, obesity, hypertension, diabetes, and c

218 Diabetic cardiomyopathy occurs as a result of the dysregulated gl

219 08 [95% CI, 1.05-1.11]; P<0.001) and dilated cardiomyopathy (odds ratio, 1.04 [95% CI, 1.01-1.06]; P=

220 The cardiomyopathy of Duchenne muscular dystrophy (DMD) is a

221 Cardiomyopathies often have a genetic cause, and the fie

222 Obstructive hypertrophic cardiomyopathy (oHCM) is characterized by unexplained le

223 estion while avoiding confounding effects of cardiomyopathy on mitochondrial phenotype, we utilized T

224 ause either arrhythmogenic right ventricular cardiomyopathy or dilated cardiomyopathy.

225 ardial inflammation with established dilated cardiomyopathy or hypokinetic nondilated phenotype, whic

226 tic discovery, and provide new insights into cardiomyopathy pathogenesis, as well.

227 d and applied retrospectively to 29 ischemic cardiomyopathy patients with contrast-enhanced computed

228 One hundred twenty-two consecutive ischemic cardiomyopathy patients with left ventricular ejection f

229 ohort comprises 217 consecutive hypertrophic cardiomyopathy patients with primary prevention ICDs imp

230 f heart failure hospitalization than dilated cardiomyopathy patients.

231 rdiovascular risk when compared with dilated cardiomyopathy patients.

232 Conclusion In the hypertrophic cardiomyopathy population, a three-dimensional convoluti

233 eria has the highest incidence of peripartum cardiomyopathy (PPCM) in the world.

234 ed by ejection fraction, sex, race, cause of cardiomyopathy, presence/absence of implantable cardiac

235 In patients with arrhythmogenic RV cardiomyopathy presenting with recurrent ventricular tac

236 antibodies (n=69, 57%), and prior peripartum cardiomyopathy pretransplant (n=57, 47%).

237 in premature ventricular contraction-induced cardiomyopathy (PVC-CM) remain unknown.

238 gnificant difference in baseline Kansas City Cardiomyopathy Questionnaire (24.5 versus 36.2, respecti

239 eported outcomes assessed by the Kansas City Cardiomyopathy Questionnaire and a novel HCM-specific in

240 th >=20-point improvement in the Kansas City Cardiomyopathy Questionnaire overall summary (KCCQ-OS) s

241 ationship between SBP change and Kansas City Cardiomyopathy Questionnaire overall summary score (KCCQ

242 between change in health status (Kansas City Cardiomyopathy Questionnaire overall summary score [KCCQ

243 he primary outcome was change in Kansas City Cardiomyopathy Questionnaire score between baseline and

244 sures, diuretic intensification, Kansas City Cardiomyopathy Questionnaire Total Symptom Score, 6-minu

245 retic intensification, symptoms (Kansas City Cardiomyopathy Questionnaire Total Symptom Score, 6-minu

246 The Kansas City Cardiomyopathy Questionnaire was administered to assess

247 er than those untreated (6-month Kansas City Cardiomyopathy Questionnaire, 68.0 [interquartile range,

248 Index, P=0.005) and HF-specific (Kansas City Cardiomyopathy Questionnaire, P=0.001) HRQOL.

249 OT gradient, pVO(2), NYHA class, Kansas City Cardiomyopathy Questionnaire-Clinical Summary Score (KCC

250 athy (DCM, n=19 921), nonamyloid restrictive cardiomyopathy (RCM, n=248), or ACM (n=46) between 2005

251 onic advanced heart failure from nonischemic cardiomyopathy receiving the Heartmate II LVAD were enro

252 Consecutive patients with dilated cardiomyopathy referred for cardiac magnetic resonance (

253 Hypertrophic cardiomyopathy registries have revealed distinct clinica

254 ternational SHaRe Registry (Sarcomeric Human Cardiomyopathy Registry) were used to describe the natur

255 ertrophic cardiomyopathy in Sarcomeric Human Cardiomyopathy Registry, 1316 patients were identified w

256 ts were identified from the Sarcomeric Human Cardiomyopathy Registry.

257 m the ongoing multinational Sarcomeric Human Cardiomyopathy Registry.

258 ent external cohort (SHaRe [Sarcomeric Human Cardiomyopathy Registry], n=285).

259 osttransplant survival compared with matched cardiomyopathy-related HTx recipients.

260 nique mutation in patients with hypertrophic cardiomyopathy remains unknown.

261 and mechanisms, especially of the associated cardiomyopathy, remains limited and effective therapeuti

262 nI-G203S mice, but not mice with established cardiomyopathy, restored cardiac myocyte mitochondrial m

263 This cardiomyopathy, similar to cirrhotic cardiomyopathy in h

264 disease Barth syndrome, which presents with cardiomyopathy, skeletal muscle weakness, fatigue, and o

265 n for Molecular Pathology and ClinGen's MYH7-cardiomyopathy specifications provide relevant guidance

266 rlying inherited arrhythmic syndromes and/or cardiomyopathies suggesting a role for these genes in ca

267 l Summary Score (KCCQ-CSS), and Hypertrophic Cardiomyopathy Symptom Questionnaire Shortness-of-Breath

268 In patients with transthyretin amyloid cardiomyopathy, tafamidis reduces all-cause mortality an

269 pasm, myocardial bridging and stress-induced cardiomyopathy (Takotsubo syndrome).

270 nd induce non-ischaemic and non-hypertensive cardiomyopathy, termed diabetic or lipotoxic cardiomyopa

271 infarction and gene correction for inherited cardiomyopathies that were unapproachable until a decade

272 -CoV-2 infection concomitant to an unrelated cardiomyopathy that led to euthanasia.

273 To explore and define therapies for DMD cardiomyopathy, the authors used DMD patient-specific hi

274 duced clinical endpoints related to diabetic cardiomyopathy, the combination of the two did not accen

275 multinational study of patients with dilated cardiomyopathy, the presence of LGE showed strong progno

276 ile disruption of the LINC complex can cause cardiomyopathy, the relevant interactions that bridge th

277 e sarcomere variants that cause hypertrophic cardiomyopathy, the titin and sarcomere variants that ca

278 k prediction model in pediatric hypertrophic cardiomyopathy to guide SCD prevention strategies.

279 cohort of all other cardiomyopathies, called cardiomyopathy-unmatched (n=41 317).

280 To this end, we tailored the ClinGen MYH7-cardiomyopathy variant interpretation framework; the spe

281 ten presents as an acute cardiac injury with cardiomyopathy, ventricular arrhythmias, and hemodynamic

282 Such Nrf2-mediated progression of diabetic cardiomyopathy was confirmed by a cardiomyocyte-restrict

283 The lowest risk for being diagnosed with a cardiomyopathy was detected at a BMI of 21 kg/m(2), with

284 Left ventricular (LV) predominant cardiomyopathy was exclusively present among patients wi

285 or PKP2, P<0.001), whereas right ventricular cardiomyopathy was present in only 14% of patients with

286 ociation between cocaine, heart failure, and cardiomyopathy, we first conducted a broad-term search i

287 Cases with childhood-onset cardiomyopathy were consecutively recruited.

288 ive unrelated probands with various forms of cardiomyopathy were evaluated.

289 ture's role in diseases such as hypertrophic cardiomyopathy where misalignment of cardiomyocytes has

290 sk with higher BMI, particularly for dilated cardiomyopathy, where a hazard ratio of 4.71 (95% CI, 2.

291 Incidence rates of cardiomyopathies, which are a common cause of heart fail

292 d with typical manifestation of hypertrophic cardiomyopathy, which can progress to heart failure and

293 icular cardiomyopathy (ARVC) is an inherited cardiomyopathy, which is associated with life-threatenin

294 The genetic literature on cardiomyopathy, which is often focused on the identifica

295 lts indicate that this approach to modelling cardiomyopathies will continue to provide critical insig

296 pn-csERRalpha/gamma knockdown mice exhibited cardiomyopathy with an arrest in mitochondrial maturatio

297 n and microcytic anemia, while one had fatal cardiomyopathy with lactic acidosis following a febrile

298 identifying markers of risk in patients with cardiomyopathy with the use of genetic testing.

299 mmarize the molecular mechanisms of diabetic cardiomyopathy, with a special emphasis on cardiac lipot

300 nd treatment of myocarditis and inflammatory cardiomyopathy, with a special focus on virus-induced an