ライフサイエンスコーパス: cardiomyopathy

1 myopathies, including heart muscle diseases (cardiomyopathy).

2 l leads to myocyte instability and a dilated cardiomyopathy.

3 Erk5 expression in Erk5-CKO hearts prevents cardiomyopathy.

4 on the genetic basis of this rare and morbid cardiomyopathy.

5 hypertrophy and in human hearts with dilated cardiomyopathy.

6 e have been linked to muscular dystrophy and cardiomyopathy.

7 umulative variant hypothesis in hypertrophic cardiomyopathy.

8 icion of genetically determined hypertrophic cardiomyopathy.

9 ncluding pulmonary arterial hypertension and cardiomyopathy.

10 cause mortality in patients with nonischemic cardiomyopathy.

11 a candidate gene for muscular dystrophy and cardiomyopathy.

12 ze and improves cardiac function in ischemic cardiomyopathy.

13 d LVNC in the absence of a family history of cardiomyopathy.

14 hythmias in patients with idiopathic dilated cardiomyopathy.

15 ntically delivered in patients with ischemic cardiomyopathy.

16 ce, including specifically those with atrial cardiomyopathy.

17 underpins the lasting and severe effects of cardiomyopathy.

18 cle (LV) ultimately transitions to a dilated cardiomyopathy.

19 arrhythmogenesis and remodeling, leading to cardiomyopathy.

20 unctional Pg is a hallmark of arrhythmogenic cardiomyopathy.

21 c remodeling from ARVC and post-inflammatory cardiomyopathy.

22 decades as a reversible form of nonischemic cardiomyopathy.

23 revention ICDs) in patients with nonischemic cardiomyopathy.

24 t MSCs (itMSCs) in patients with nonischemic cardiomyopathy.

25 latives, and 9 with noncompaction or dilated cardiomyopathy.

26 evaluation of all patients with hypertrophic cardiomyopathy.

27 behavior in an animal model of hypertrophic cardiomyopathy.

28 may increase risk for human arrhythmias and cardiomyopathy.

29 rate of children with chronic HF and dilated cardiomyopathy.

30 B species were found in type 1 diabetes and cardiomyopathy.

31 utic solutions to treat CVD such as ischemic cardiomyopathy.

32 l) in at least 100 patients with nonischemic cardiomyopathy.

33 se mortality among patients with nonischemic cardiomyopathy.

34 VCL knockout mice prior to the appearance of cardiomyopathy.

35 ly prevented the development of hypertrophic cardiomyopathy.

36 as Chagasic, other nonischemic, or ischemic cardiomyopathy.

37 fibroadipocytes, as in human arrhythmogenic cardiomyopathy.

38 imal models of both AMI and chronic ischemic cardiomyopathy.

39 nvolved in the development of HIV-associated cardiomyopathy.

40 that leads to chronic remodeling and dilated cardiomyopathy.

41 m for mitochondrial dysfunction in lipotoxic cardiomyopathy.

42 isease mimicking nonobstructive hypertrophic cardiomyopathy.

43 and none to arrhythmogenic right ventricular cardiomyopathy.

44 d cDKOs), which develops adult-onset dilated cardiomyopathy.

45 matic PVCs, and 29 (4.7%) had IVA-associated cardiomyopathy.

46 ontribute to the pathophysiology of diabetic cardiomyopathy.

47 dense regions of myocardium, in postinfarct cardiomyopathy.

48 serve as therapeutic targets in inflammatory cardiomyopathies.

49 c remodeling from ARVC and post-inflammatory cardiomyopathies.

50 omes of patients with ischemic or idiopathic cardiomyopathies.

51 idemiology, cause, and outcomes of pediatric cardiomyopathies.

52 ted in about one-third of idiopathic dilated cardiomyopathies.

53 oing cardiac transplantation are affected by cardiomyopathies.

54 pathogenesis and pathobiology of individual cardiomyopathies.

55 his gene as an important cause of structural cardiomyopathies.

56 s are the leading cause of inherited primary cardiomyopathies.

57 mpared with those with LVNC and co-occurring cardiomyopathy (0% versus 12%, respectively; P<0.01).

58 Among all patients (164 ischemic cardiomyopathy, 150 nonischemic dilated cardiomyopathy),

59 ease (35.7%) compared with those with Chagas cardiomyopathy (36.8%) (P=1.000).

60 were included, most of them having ischemic cardiomyopathy (65.4%).

61 ias (69% and 52%, respectively), and dilated cardiomyopathy (74% and 14%, respectively).

62 Cirrhotic cardiomyopathy, a condition characterized by increased c

63 Arrhythmogenic cardiomyopathy (AC) is an inherited heart muscle disease

64 Diagnostic screening for Anderson-Fabry cardiomyopathy (AFC) is performed in the presence of spe

65 mous LMNA VUS, demonstrated segregation with cardiomyopathy affection status and altered cardiac LMNA

66 its are characteristic of the desmin-related cardiomyopathies and crystallin cardiomyopathic diseases

67 ng hypertrophic, dilated, and arrhythmogenic cardiomyopathies and inherited arrhythmias.

68 numerous z-disc proteins are associated with cardiomyopathies and muscle diseases.

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

70 on in patients with obstructive hypertrophic cardiomyopathy and advanced heart failure.

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

72 s were used to examine a family with dilated cardiomyopathy and atrial and ventricular arrhythmias.

73 a subset of 517 epigenetic loci with dilated cardiomyopathy and cardiac gene expression.

74 ated on K1479 in the hearts of patients with cardiomyopathy and clinical conduction disease.

75 obtained from patients with newly diagnosed cardiomyopathy and clinical suspicion of myocarditis.

76 al tissue and blood of patients with dilated cardiomyopathy and controls.

77 mation and myocardial fibrosis, resulting in cardiomyopathy and death.

78 elopmental delay, failure to thrive, dilated cardiomyopathy and epilepsy, ultimately leading to death

79 luate known human congenital heart diseases: cardiomyopathy and heterotaxy.

80 esponsiveness in a model of familial dilated cardiomyopathy and improve cardiac function and morpholo

81 mmation in patients with nonischemic dilated cardiomyopathy and inflammatory cardiomyopathy (iCMP).

82 eview, we will review cancer therapy-induced cardiomyopathy and ischemia.

83 isease or environmental condition, can cause cardiomyopathy and lead to heart failure.

84 dverse outcome in patients with hypertrophic cardiomyopathy and may help to optimize risk stratificat

85 stability encountered in muscle diseases and cardiomyopathy and may underlie potential target treatme

86 in addition to the neuropathy, for example, cardiomyopathy and neuropathy.

87 , two deaths were attributed to hypertrophic cardiomyopathy and none to arrhythmogenic right ventricu

88 with relevance to ventricular noncompaction cardiomyopathy and regenerative medicine.

89 Regular surveillance and early treatment for cardiomyopathy and respiratory muscle weakness is advoca

90 umab 100 mg group; the patient had alcoholic cardiomyopathy and steatohepatitis, and adjudication was

91 coupling interval (CI) increases the risk of cardiomyopathy and sudden death.

92 abradine in paediatric patients with dilated cardiomyopathy and symptomatic chronic heart failure fro

93 nship of ivabradine in children with dilated cardiomyopathy and symptomatic chronic HF.

94 n contributes to the pathophysiology of LMNA cardiomyopathy and that drugs activating beta-catenin ma

95 nts, 11 ischemic heart disease, nine dilated cardiomyopathy, and 11 nonfailing donors.

96 37 patients with prior (>12-month) takotsubo cardiomyopathy, and 37 age-, sex-, and comorbidity-match

97 ction occurs in 20% of children with dilated cardiomyopathy, and 40% die or undergo transplantation.

98 h as myocardial infarction, various types of cardiomyopathy, and atherosclerosis.

99 ulation of development, ischemic and dilated cardiomyopathy, and myocardial infarction.

100 ted with fatal infantile lactic acidosis and cardiomyopathy, and was found to have profoundly decreas

101 The restrictive cardiomyopathies are a heterogenous group of myocardial

102 Pediatric cardiomyopathies are rare diseases with an annual incide

103 Dilated and hypertrophic cardiomyopathies are the most common; restrictive, nonco

104 uble mutations in patients with hypertrophic cardiomyopathy are much less common than previously esti

105 uble mutations in patients with hypertrophic cardiomyopathy are not rare and are associated with a mo

106 adverse events in patients with hypertrophic cardiomyopathy are still limited.

107 pecifically arrhythmogenic right ventricular cardiomyopathy (ARVC).

108 f arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C).

109 We defined IVA-associated cardiomyopathy as a drop in ejection fraction of >/=10%

110 They review evidence implicating atrial cardiomyopathy as an independent contributor to the risk

111 nonsynonymous or splice-site variations in 6 cardiomyopathy-associated genes (BAG3, DSP, PKP2, RYR2,

112 The hypertrophic cardiomyopathy-associated mutant D145E, in cardiac tropo

113 ycardia syndromes) should also be considered cardiomyopathies because of electric myocyte dysfunction

114 variants are misinterpreted as hypertrophic cardiomyopathy because of the lack of extracardiac organ

115 S identified variants in genes implicated in cardiomyopathy but not included in prior panel testing:

116 ts cause hypertrophic (HCM) or dilated (DCM) cardiomyopathy by disrupting sarcomere contraction and r

117 endent cardiac phenotypes, including dilated cardiomyopathy, cardiac conduction disturbance, atrial f

118 In Latin America, cardiomyopathy caused by Chagas disease is endemic.

119 myopathies, with an emphasis on hypertrophic cardiomyopathy caused by sarcomeric mutations.

120 Chronic Chagas disease cardiomyopathy, caused by Trypanosoma cruzi infection, i

121 Although several cardiomyopathy-causing mutations have been identified in

122 e also propose potential mechanisms by which cardiomyopathy-causing mutations may lead to proteasome

123 The regulation is putatively impaired by cardiomyopathy-causing mutations that affect the intramo

124 nfected patients will develop chronic Chagas cardiomyopathy (CCC), an inflammatory cardiomyopathy cha

125 ost frequently occurred because hypertrophic cardiomyopathy centers had access to different privately

126 in variant classification among hypertrophic cardiomyopathy centers is largely attributable to privat

127 myopathy probands at 5 tertiary hypertrophic cardiomyopathy centers.

128 Chagas cardiomyopathy (CCC), an inflammatory cardiomyopathy characterized by hypertrophy, fibrosis, a

129 Restrictive cardiomyopathy (RCM) is a rare cardiomyopathy characterized by impaired diastolic ventr

130 5.98-66.97; P=0.02) and improved Kansas City Cardiomyopathy clinical summary (+5.22, 95% confidence i

131 3 ATTR-ACT study (Tafamidis in Transthyretin Cardiomyopathy Clinical Trial), an international, multic

132 ing should be considered in individuals with cardiomyopathy co-occurring with LVNC.

133 d expression of neuropilin 1 that attenuates cardiomyopathy compared to diabetic male rats.

134 In pediatric patients with dilated cardiomyopathy, compared with dimension and area methods

135 them with samples from patients with dilated cardiomyopathy (DCM) and inflammatory cardiomyopathy (IC

136 ABSTRACT: Dilated cardiomyopathy (DCM) can be caused by mutations in sarco

137 Diabetic cardiomyopathy (DCM) has been increasingly considered as

138 Dilated cardiomyopathy (DCM) is a condition of abnormal myocardi

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

140 The cause of idiopathic dilated cardiomyopathy (DCM) is unknown by definition, but its f

141 trophic cardiomyopathy (HCM) and two dilated cardiomyopathy (DCM) mutants were studied by biochemical

142 eveal reduced force generation and a dilated cardiomyopathy (DCM) phenotype.

143 Peripartum cardiomyopathy (PPCM) and dilated cardiomyopathy (DCM) show similarities in clinical prese

144 ting variants (TTNtv) commonly cause dilated cardiomyopathy (DCM).

145 muscular dystrophy (EDMD) as well as dilated cardiomyopathy (DCM).

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

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

148 Patients with myocarditis or dilated cardiomyopathy develop autoantibodies to SERCA2a suggest

149 The diagnosis of arrhythmogenic cardiomyopathy does not rely on a single gold standard t

150 ty control, we used a mouse model of dilated cardiomyopathy driven by cardiac restricted overexpressi

151 evalence in arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) varies depending on st

152 th inherited left ventricular arrhythmogenic cardiomyopathy/dysplasia and a high incidence of adverse

153 h inherited arrhythmogenic right ventricular cardiomyopathy/dysplasia, although their cellular and mo

154 of inherited left ventricular arrhythmogenic cardiomyopathy/dysplasia.

155 at are significantly associated with dilated cardiomyopathy (false discovery corrected P</=0.05), wit

156 e survival of children with familial dilated cardiomyopathy (FDCM) to that of children with idiopathi

157 m cells (hMSCs) have been tested in ischemic cardiomyopathy, few studies exist in chronic nonischemic

158 erter defibrillator in patients with dilated cardiomyopathy for the primary prevention of sudden card

159 Overall, 75 individuals had either cardiomyopathy gene panel (n=65) or known variant testin

160 These data do not suggest an indication for cardiomyopathy gene panel testing in individuals with is

161 The yield of cardiomyopathy gene panel testing was 9%.

162 th LVNC, we sought to determine the yield of cardiomyopathy gene panel testing, distinguish the yield

163 Both arrhythmia and cardiomyopathy genes are implicated.

164 We also suggest inclusion of cardiomyopathy genes as well as other candidate SUD gene

165 t an evaluation of cardiac channelopathy and cardiomyopathy genes in a large, demographically diverse

166 nd surveillance of cardiac channelopathy and cardiomyopathy genes represents the latest molecular aut

167 olecular autopsy for electrical disorder and cardiomyopathy genes, using ACMG guidelines for variant

168 54 previously identified LVNC or other known cardiomyopathy genes.

169 athy who had undergone targeted hypertrophic cardiomyopathy genetic testing (either multigene panel o

170 may prove to reduce stroke risk from atrial cardiomyopathy given its parallels to atrial fibrillatio

171 um biomarkers, patients with prior takotsubo cardiomyopathy had impaired cardiac deformation indices

172 ractory symptoms of obstructive hypertrophic cardiomyopathy has long been debated and is primarily ce

173 Novel cardiomyopathies have been discovered (arrhythmogenic, r

174 Although adult and pediatric cardiomyopathies have similar morphological and clinical

175 i.e., cardiogenic shock complicating chronic cardiomyopathy) have not yet been reported.

176 ing, and apply the technique in hypertrophic cardiomyopathy (HCM) and DCM.

177 tations in the TNT1 region, six hypertrophic cardiomyopathy (HCM) and two dilated cardiomyopathy (DCM

178 Hypertrophic cardiomyopathy (HCM) is a clinically and genetically het

179 Hypertrophic cardiomyopathy (HCM) is a genetic disorder that is chara

180 RATIONALE: Hypertrophic cardiomyopathy (HCM) is a prototypic single-gene disease

181 The natural history of hypertrophic cardiomyopathy (HCM) is complex and may include progress

182 Yield of causative variants in hypertrophic cardiomyopathy (HCM) is increased in some probands, sugg

183 ical red flags in patients with hypertrophic cardiomyopathy (HCM) older than 25 years.

184 common sustained arrhythmia in hypertrophic cardiomyopathy (HCM), is capable of producing symptoms t

185 on, which is exhibited in human hypertrophic cardiomyopathy (HCM), to investigate the influence of HC

186 ns in hVELC are associated with hypertrophic cardiomyopathy (HCM).

187 (FLNC) as a candidate gene for hypertrophic cardiomyopathy (HCM).

188 Proteasome impairment has been detected in cardiomyopathies, heart failure, myocardial ischaemia, a

189 s more at risk of ischemic heart disease and cardiomyopathy/heart failure death, respectively, than e

190 ), 10 patients with hypertrophic obstructive cardiomyopathy (HOCM), 10 patients with aortic valve ste

191 rter defibrillator (ICD) therapy in ischemic cardiomyopathy (ICM) and nonischemic cardiomyopathy (NIC

192 ilated cardiomyopathy (DCM) and inflammatory cardiomyopathy (ICM).

193 ronic postinfarction heart failure (ischemic cardiomyopathy [ICM]).

194 emic dilated cardiomyopathy and inflammatory cardiomyopathy (iCMP).

195 to that of children with idiopathic dilated cardiomyopathy (IDCM) has produced conflicting results.

196 The most common cause of inflammatory cardiomyopathies in developed countries is lymphocytic m

197 s should be aware of rare cases of takotsubo cardiomyopathy in MS relapses.

198 atients developing neurological deficits and cardiomyopathy in the long-term, among other complicatio

199 rare variants in patients with hypertrophic cardiomyopathy in the setting of comprehensive and targe

200 myopathy, ischemic heart disease, or dilated cardiomyopathy, in comparison to nonfailing hearts.

201 advances were achieved in the nosography of cardiomyopathies, influencing the definition and taxonom

202 We conclude that NS-cardiomyopathy involves cardiomyocytes, ECs and fibrobla

203 hogenesis of isolated or syndromic pediatric cardiomyopathies is becoming apparent.

204 The new catchphrase in the evaluation of cardiomyopathies is multimodality imaging, which is purp

205 Hypertrophic cardiomyopathy is a genetically heterogeneous myocardial

206 Dystrophic cardiomyopathy is a leading cause of death in Duchenne m

207 Because a common finding in dilated cardiomyopathy is a reduction in the myofilament-Ca(2)(+

208 Takotsubo cardiomyopathy is an increasingly recognized acute heart

209 Arrhythmogenic cardiomyopathy is an inherited heart muscle disorder, pr

210 commendations for patients with hypertrophic cardiomyopathy is challenging because of concern about t

211 Sickle cell anemia (SCA)-related cardiomyopathy is characterized by diastolic dysfunction

212 ycardia (NSVT) in patients with hypertrophic cardiomyopathy is incompletely resolved.

213 uently; and arrhythmogenic right ventricular cardiomyopathy is rare.

214 in viral RNA replication.IMPORTANCE Dilated cardiomyopathy is the most common indication for heart t

215 apoptosis in pre-diabetic stages of diabetic cardiomyopathy is unknown.

216 link between metabolic stress and associated cardiomyopathy is unknown.

217 n are reported in patients with hypertrophic cardiomyopathy, ischemic heart disease, diabetes mellitu

218 on of genes with altered abundance in septic cardiomyopathy, ischemic heart disease, or dilated cardi

219 ed evolution of a sarcomeric to infiltrative cardiomyopathy, leading to an ominous outcome in which t

220 , those with DM had higher rates of ischemic cardiomyopathy, LVAD implantation as destination therapy

221 Such an atrial cardiomyopathy may explain many cases of embolic stroke

222 In patients with dilated cardiomyopathy, myocardial Gal-3 expression correlated w

223 c & Translational Research, Cardiac Failure, Cardiomyopathies/Myocardial & Pericardial Diseases, Cong

224 schemic cardiomyopathy (ICM) and nonischemic cardiomyopathy (NICM) patients and to evaluate 4 LGE bor

225 pacing (CRT-P) for patients with nonischemic cardiomyopathy (NICM).

226 rmation in patients with nonischemic dilated cardiomyopathy (NIDCM).

227 studies exist in chronic nonischemic dilated cardiomyopathy (NIDCM).

228 d with progressive external ophthalmoplegia, cardiomyopathy, nonsyndromic intellectual disability, ap

229 ommon; restrictive, noncompaction, and mixed cardiomyopathies occur infrequently; and arrhythmogenic

230 Although takotsubo cardiomyopathy occurred 20 (range 13-39) months before t

231 Pediatric cardiomyopathies often occur in the absence of comorbidi

232 ciate with a life-threatening arrhythmogenic cardiomyopathy, often of right ventricular predominance.

233 sarcomere hypercontractility of hypertrophic cardiomyopathy, one of the most prevalent heritable card

234 Cardiomyopathy patients are at risk of sudden death, typ

235 ETHODS AND Clinical data of all hypertrophic cardiomyopathy patients with 2 rare genetic variants wer

236 eter to predict new-onset AF in hypertrophic cardiomyopathy patients with LA diameter <45 mm, which t

237 Finally, SNRK is increased in cardiomyopathy patients, and SNRK reduces infarct size a

238 ventricular tachyarrhythmias in ICD-eligible cardiomyopathy patients.

239 le cardioverter-defibrillator (ICD)-eligible cardiomyopathy patients.

240 ur findings demonstrate that after takotsubo cardiomyopathy, patients develop a persistent, long-term

241 e each important determinants of the dilated cardiomyopathy phenotype and are controlled by genetic f

242 he knockout strategy ameliorates the dilated cardiomyopathy phenotype in vitro.

243 an occur in isolation or can co-occur with a cardiomyopathy phenotype or cardiovascular malformation.

244 among patients with dilated and restrictive cardiomyopathies, pointed to this gene as an important c

245 Peripartum cardiomyopathy (PPCM) and dilated cardiomyopathy (DCM) s

246 Peripartum cardiomyopathy (PPCM) disproportionately affects women o

247 isk factor for the development of peripartum cardiomyopathy (PPCM), but it is unknown whether preecla

248 ll number of individuals with IVA-associated cardiomyopathy precluded any formal testing.

249 ed on 358 consecutive genotyped hypertrophic cardiomyopathy probands at 5 tertiary hypertrophic cardi

250 changes preceded the onset of iron overload cardiomyopathy, providing an early biomarker of disease

251 h, 1 year, and 2 years using the Kansas City Cardiomyopathy Questionnaire (KCCQ) (23 items covering p

252 uality-of-life measurements, the Kansas City Cardiomyopathy Questionnaire (KCCQ) overall summary and

253 and health status as assessed by Kansas City Cardiomyopathy Questionnaire (KCCQ, range 0-100, higher

254 ducation (P<0.01), including the Kansas City Cardiomyopathy Questionnaire (P=0.009), depressive sympt

255 and 1 year after TAVR using the Kansas City Cardiomyopathy Questionnaire overall summary (KCCQ-OS) s

256 Kansas City Cardiomyopathy Questionnaire score increased (mean: 43.1

257 EQ-5D-3L visual analog scale and Kansas City Cardiomyopathy Questionnaire-12 summary scores pre-impla

258 ty of life was assessed with the Kansas City Cardiomyopathy Questionnaire.

259 Restrictive cardiomyopathy (RCM) is a rare cardiomyopathy characteri

260 Restrictive cardiomyopathy (RCM) is characterized by nondilated left

261 METHODS AND Thirty patients with ischemic cardiomyopathy received in a blinded manner either 20 mi

262 In contrast, inflammatory cardiomyopathies refer to a diverse group of disorders i

263 (Pediatric Cardiomyopathy Registry [PCMR]; NCT00005391).

264 , Lung, and Blood Institute-funded Pediatric Cardiomyopathy Registry.

265 From 1990 he directed the heart failure and cardiomyopathy research programs.

266 ients clinically diagnosed with hypertrophic cardiomyopathy resulted in identification of 8 individua

267 rting the importance of NSVT in hypertrophic cardiomyopathy risk stratification.

268 young white adults raises the possibility of cardiomyopathy, specifically arrhythmogenic right ventri

269 herapeutic approach for restoring dystrophic cardiomyopathy structurally and functionally.

270 ntric hypertrophy does progress to a dilated cardiomyopathy, such a transition would occur over a muc

271 2P/H222P mouse, a small animal model of LMNA cardiomyopathy, suggested decreased WNT/beta-catenin sig

272 pression differs between adult and pediatric cardiomyopathies, suggesting that treatment response may

273 a patient suffering from idiopathic dilated cardiomyopathy, suggesting that such mutant viruses may

274 Tachycardiomyopathy or tachycardia-induced cardiomyopathy (TCM) has been known for decades as a rev

275 pe gene SYNE1 in a child with severe dilated cardiomyopathy that underwent transplant, as well as in

276 emic cardiomyopathy, 150 nonischemic dilated cardiomyopathy), the mean left ventricular ejection frac

277 ential for treating metabolic stress-induced cardiomyopathy.The mechanistic link between metabolic st

278 in mice with large infarcts, and in ischemic cardiomyopathy, they improve LV function, effects appare

279 cts the peripheral nerves, and transthyretin cardiomyopathy (TTR-CM), which primarily affects the hea

280 1) and this was consistent for QRSp for both cardiomyopathy types.

281 It is a cell-to-cell junction cardiomyopathy, typically caused by genetically determin

282 tients with ischemic or non-ischemic dilated cardiomyopathy undergoing prophylactic ICD implantation

283 hemic heart disease, and discuss nonischemic cardiomyopathies unique to or prevalent in women.

284 that different gene mutations induce dilated cardiomyopathy via diverse cellular pathways.

285 , traditionally associated with hypertrophic cardiomyopathy, was the commonest pattern of ventricular

286 echanism driving the development of diabetic cardiomyopathy, we studied a unique model of T2DM: lipod

287 variants in genes associated with inherited cardiomyopathies were significantly enriched in AM-AVM p

288 lterations in messenger RNA levels in septic cardiomyopathy were both distinct from and more profound

289 >/=2) variants in patients with hypertrophic cardiomyopathy were described 10 years ago with a preval

290 evels in explanted human hearts with dilated cardiomyopathy were elevated despite ACE inhibition with

291 arently unrelated families with hypertrophic cardiomyopathy were evaluated.

292 polio syndrome, type 1 diabetes, and chronic cardiomyopathy were investigated.

293 Gottingen swine with experimental ischemic cardiomyopathy were randomized to receive transendocardi

294 Frataxin KO results in fatal cardiomyopathy, whereas skeletal muscle was asymptomatic

295 The term atrial cardiomyopathy, which has been used sporadically in the

296 this review, left ventricular noncompaction cardiomyopathy, which is often caused by mutations in sa

297 ODS AND Forty-one patients with hypertrophic cardiomyopathy who had undergone targeted hypertrophic c

298 have been implicated in the pathogenesis of cardiomyopathies with different etiologies.

299 ouse heart for the first time during dilated cardiomyopathy with heart failure.

300 ggest UPS dysfunction is a common feature of cardiomyopathies, with an emphasis on hypertrophic cardi