ライフサイエンスコーパス: arrhythmogenic

1 rophin deficient), the SSC was excessive and arrhythmogenic.

2 educing its slope, rendering the tissue less arrhythmogenic.

3 ng-induced cardiomyopathy and attenuation of arrhythmogenic activity.

4 o 48 hours of exposure to the drug generated arrhythmogenic afterdepolarizations and >/=15-fold incre

5 al cardiac cells, in turn, is accompanied by arrhythmogenic afterdepolarizations thought to trigger t

6 ayed prolonged action potential duration and arrhythmogenic afterdepolarizations.

7 dispersion of repolarization is potentially arrhythmogenic and, intriguingly, was less evident durin

8 problem differently making the prediction of arrhythmogenic and/or antiarrhythmic effects difficult.

9 Kcne3 deletion is therefore arrhythmogenic by a novel mechanism in which secondary h

10 oportion of A103V-CaM is sufficient to evoke arrhythmogenic Ca disturbances via ryanodine receptor 2

11 roportion of CPVT-CaM is sufficient to evoke arrhythmogenic Ca disturbances, whereas LQTS-CaMs do not

12 ) levels, contractility and the frequency of arrhythmogenic Ca(2+) fluctuations in ventricular myocyt

13 otentially protective mechanisms against pro-arrhythmogenic Ca(2+) release during beta-adrenergic sti

14 Here, we report a new role for NAADP in arrhythmogenic Ca(2+) release in cardiac myocytes evoked

15 itates spontaneous Ca(2+) release in form of arrhythmogenic Ca(2+) waves and spontaneous action poten

16 he myocyte level, PLN ablation converted the arrhythmogenic Ca(2+) waves evoked by high extracellular

17 ulum, and the frequency of Ca(2+) sparks and arrhythmogenic Ca(2+) waves remains low.

18 The higher propensity of arrhythmogenic Ca(2+) waves resulted from the combined a

19 lls were also more susceptible to developing arrhythmogenic Ca(2+) waves which might form the substra

20 waves and a larger fraction of waves (termed arrhythmogenic Ca(2+) waves) triggered APs and global Ca

21 Ca2+ sparks, arrhythmogenic Ca2+ waves, sarcoplasmic reticulum (SR) C

22 sitive inotropic effects, it can also induce arrhythmogenic Ca2+ waves.

23 critical level leading to the generation of arrhythmogenic Ca2+ waves.

24 a release channels in the heart, but whether arrhythmogenic CaM mutants alter RyR2 function is not kn

25 This is in stark contrast to the actions of arrhythmogenic CaM mutations N54I, D96V, N98S, and D130G

26 growth and viability, yet the effect of the arrhythmogenic CaM mutations on cell viability, as well

27 f RyR2 as well as the mechanistic effects of arrhythmogenic CaM mutations.

28 a by gene transfer will significantly reduce arrhythmogenic cardiac alternans in the failing heart.

29 s a powerful tool for cause determination of arrhythmogenic cardiac diseases, efficient screening of

30 Brugada syndrome (BrS) is a highly arrhythmogenic cardiac disorder, associated with an incr

31 milies, including hypertrophic, dilated, and arrhythmogenic cardiomyopathies and inherited arrhythmia

32 pping phenotype of dilated and left-dominant arrhythmogenic cardiomyopathies complicated by frequent

33 ause hypertrophic, dilated, restrictive, and arrhythmogenic cardiomyopathies.

34 and the development of high-risk dilated and arrhythmogenic cardiomyopathies.

35 Desmoglein 2 gene (DSG2) mutations cause arrhythmogenic cardiomyopathy (AC) in human and transgen

36 Arrhythmogenic cardiomyopathy (AC) is a hereditary cardi

37 Arrhythmogenic cardiomyopathy (AC) is a hereditary disea

38 Arrhythmogenic cardiomyopathy (AC) is an inherited heart

39 Arrhythmogenic cardiomyopathy (AC) is associated with mu

40 e mutation of which has been associated with arrhythmogenic cardiomyopathy (AC).

41 pot for pathogenic mutations associated with arrhythmogenic cardiomyopathy (AC).

42 r early cardiac arrhythmias in patients with arrhythmogenic cardiomyopathy and cardiocutaneous syndro

43 ith Naxos disease, which is characterized by arrhythmogenic cardiomyopathy and the cutaneous disorder

44 as sarcomeric, force generation disease; and arrhythmogenic cardiomyopathy as desmosome, cell junctio

45 Cardiomyocyte ILK deletion produces a lethal arrhythmogenic cardiomyopathy associated with important

46 rdium has revealed mechanistic insights into arrhythmogenic cardiomyopathy but cardiac samples are di

47 The diagnosis of arrhythmogenic cardiomyopathy does not rely on a single

48 Arrhythmogenic cardiomyopathy is an inherited heart musc

49 RATIONALE: Arrhythmogenic cardiomyopathy is caused primarily by mut

50 Buccal mucosa cells from arrhythmogenic cardiomyopathy patients exhibit changes i

51 kedly diminished in buccal mucosa cells from arrhythmogenic cardiomyopathy patients with known desmos

52 on of Jup in cardiomyocytes in mice leads to arrhythmogenic cardiomyopathy similar to Naxos disease i

53 re responsible for a subset of patients with arrhythmogenic cardiomyopathy who exhibit cardiac arrhyt

54 of titin's spring region is associated with arrhythmogenic cardiomyopathy, a disease characterized b

55 human PKP2 associate with a life-threatening arrhythmogenic cardiomyopathy, often of right ventricula

56 lar junction proteins are the major cause of arrhythmogenic cardiomyopathy, whereas recessive mutatio

57 cause loss of junctional Pg is a hallmark of arrhythmogenic cardiomyopathy.

58 in is the first sarcomeric protein linked to arrhythmogenic cardiomyopathy.

59 ed phenotype of an early onset biventricular arrhythmogenic cardiomyopathy.

60 excess cardiac fibroadipocytes, as in human arrhythmogenic cardiomyopathy.

61 2 (PKP2), is the most common causal gene for arrhythmogenic cardiomyopathy.

62 and drug screens for effective therapies in arrhythmogenic cardiomyopathy.

63 anish family with inherited left ventricular arrhythmogenic cardiomyopathy/dysplasia and a high incid

64 nts presented data consistent with inherited arrhythmogenic cardiomyopathy/dysplasia phenotype with v

65 auses predominant inherited left ventricular arrhythmogenic cardiomyopathy/dysplasia with a high inci

66 histochemistry was compatible with inherited arrhythmogenic cardiomyopathy/dysplasia, and the functio

67 ion as a cause of inherited left ventricular arrhythmogenic cardiomyopathy/dysplasia.

68 Arrhythmogenic cardiovascular disease is associated with

69 ven to be a useful model system to delineate arrhythmogenic cardiovascular disease mechanisms.

70 y sustained high atrial activation rates and arrhythmogenic cellular Ca2+ signaling instability; howe

71 rhythmias in vitro by preventing potentially arrhythmogenic changes in action potential characteristi

72 Atrial fibrillation (AF) requires arrhythmogenic changes in atrial ion channels/receptors

73 T syndrome, its role in non-long-QT syndrome arrhythmogenic channelopathies and cardiomyopathies is l

74 In arrhythmogenic conditions, such as cardiac hypertrophy a

75 GF-beta1 signaling completely abolished both arrhythmogenic conditions.

76 KCNE1 association protects KCNQ1 from an arrhythmogenic (constitutive current-inducing) effect of

77 rome (ACS) and a marker of increased risk of arrhythmogenic death.

78 -tubules may contribute to the generation of arrhythmogenic delayed and early afterdepolarisations, a

79 The spectrum of arrhythmogenic disease included catecholaminergic polymo

80 Over a few years, the field of inherited arrhythmogenic diseases has rapidly expanded, thus resha

81 Congenital Long QT syndrome (LQTS) is an arrhythmogenic disorder that causes syncope and sudden d

82 Brugada syndrome (BrS) is an arrhythmogenic disorder that has been linked to mutation

83 ern of NaV1.5 subunits associated with these arrhythmogenic disorders and the associated channel regu

84 and may contribute to CaMKIIdeltac-dependent arrhythmogenic disorders in failing hearts.

85 e specific needs of individual patients with arrhythmogenic disorders may become future applications

86 ations in several ion currents contribute to arrhythmogenic drug activity.

87 y associated with QT prolongation and may be arrhythmogenic during AVB.

88 ated late sodium current is known to mediate arrhythmogenic early afterdepolarizations in heart, and

89 explore the potential antiarrhythmic and/or arrhythmogenic effect of modulation of the autonomic ner

90 iological models of hMSCs, predicts possible arrhythmogenic effects of hMSCs when directly coupled to

91 Arrhythmogenic effects were studied using caffeine.

92 lore the potential role of Wnt signalling in arrhythmogenic electrical remodelling, we examined volta

93 aps before and after ajmaline determined the arrhythmogenic electrophysiological substrate (AES) as c

94 d provide a substrate for synchronization of arrhythmogenic events at the tissue level in hearts pron

95 system development and the observation that arrhythmogenic foci can originate in areas near the atri

96 tissue correspond to a region enriched with arrhythmogenic foci, which may reflect a common developm

97 ve been used to study the pathophysiology of arrhythmogenic heart diseases, such as the long-QT syndr

98 Some but not all drugs designated as arrhythmogenic IKr blockers can generate arrhythmias by

99 btype of the adenosine receptors (A(1)AR) is arrhythmogenic in the developing heart, little is known

100 anied by activation of large and potentially arrhythmogenic inward INCX.

101 diac hypertrophy and Epac2 activation can be arrhythmogenic, it is unknown whether distinct subcellul

102 did not bind to the main binding site of the arrhythmogenic KV11.1 blockers (the Phe656 pore residue)

103 radigm to screen drugs for QT prolonging and arrhythmogenic liability.

104 perties thought to predict QT prolonging and arrhythmogenic liability.

105 ions such as carbon-12 ((12)C), delivered to arrhythmogenic locations of the heart could be a promisi

106 d Ca2+ channels, suggesting that FHFs may be arrhythmogenic loci, leading to arrhythmias through a no

107 in R33Q myocytes synergize to provide a new arrhythmogenic mechanism for catecholaminergic polymorph

108 We propose a previously unrecognized arrhythmogenic mechanism related to PKP2 expression and

109 olarization and may protect hearts from this arrhythmogenic mechanism.

110 otential (AP) duration (APD) is a well-known arrhythmogenic mechanism.

111 rdiac arrhythmia syndromes has unearthed new arrhythmogenic mechanisms and given rise to a number of

112 CaL.) These data provide novel insights into arrhythmogenic mechanisms during beta-adrenergic stimula

113 Several arrhythmogenic mechanisms have been inferred from animal

114 d of familial and genetic screening, and the arrhythmogenic mechanisms in the largest cohort of short

115 extracardiac pathogenesis when investigating arrhythmogenic mechanisms, even in inherited, monogenic

116 , elucidating new molecular pathways and new arrhythmogenic mechanisms.

117 ls have proven challenging to use, targeting arrhythmogenic metabolic changes and redox imbalance may

118 mechanisms by which autonomic activation is arrhythmogenic or antiarrhythmic are complex and differe

119 different types of cardiac disease, such as arrhythmogenic or hypertrophic cardiomyopathy.

120 probands previously diagnosed with dilated, arrhythmogenic, or restrictive cardiomyopathies.

121 Collagen did not alter the arrhythmogenic outcome resulting from the other fibrosis

122 ile both ischemia and severe hypothermia are arrhythmogenic, patients undergoing therapeutic hypother

123 us diastolic Ca(2+) release (DCR) can induce arrhythmogenic plasma membrane depolarizations, although

124 ular myocyte to interrogate this potentially arrhythmogenic positive feedback in both control conditi

125 rt, for the induction of tachycardia and the arrhythmogenic potency of this drug.

126 However, the observed increase in arrhythmogenic potential is not due to a steepening of t

127 aneous action potentials, thus enhancing the arrhythmogenic potential of atrial cells.

128 1-active hMSCs supports the claim of reduced arrhythmogenic potential of this cell type with low hMSC

129 the intercalated disk explains its clinical arrhythmogenic potential.

130 ients with heart failure, causes potentially arrhythmogenic reductions in slow delayed-rectifier K(+)

131 ram fractionation may be helpful to identify arrhythmogenic regions in the postinfarction heart.

132 ustained VT can distinguish exercise-induced arrhythmogenic remodeling from ARVC and post-inflammator

133 rn may allow distinguishing exercise-induced arrhythmogenic remodeling from ARVC and post-inflammator

134 Novel cardiomyopathies have been discovered (arrhythmogenic, restrictive, and noncompacted) and added

135 elates of left ventricular (LV) substrate in arrhythmogenic right ventricular (RV) cardiomyopathy are

136 etic resonance (MR) imaging in patients with arrhythmogenic right ventricular (RV) dysplasia/cardiomy

137 pholamban R14del mutation causes dilated and arrhythmogenic right ventricular cardiomyopathies and is

138 ic polymorphic ventricular tachycardia (4%), arrhythmogenic right ventricular cardiomyopathy (4%), an

139 rtrophy (LVH) and/or fibrosis (n = 59, 16%); arrhythmogenic right ventricular cardiomyopathy (ARVC) (

140 Although the Task Force Criteria for arrhythmogenic right ventricular cardiomyopathy (ARVC) h

141 Although overlap with arrhythmogenic right ventricular cardiomyopathy (ARVC) h

142 Arrhythmogenic right ventricular cardiomyopathy (ARVC) i

143 Arrhythmogenic right ventricular cardiomyopathy (ARVC) i

144 ould expose a latent electrical substrate of arrhythmogenic right ventricular cardiomyopathy (ARVC) i

145 Arrhythmogenic right ventricular cardiomyopathy (ARVC) i

146 Arrhythmogenic right ventricular cardiomyopathy (ARVC) i

147 The hallmark lesion of arrhythmogenic right ventricular cardiomyopathy (ARVC) i

148 Arrhythmogenic right ventricular cardiomyopathy (ARVC) i

149 Arrhythmogenic right ventricular cardiomyopathy (ARVC) i

150 Arrhythmogenic right ventricular cardiomyopathy (ARVC) i

151 Arrhythmogenic right ventricular cardiomyopathy (ARVC) i

152 Arrhythmogenic right ventricular cardiomyopathy (ARVC) i

153 Exercise has been proposed as a trigger for arrhythmogenic right ventricular cardiomyopathy (ARVC) p

154 k Force Criteria (rTFC) for the diagnosis of arrhythmogenic right ventricular cardiomyopathy (ARVC).

155 on (TWI), may create diagnostic overlap with arrhythmogenic right ventricular cardiomyopathy (ARVC).

156 osomal proteins are the most common cause of arrhythmogenic right ventricular cardiomyopathy (ARVC).

157 possibility of cardiomyopathy, specifically arrhythmogenic right ventricular cardiomyopathy (ARVC).

158 malities precede overt structural disease in arrhythmogenic right ventricular cardiomyopathy (ARVC).

159 Our aim was to screen 315 patients with arrhythmogenic right ventricular cardiomyopathy (n = 111

160 hy (n=1), ischemic cardiomyopathy (n=1), and arrhythmogenic right ventricular cardiomyopathy (n=1).

161 had a diagnosis of cardiomyopathy, including arrhythmogenic right ventricular cardiomyopathy (n=3) an

162 onischemic dilated cardiomyopathy [NICM], 15 arrhythmogenic right ventricular cardiomyopathy [ARVC])

163 e shocks in primary prevention patients with arrhythmogenic right ventricular cardiomyopathy and hype

164 The higher appropriate discharge rates in arrhythmogenic right ventricular cardiomyopathy and hype

165 rdioverter defibrillator (ICD) in males with arrhythmogenic right ventricular cardiomyopathy caused b

166 Arrhythmogenic right ventricular cardiomyopathy had bett

167 Thus, the hypothesis of an exercise-induced arrhythmogenic right ventricular cardiomyopathy has to b

168 ablation of ventricular tachycardia (VT) in arrhythmogenic right ventricular cardiomyopathy improves

169 9 (53%), valvular heart disease in 34 (15%), arrhythmogenic right ventricular cardiomyopathy in 37 (1

170 In diagnosed channelopathy or arrhythmogenic right ventricular cardiomyopathy index ca

171 and adjuvant EPI substrate ablation of VT in arrhythmogenic right ventricular cardiomyopathy is good.

172 xed cardiomyopathies occur infrequently; and arrhythmogenic right ventricular cardiomyopathy is rare.

173 at a Dsg2 mutant, V977fsX1006, identified in arrhythmogenic right ventricular cardiomyopathy patients

174 cutive patients with Task Force criteria for arrhythmogenic right ventricular cardiomyopathy referred

175 was higher in nonischemic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy than in

176 for a possible primary electric syndrome or arrhythmogenic right ventricular cardiomyopathy were ana

177 physiology of inherited arrhythmias (such as arrhythmogenic right ventricular cardiomyopathy) are dis

178 pathy, 15 nonischemic cardiomyopathy, and 14 arrhythmogenic right ventricular cardiomyopathy) with a

179 opathies (i.e., hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy).

180 ar tachycardia, 3; short QT syndrome, 1; and arrhythmogenic right ventricular cardiomyopathy, 23).

181 Long-QT, arrhythmogenic right ventricular cardiomyopathy, and cat

182 cause life-threatening conditions including arrhythmogenic right ventricular cardiomyopathy, and des

183 se each (3%) of hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, long QT

184 In patients with arrhythmogenic right ventricular cardiomyopathy, those d

185 that a mutation in alphaT-catenin linked to arrhythmogenic right ventricular cardiomyopathy, V94D, p

186 hies such as hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy, which a

187 EPI) substrate modification in patients with arrhythmogenic right ventricular cardiomyopathy.

188 d to hypertrophic cardiomyopathy and none to arrhythmogenic right ventricular cardiomyopathy.

189 electric and histological features known for arrhythmogenic right ventricular cardiomyopathy.

190 S mutations were also found in patients with arrhythmogenic right ventricular cardiomyopathy.

191 attern can also be the first presentation of arrhythmogenic right ventricular cardiomyopathy.

192 n defects of desmin mutants, associated with arrhythmogenic right ventricular cardiomyopathy.

193 ns were described in patients with inherited arrhythmogenic right ventricular cardiomyopathy/dysplasi

194 Heart failure (HF) prevalence in arrhythmogenic right ventricular cardiomyopathy/dysplasi

195 cardiomyopathy, dilated cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy/dysplasi

196 ers for risk stratification in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasi

197 EVM in a consecutive series of patients with arrhythmogenic right ventricular cardiomyopathy/dysplasi

198 R420W, and L433P, which are associated with arrhythmogenic right ventricular displasia type 2, also

199 Ventricular tachycardia ablation in arrhythmogenic right ventricular dysplasia (ARVD) is mor

200 netically uncharacterized diseases including arrhythmogenic right ventricular dysplasia 3.

201 Mutations in PTPLa correlated with arrhythmogenic right ventricular dysplasia in humans and

202 Arrhythmogenic right ventricular dysplasia/cardiomyopath

203 M and they were diagnostic or suggestive for arrhythmogenic right ventricular dysplasia/cardiomyopath

204 ow overlap in the clinical presentation with arrhythmogenic right ventricular dysplasia/cardiomyopath

205 lete penetrance and variable expressivity of arrhythmogenic right ventricular dysplasia/cardiomyopath

206 can in turn facilitate ablation of the VT in arrhythmogenic right ventricular dysplasia/cardiomyopath

207 imaging in arrhythmic risk stratification of arrhythmogenic right ventricular dysplasia/cardiomyopath

208 Arrhythmogenic right ventricular dysplasia/cardiomyopath

209 entricular contractions (PVCs) are common in arrhythmogenic right ventricular dysplasia/cardiomyopath

210 Arrhythmogenic right ventricular dysplasia/cardiomyopath

211 We hypothesized that VT in arrhythmogenic right ventricular dysplasia/cardiomyopath

212 entricular arrhythmias in patients harboring arrhythmogenic right ventricular dysplasia/cardiomyopath

213 ermine how exercise influences penetrance of arrhythmogenic right ventricular dysplasia/cardiomyopath

214 hythmic risk stratification in patients with arrhythmogenic right ventricular dysplasia/cardiomyopath

215 The study population included 16 consecutive arrhythmogenic right ventricular dysplasia/cardiomyopath

216 acycline cardiomyopathy, cardiac tumors, and arrhythmogenic right ventricular dysplasia/cardiomyopath

217 earch has described the arrhythmic course of arrhythmogenic right ventricular dysplasia/cardiomyopath

218 r tachycardia (VT) ablation in patients with arrhythmogenic right ventricular dysplasia/cardiomyopath

219 Arrhythmogenic right ventricular dysplasia/cardiomyopath

220 ricular tachycardia (VT) among patients with arrhythmogenic right ventricular dysplasia/cardiomyopath

221 yopathy, left ventricular noncompaction, and arrhythmogenic right ventricular dysplasia; and delineat

222 pathies are clinically characterized by high arrhythmogenic risk and caused by LMNA mutations.

223 spersion of repolarization, which could pose arrhythmogenic risk in LQTS patients.

224 The arrhythmogenic risk of such direct electrical interactio

225 issing and would assist in the evaluation of arrhythmogenic risk.

226 too much IKs under basal conditions poses an arrhythmogenic risk.

227 e heart's contractile activity and increased arrhythmogenic risks.

228 Thirty-two patients with arrhythmogenic RV cardiomyopathy (47+/-14 years; 6 women

229 cardiac magnetic resonance (CMR) imaging in arrhythmogenic RV cardiomyopathy (ARVC) may be inadequat

230 Further investigation did not diagnose arrhythmogenic RV cardiomyopathy in any athlete.

231 As, the potential for erroneous diagnosis of arrhythmogenic RV cardiomyopathy is considerably greater

232 ment compatible with diagnostic criteria for arrhythmogenic RV cardiomyopathy was frequently observed

233 LV substrate is frequent in arrhythmogenic RV cardiomyopathy, but poorly identified

234 commonly exhibit ECG anomalies that resemble arrhythmogenic RV cardiomyopathy.

235 domain residues 2460-2495 recapitulates this arrhythmogenic RyR2 leakiness by unzipping N-terminal an

236 ctive Epac activation can induce potentially arrhythmogenic sarcoplasmic reticulum (SR) Ca(2+) releas

237 c2 is located at the T tubules and regulates arrhythmogenic sarcoplasmic reticulum Ca leak.

238 We targeted arrhythmogenic scar regions by combining anatomical imag

239 r own appear as essential components of this arrhythmogenic scheme.

240 n the ischemic zone and activated to release arrhythmogenic secretome.

241 ccelerates Ca(2)(+) sequestration and aborts arrhythmogenic spontaneous Ca(2)(+) waves (SCWs).

242 the propensity and reduced the threshold for arrhythmogenic spontaneous Ca(2+) release in HEK293 cell

243 PLN ablation aborts the arrhythmogenic SR Ca(2+) waves of S2814D(+/+) and transf

244 ic stability through the amelioration of key arrhythmogenic substrate (ie, cardiac alternans) and tri

245 front may increase the sensitivity to detect arrhythmogenic substrate and critical sites for ventricu

246 l fibrillation are important elements of the arrhythmogenic substrate and result from endo-epicardial

247 d its possible value in the detection of the arrhythmogenic substrate associated with atrial fibrilla

248 LCS may provide an arrhythmogenic substrate by slowing the Ca(2+) transient

249 of cardiac activation before ablation of the arrhythmogenic substrate can reduce electrophysiological

250 A more extensive epicardial (Epi) arrhythmogenic substrate could explain the low efficacy.

251 rial conduction abnormalities, presenting an arrhythmogenic substrate for atrial re-entry.

252 tions provide a well-established ventricular arrhythmogenic substrate for SCD.

253 ardiomyopathy (ARVC) has been suggested, the arrhythmogenic substrate for VTs in athletes is unknown.

254 adin, and/or junctin and RyR2 may produce an arrhythmogenic substrate in anthracycline-induced cardio

255 al fibrosis is an important component of the arrhythmogenic substrate in patients with atrial fibrill

256 osis is likely to be a critical component of arrhythmogenic substrate in patients with nonischemic ca

257 e enabled characterization of the structural arrhythmogenic substrate in patients with VT with increa

258 ardial wall thinning (WT) imaged by MDCT and arrhythmogenic substrate in postinfarction ventricular t

259 Its arrhythmogenic substrate in the intact human heart remai

260 Defining the arrhythmogenic substrate is essential for successful abl

261 cardiac arrhythmia, but our knowledge of the arrhythmogenic substrate is incomplete.

262 assess whether prophylactic ablation of the arrhythmogenic substrate reduces or prevents the recurre

263 ial function is thought to contribute to the arrhythmogenic substrate, but how mitochondria contribut

264 t the LV/RV junction, and may potentiate the arrhythmogenic substrate, particularly in patients with

265 in, consistent with anatomic location of the arrhythmogenic substrate.

266 F, indicating that reduced Pitx2 promotes an arrhythmogenic substrate.

267 ing early formation and stabilization of the arrhythmogenic substrate.

268 n lesions are of insufficient depth to reach arrhythmogenic substrate.

269 osis in the remodeled heart, resulting in an arrhythmogenic substrate.

270 effect size that may contribute to an atrial arrhythmogenic substrate.

271 rial electrophysiology and predisposes to an arrhythmogenic substrate.

272 trophy or ischemia, thus contributing to the arrhythmogenic substrate.

273 There are limited data on typical arrhythmogenic substrates and associated ventricular tac

274 from electrocardiographic imaging studies of arrhythmogenic substrates associated with human clinical

275 Most studies of arrhythmia mechanisms and arrhythmogenic substrates have been conducted in animal

276 septal and inferolateral) account for 89% of arrhythmogenic substrates in patients with nonischemic c

277 PD rate adaptation and their contribution to arrhythmogenic substrates in the in vivo human heart usi

278 l redox state during cardiac diseases foment arrhythmogenic substrates through direct or indirect mod

279 age heart failure, beta2-stimulation creates arrhythmogenic substrates via conduction velocity regula

280 ay predispose to the pathogenesis of a fatal arrhythmogenic subtype of HCM.

281 rivascular fibrosis, which may contribute to arrhythmogenic sudden cardiac death.

282 tent to which PI3K inhibition contributes to arrhythmogenic susceptibility.

283 able cardioverter defibrillator shock or (2) arrhythmogenic syncope, seizures, or aborted cardiac arr

284 ation, sustained ventricular tachycardia, or arrhythmogenic syncope.

285 ndrome (SQTS) is a rare and life-threatening arrhythmogenic syndrome characterized by abbreviated rep

286 CPVT is a familial arrhythmogenic syndrome characterized by abnormal calciu

287 An arrhythmogenic syndrome was the predominant diagnosis in

288 he results achieved by iPS investigations in arrhythmogenic syndromes and discuss the existing challe

289 e identified a similar proportion of primary arrhythmogenic syndromes to a contemporary series of SAD

290 new genes associated with monogenic familial arrhythmogenic syndromes, giving the opportunity to deli

291 e potential of hiPSCs for studying inherited arrhythmogenic syndromes, in general, and CPVT specifica

292 have been associated with various inherited arrhythmogenic syndromes, including Brugada syndrome and

293 have been associated with various inherited arrhythmogenic syndromes, including cases of Brugada syn

294 on targeting structural disorders or primary arrhythmogenic syndromes, respectively.

295 beta2-Stimulation is, therefore, more arrhythmogenic than beta1-stimulation.

296 the first report on bioenzymatic ablation of arrhythmogenic tissue as an alternative strategy for les

297 exposed hearts showed increased incidence of arrhythmogenic-triggered activities in female ventricula

298 nalling silencing) and Ca(2+) destabilizing (arrhythmogenic unstable Ca(2+) signalling) factors.

299 Arrhythmogenic ventricular remodeling is hallmarked by b

300 Ca(2+)-sensing protein calmodulin (CaM) are arrhythmogenic, yet their underlying mechanisms are not