ライフサイエンスコーパス: long QT syndrome

1 lymorphic ventricular tachycardia (CPVT) and long QT syndrome.

2 in normal cells and in cells with simulated long QT syndrome.

3 potent in the 'disease setting' of inherited long QT syndrome.

4 are being developed for congenital/acquired long QT syndrome.

5 trigger cardiac arrhythmias associated with long QT syndrome.

6 , are present in a minority of patients with long QT syndrome.

7 ell established in certain diseases, such as long QT syndrome.

8 style changes for patients and families with long QT syndrome.

9 important factor in acquired and congenital long QT syndrome.

10 in principle, prove useful for treatment of long QT syndrome.

11 gation on the surface ECG is the hallmark of long QT syndrome.

12 as a common reason for the acquired form of long QT syndrome.

13 hmias associated with inherited and acquired long QT syndrome.

14 xpression level of hERG channels, leading to long QT syndrome.

15 idocaine administration in clinical acquired long QT syndrome.

16 s associated with increased risk of acquired long QT syndrome.

17 nosis and treatment of autoimmune-associated long QT syndrome.

18 treatments for cardiac disorders such as the long QT syndrome.

19 to arrhythmogenic phenotypes associated with long-QT syndrome.

20 mmon genetic variation at KCNQ1 with risk of long-QT syndrome.

21 ression of Kv11.1a and Kv11.1a-USO can cause long-QT syndrome.

22 nts a novel mechanism in the pathogenesis of long-QT syndrome.

23 a large referral population of patients with long-QT syndrome.

24 loci included genes implicated in mendelian long-QT syndrome.

25 ventricular arrhythmia syndromes other than long-QT syndrome.

26 stimulation of I(Ks), which can give rise to long-QT syndrome.

27 is other than autosomal dominant or sporadic long-QT syndrome.

28 the settings of both inherited and acquired long-QT syndrome.

29 humans with restrictive cardiomyopathies and long QT syndromes.

30 ay provide therapeutic efficacy for treating long QT syndromes.

31 d in myocardial repolarization and mendelian long-QT syndromes.

32 in 20% of Brugada syndrome (2/10) and 50% of long QT syndrome (1/2) and catecholaminergic polymorphic

33 pe in >/=1 relatives: 14 Brugada syndrome; 4 long-QT syndrome; 1 catecholaminergic polymorphic ventri

34 inite or probable diagnosis (17%), including Long-QT syndrome (13%), catecholaminergic polymorphic ve

35 rgic polymorphic ventricular tachycardia and long QT syndrome (17 [6%] and 11 [4%], respectively).

36 Congenital long QT syndrome 2 (LQT2) is caused by loss-of-function

37 the ventricular action potential that causes long QT syndrome 2 (LQT2), with increased propensity for

38 atment with E-4031 to block I(Kr) (mimicking long QT syndrome 2) or with sea anemone toxin II to impa

39 om patients with the cardiac rhythm disorder long QT syndrome 3 (LQT3) carrying SCN5A sodium channel

40 Long QT Syndrome 3 (LQTS3) arises from gain-of-function

41 rhythmogenic activity in patients harbouring long QT syndrome 3 but much less so for other common for

42 impair Na(+) channel inactivation (mimicking long QT syndrome 3) prolonged AP duration (APD); however

43 5%) families: Brugada syndrome, 13/18 (72%); long QT syndrome, 3/18 (17%); and catecholaminergic poly

44 Most mutations were found in families with long-QT syndrome (47%) or hypertrophic cardiomyopathy (4

45 ilies (25%), including Brugada syndrome (7), long QT syndromes (5), dilated cardiomyopathy (2), and h

46 cytoplasmic loop of Ca(V)1.2 channels causes long QT syndrome 8 (LQT8), a disease also known as Timot

47 Of 16 participants, 13 (81%) had long QT syndrome, 9 (56%) were female, and median age wa

48 ion implantable cardioverter-defibrillators (long QT syndrome, 9; Brugada syndrome, 8; catecholaminer

49 Dysfunction of IKr causes long QT syndrome, a cardiac electrical disorder that pre

50 CaM contain targets for mutations linked to long-QT syndrome, a type of inherited arrhythmia.

51 oal compound that clinically causes acquired long QT syndrome (acLQTS), which is associated with prol

52 ardiac events by antidepressants is acquired long QT syndrome (acLQTS), which produces electrocardiog

53 ntly discovered preferential transmission of long QT syndrome alleles to daughters as compared with s

54 been reported as a risk factor for acquired long-QT syndrome (aLQTS) and torsades de pointes (TdP).

55 the WT may have predisposed to the observed long QT syndrome and associated TdP.

56 hannel have been identified in patients with Long QT syndrome and cardiac arrhythmia.

57 All patients diagnosed with long QT syndrome and catecholaminergic polymorphic ventr

58 utations are associated with severe forms of long QT syndrome and catecholaminergic polymorphic ventr

59 mutations in hERG1 channels cause inherited long QT syndrome and increased risk of cardiac arrhythmi

60 mechanism by which inherited mutations cause long QT syndrome and potentially lethal arrhythmias.

61 alance the reduced repolarization reserve in long QT syndrome and prevent EADs and PVTs.

62 ce in situ hybridization has identified that long QT syndrome and sudden cardiac death may occur as a

63 ergic polymorphic ventricular tachycardia or long QT syndrome and sudden cardiac death.

64 Dysfunction of hERG causes long QT syndrome and sudden death, which occur in patien

65 ation or pharmacological inhibition produces Long QT syndrome and the lethal cardiac arrhythmia torsa

66 bulbar effect, quinidine can induce acquired long QT syndrome and torsade de pointes through its inte

67 sition of women to acquired and drug-induced long QT syndrome and torsades de pointes.

68 Genetic perturbations in SCN5A cause type 3 long QT syndrome and type 1 Brugada syndrome, two distin

69 ities in the duration (for example, short or long QT syndromes and heart failure) or pattern (for exa

70 e-phenotype association in the ten different long QT syndromes and the five different short QT syndro

71 athogenicity of Kir2.1-52V in 1 patient with long-QT syndrome and also supports the use of isogenic h

72 herited arrhythmia syndromes (eg, congenital long-QT syndrome and Brugada syndrome).

73 ns associated with cardiac arrest, including long-QT syndrome and catecholaminergic polymorphic ventr

74 ns in the ankyrin-B gene (ANK2) cause type 4 long-QT syndrome and have been described in kindreds wit

75 For Brugada syndrome, long QT syndrome, and DPP6 the efficacy of an ICD for pr

76 een implicated in diseases such as epilepsy, long QT syndrome, and heart failure.

77 ymorphic ventricular tachycardia, congenital long QT syndrome, and hypertrophic cardiomyopathy.

78 kcnh2, affected in Romano-Ward syndrome and long-QT syndrome, and cardiac troponin T gene, tnnt2, af

79 d acquired (drug-induced) forms of the human long-QT syndrome are associated with alterations in Kv11

80 blished in long-QT syndrome, its role in non-long-QT syndrome arrhythmogenic channelopathies and card

81 l-developed case of acquired or drug-induced long QT syndrome as an exemplar case.

82 arge rearrangements in genes responsible for long QT syndrome as part of the molecular autopsy of a 3

83 responsible for the female predisposition to long QT syndromes as well as the higher male predisposit

84 ing in a patient presenting with symptoms of long-QT syndrome as a proof of principle, we demonstrate

85 Long QT syndrome associated mutations of this site lower

86 We find that several Long QT syndrome-associated IKs channel mutations shift

87 with genetic ion channel disorders including long QT syndrome, Brugada syndrome, catecholaminergic po

88 ecific genetic arrhythmia disorders, such as long QT syndrome, Brugada Syndrome, or Catecholaminergic

89 pts, the experience obtained in the study of long-QT syndrome, Brugada syndrome, and arrhythmogenic c

90 or an initial diagnosis of exercise-induced long QT syndrome but with QTc <480 ms and a subsequent n

91 potential to be used as pharmacotherapy for long QT syndrome, but can also be proarrhythmic.

92 ngly, some drugs that were thought to induce long-QT syndrome by direct block of the rapid delayed re

93 esponsible for a novel autoimmune-associated long-QT syndrome by targeting the hERG potassium channel

94 Vs identified across 388 clinically definite long-QT syndrome cases and 1344 ostensibly healthy contr

95 pathogenic/benign status to nsSNVs from 2888 long-QT syndrome cases, 2111 Brugada syndrome cases, and

96 rived cardiomyocytes have been used to study long QT syndrome, catecholaminergic polymorphic ventricu

97 e understanding by practicing cardiologists: long QT syndrome, catecholaminergic polymorphic ventricu

98 nt of future IKs channel activators to treat Long QT syndrome caused by diverse IKs channel mutations

99 ve been withdrawn from the market due to the long QT syndrome caused by hERG inhibition.

100 yndrome, a rare, autosomal-recessive form of long-QT syndrome characterized by deafness, marked QT pr

101 ythmogenic right ventricular cardiomyopathy, long QT syndrome, commotio cordis, and Kawasaki disease.

102 Long-QT syndrome could, therefore, benefit from having a

103 effect of CaM mutations causing CPVT (N53I), long QT syndrome (D95V and D129G), or both (CaM N97S) on

104 Compared with long QT syndrome D96V-CaM, A103V-CaM had significantly l

105 ; P<0.0001) with 17 Brugada syndromes and 15 long QT syndromes diagnosed based on pharmacological tes

106 Drug-induced long QT syndrome (diLQTS) and congenital LQTS (cLQTS) sh

107 Drug-induced long-QT syndrome (diLQTS) is an adverse drug effect that

108 D causation have been found, particularly in long QT syndrome (e.g., KCNJ5, AKAP9, SNTA1), idiopathic

109 Long QT syndrome, either inherited or acquired from drug

110 rgic polymorphic ventricular tachycardia and long QT syndrome, especially the RYR2 gene, as well as t

111 kade contributes importantly to drug-induced long QT syndrome, especially when repolarization reserve

112 ions in genes responsible for the congenital long-QT syndrome, especially SCN5A, have been identified

113 retrospective analysis of all patients with long-QT syndrome evaluated from July 1998 to April 2012

114 ealthy subjects and patients with hereditary long QT syndrome, familial hypertrophic cardiomyopathy,

115 pathogenicity of gene variants identified in long QT syndrome genetic screening.

116 t with QTc <480 ms and a subsequent negative long QT syndrome genetic test (n = 45).

117 rging algorithms for interpreting a positive long QT syndrome genetic test, the zebrafish cardiac ass

118 2000 and December 2009 in the Mayo Clinic's Long QT Syndrome/Genetic Heart Rhythm Clinic, all 24 (16

119 Long QT syndrome has been associated with sudden cardiac

120 This syndrome of drug-induced long QT syndrome has moved from an interesting academic

121 derstanding the biophysical underpinnings of long QT syndrome have provided growing insight into the

122 Although genetic studies of familial long-QT syndromes have uncovered several key genes in ca

123 o EAD formation in clinical settings such as long QT syndromes, heart failure, and increased sympathe

124 sted the ability of previously characterized Long QT Syndrome hERG1 mutations and polymorphisms to re

125 ardiotoxicity profiles for healthy subjects, long QT syndrome, hypertrophic cardiomyopathy, and dilat

126 Disease phenotypes were verified in long QT syndrome, hypertrophic cardiomyopathy, and dilat

127 in patients with potassium channel-mediated long QT syndrome (ie, LQT1 and LQT2) has not been invest

128 A test was considered positive for long-QT syndrome if the absolute QT interval prolonged b

129 There was stronger clinical evidence of long QT syndrome in carriers (38.6% versus 5.5%, P=0.000

130 Testing was positive for long-QT syndrome in 31 patients (18%) and borderline in

131 athematical models of acquired and inherited long-QT syndrome in male and female ventricular human my

132 aling pathway as the cause of a drug-induced long-QT syndrome in which alterations in several ion cur

133 otype may represent a more common pattern of long-QT syndrome inheritance than previously anticipated

134 Type 2 long QT syndrome involves mutations in the human ether a

135 Long QT syndrome is a potentially lethal yet highly trea

136 Drug-induced long QT syndrome is generally ascribed to inhibition of

137 Genetic testing for Long QT Syndrome is now a standard and integral componen

138 Long-QT syndrome is a potentially fatal condition for wh

139 Long-QT syndrome is an inherited cardiac channelopathy c

140 ic denervation (LCSD) is well established in long-QT syndrome, its role in non-long-QT syndrome arrhy

141 contrast to the autosomal dominant forms of long QT syndrome, JLNS is a recessive trait, resulting f

142 disparate mutant ion channels that underlie long QT syndrome (LQT) and cystic fibrosis (CF).

143 The pro-arrhythmic Long QT syndrome (LQT) is linked to 10 different genes (

144 a subunit, KCNQ1, constitute the majority of long QT syndrome (LQT-1) cases, we have carried out a de

145 which cause cardiac arrhythmias, such as the long-QT syndrome (LQT) and atrial fibrillation.

146 he main trigger for cardiac events in type 1 long-QT syndrome (LQT1).

147 he dominant mechanism associated with type 2 Long QT syndrome (LQT2) caused by Kv11.1 potassium chann

148 ng a novel transgenic rabbit model of type 2 long QT syndrome (LQT2).

149 The majority of type 2 long-QT syndrome (LQT2) stems from trafficking defective

150 patients with sodium channel-mediated type 3 long QT syndrome (LQT3).

151 Insight into type 6 long-QT syndrome (LQT6), stemming from mutations in the

152 es, have been associated with the congenital long-QT syndrome (LQT9).

153 s identified in 115 (51%) of 225 RSCA cases: long QT syndrome (LQTS) (n = 48 [42%]), hypertrophic car

154 or their associated proteins cause inherited long QT syndrome (LQTS) and account for approximately 75

155 Changes in hERG channel function underlie long QT syndrome (LQTS) and are associated with cardiac

156 Long QT syndrome (LQTS) and catecholaminergic polymorphi

157 e the efficacy of different beta-blockers in long QT syndrome (LQTS) and in genotype-positive patient

158 Patients with long QT syndrome (LQTS) are predisposed to life-threaten

159 The heart rhythm disorder long QT syndrome (LQTS) can result in sudden death in th

160 Inherited long QT syndrome (LQTS) caused by loss-of-function mutat

161 Long QT syndrome (LQTS) exhibits great phenotype variabi

162 As genetic testing for long QT syndrome (LQTS) has become readily available, im

163 Fetal arrhythmias characteristic of long QT syndrome (LQTS) include torsades de pointes (TdP

164 The hereditary long QT syndrome (LQTS) is a genetic channelopathy with

165 Long QT syndrome (LQTS) is a genetic disease characteriz

166 Long QT syndrome (LQTS) is a leading cause of sudden car

167 Long QT syndrome (LQTS) is a potentially lethal but high

168 Long QT syndrome (LQTS) is a potentially lethal cardiac

169 Congenital Long QT syndrome (LQTS) is an arrhythmogenic disorder th

170 Long QT syndrome (LQTS) is an inherited or drug induced

171 Fetal long QT syndrome (LQTS) is associated with complex arrhy

172 Long QT syndrome (LQTS) is caused by the abnormal functi

173 Congenital long QT syndrome (LQTS) is characterized by QT prolongat

174 The diagnosis of long QT syndrome (LQTS) is rather straightforward.

175 A puzzling feature of the long QT syndrome (LQTS) is that family members carrying

176 Long QT syndrome (LQTS) is the first described and most

177 Long QT syndrome (LQTS) is the most common cardiac chann

178 Long QT syndrome (LQTS) may contribute to this problem.

179 entify risk factors for fatal arrhythmias in long QT syndrome (LQTS) patients presenting with syncope

180 nvestigate the clinical course of women with long QT syndrome (LQTS) throughout their potential child

181 reflexes, might identify high- and low-risk long QT syndrome (LQTS) type 1 (LQT1) patients.

182 Mutations in these channels can cause Long QT Syndrome (LQTS) which increases the risk for ven

183 f which harbor pathogenic variants linked to long QT syndrome (LQTS) with early and severe expressivi

184 hERG that perturb deactivation are linked to long QT syndrome (LQTS), a catastrophic cardiac arrhythm

185 um channel ancillary subunit, associate with long QT syndrome (LQTS), a defect in ventricular repolar

186 acquired prolongation of the QT interval, or long QT syndrome (LQTS), are at risk of life-threatening

187 atification is of clinical importance in the long QT syndrome (LQTS), however, little genotype-specif

188 This review will focus on the long QT syndrome (LQTS), the most common of the potentia

189 ing sequence of the KCNH2 gene implicated in Long QT Syndrome (LQTS), which occurred once in 500 whol

190 patients at the highest phenotypic risk for long QT syndrome (LQTS)-associated life-threatening card

191 ening arrhythmia in a 10-day-old infant with long QT syndrome (LQTS).

192 ss-of-function mutations in KCNQ1 have KCNQ1 long QT syndrome (LQTS).

193 y life-threatening arrhythmia syndromes like long QT syndrome (LQTS).

194 olymorphic ventricular tachycardia (CPVT) or long QT syndrome (LQTS).

195 resentation and management of the fetus with long QT syndrome (LQTS).

196 ive genes involved in the Mendelian disorder long QT syndrome (LQTS).

197 the efficacy of beta-blockers in congenital long QT syndrome (LQTS).

198 her variations in NOS1AP affect drug-induced long QT syndrome (LQTS).

199 ients with acquired (a-) and congenital (c-) long QT syndrome (LQTS).

200 intes (TdP) in patients with drug-associated long QT syndrome (LQTS).

201 nq1 gene are the leading cause of congenital long QT syndrome (LQTS).

202 ponsible for the cardiac arrhythmia disease, long QT syndrome (LQTS).

203 kade significantly reduces cardiac events in long QT syndrome (LQTS).

204 Long QT syndromes (LQTS) arise from many genetic and non

205 diac sympathetic denervation reduces risk in long-QT syndrome (LQTS) and catecholaminergic polymorphi

206 ening cardiac arrhythmias such as congenital long-QT syndrome (LQTS) and catecholaminergic polymorphi

207 e disease, cardiomyopathy, and most recently long-QT syndrome (LQTS) and sudden infant death syndrome

208 genetic modifiers of disease severity in the long-QT syndrome (LQTS) as their identification may cont

209 Genetic testing for long-QT syndrome (LQTS) has diagnostic, prognostic, and

210 g cardiac events in patients with congenital long-QT syndrome (LQTS) have focused mainly on the first

211 Although the hallmark of long-QT syndrome (LQTS) is abnormal cardiac repolarizati

212 The congenital long-QT syndrome (LQTS) is an important cause of sudden

213 Inherited long-QT syndrome (LQTS) is associated with risk of sudde

214 Long-QT syndrome (LQTS) is characterized by a prolonged

215 Long-QT syndrome (LQTS) is characterized by such strikin

216 Long-QT syndrome (LQTS) may result in syncope, seizures,

217 The Brugada syndrome (BrS) and long-QT syndrome (LQTS) present as congenital or acquire

218 herited arrhythmia clinics and the Rochester long-QT syndrome (LQTS) registry.

219 In long-QT syndrome (LQTS) type 1, severely increased morta

220 ythmia syndromes capable of producing severe long-QT syndrome (LQTS) with mutations involving CALM1,

221 for life-threatening events in patients with long-QT syndrome (LQTS) with normal corrected QT (QTc) i

222 Long-QT syndrome (LQTS), a cardiac arrhythmia disorder w

223 harbors hereditary mutations associated with long-QT syndrome (LQTS), a potentially lethal cardiac ar

224 enetic disorders of the RAS/MAPK pathway and long-QT syndrome (LQTS), and future directions for the f

225 presence of the potentially lethal mendelian long-QT syndrome (LQTS).

226 phase of action potentials, is a hallmark of long-QT syndrome (LQTS).

227 eart and a target for inherited and acquired long-QT syndrome (LQTS).

228 thy (HCM) or cardiac channelopathies such as long-QT syndrome (LQTS); however, the underlying molecul

229 ones are crucial for glucose regulation, and long-QT syndrome may cause disturbed glucose regulation.

230 gradients present on regular stimulation in long-QT syndrome models.

231 ation since it was identified as a target of long QT syndrome more than 20 years ago.

232 ells in the absence of WT CaM except for the long QT syndrome mutant CaM D129G.

233 ectrophysiological analysis of corresponding long QT syndrome mutants suggested impaired PIP2 regulat

234 o exert these same effects on a prototypical long QT syndrome mutation (delKPQ).

235 2), left ventricular noncompaction (n=1), or long-QT syndrome (n=2).

236 f arrhythmogenic heart diseases, such as the long-QT syndrome or catecholaminergic polymorphic ventri

237 y prevention patients with Brugada syndrome, long QT syndrome, or carrying the DPP6 haplotype approac

238 ations are found in 13% of genotype-negative long QT syndrome patients, but the prevalence of CaM mut

239 of abnormal patients was positive in 17% of long-QT syndrome patients and 13% of catecholaminergic p

240 s a major factor in triggering TdP in female long-QT syndrome patients.

241 ent, monogenetic substrate for the patient's long-QT syndrome phenotype.

242 potassium current (IKr) blockade to predict long QT syndrome prolongation and arrhythmogenesis.

243 ubjects with 34 mutations from multinational long QT syndrome registries were studied.

244 Patients with hereditary short-QT or long-QT syndromes, representing the very extremes of the

245 on of SGK1 in a zebrafish model of inherited long QT syndrome rescues the long QT phenotype.

246 otentially fatal human arrhythmias including long QT syndrome, short QT syndrome, Brugada syndrome, a

247 The main inherited cardiac arrhythmias are long QT syndrome, short QT syndrome, catecholaminergic p

248 For the primary care provider, long QT syndrome should be considered during the evaluat

249 ese cases should be treated as a higher-risk long-QT syndrome subset similar to their Jervell and Lan

250 at CACNA1C is a bona fide, definite evidence long-QT syndrome susceptibility gene.

251 s) have been identified in the 2 most common long-QT syndrome-susceptibility genes (KCNQ1 and KCNH2).

252 A mutational analysis of the major long-QT syndrome-susceptibility genes (KCNQ1, KCNH2, and

253 ial and is the predominant cause of acquired long QT syndrome that can lead to fatal cardiac arrhythm

254 forms, potentially aiding the study of short/long QT syndromes that result from abnormal changes in a

255 the majority of drugs implicated in acquired long QT syndrome, the most common cause of drug-induced

256 hannel dysfunction with patient phenotype in long QT syndrome, these have been largely unsuccessful.

257 mmonly used to estimate the risk of acquired long QT syndrome, this approach is crude, and it is wide

258 In long-QT syndrome, transmembrane segments S3-S5+S6 and th

259 outcomes and to risk-stratify patients with long QT syndrome type 1 (LQT1).

260 (c.671C>T, p.T224M), a gene associated with long QT syndrome type 1, which can cause syncope and sud

261 her go-go (HERG) potassium channels underlie long QT syndrome type 2 (LQT2) and are associated with f

262 on of polymorphic ventricular tachycardia in long QT syndrome type 2 (LQT2) has been associated with

263 K(+)] and T-wave, we also analysed data from long QT syndrome type 2 (LQT2) patients, testing the hyp

264 d have key roles in diseases such as cardiac long QT syndrome type 2 (LQT2), epilepsy, schizophrenia

265 RNA decay (NMD) is an important mechanism of long QT syndrome type 2 (LQT2).

266 ions in the cardiac Kv11.1 channel can cause long QT syndrome type 2 (LQTS2), a heart rhythm disorder

267 Cardiac long QT syndrome type 2 is caused by mutations in the hu

268 Confocal Ca(2+) imaging of long QT syndrome type 2 myocytes revealed that GS967 sho

269 by GS967 prevents EADs and abolishes PVT in long QT syndrome type 2 rabbits by counterbalancing the

270 revealed that I(NaL) potentiates EADs in the long QT syndrome type 2 setting through (1) providing ad

271 VT induction in a transgenic rabbit model of long QT syndrome type 2 using intact heart optical mappi

272 Long QT syndrome type 3 (LQT3) is a lethal disease cause

273 on) had a variant previously associated with long QT syndrome type 3 (LQTS3).

274 otentially fatal arrhythmias associated with long QT syndrome type 3.

275 beta-Blockers are extremely effective in long-QT syndrome type 1 and should be administered at di

276 Beta-blocker efficacy in long-QT syndrome type 1 is good but variably reported, a

277 surrounding cardiac events in 216 genotyped long-QT syndrome type 1 patients treated with beta-block

278 e that the recessive inheritance of a severe long-QT syndrome type 1 phenotype in the absence of an a

279 v11.1 voltage-gated potassium channel) cause long-QT syndrome type 2 (LQT2) because of prolonged card

280 ed sodium channel [NaV1.5]) cause congenital long-QT syndrome type 3 (LQT3).

281 get block of IKr in the setting of inherited long-QT syndrome type 3 and heart failure.

282 gers in bradycardia-dependent arrhythmias in long-QT syndrome type 3 as well tachyarrhythmogenic trig

283 A long-QT syndrome type 3 child experienced paradoxical QT

284 m increased INaL from inherited defects (eg, long-QT syndrome type 3 or disease-induced electric remo

285 kers are used as gene-specific treatments in long-QT syndrome type 3, which is caused by mutations in

286 hannels in the setting of normal physiology, long-QT syndrome type 3-linked DeltaKPQ mutation, and he

287 The basic defect in long-QT syndrome type III (LQT3) is an excessive inflow

288 mmonly implicated in the pathogenesis of the long QT syndrome, type 2 (LQT2).

289 ses, such as hypertrophic cardiomyopathy and long-QT syndrome, uncovered large-effect genetic variant

290 An emerging standard-of-care for long-QT syndrome uses clinical genetic testing to identi

291 ur report describes a novel form of acquired long QT syndrome where the target modified by As(2)O(3)

292 ted pathways involved in arrhythmogenesis in long QT syndrome, whereas proarrhythmic changes in intra

293 Reduction in I(Kr) causes long QT syndrome, which can lead to fatal arrhythmias tr

294 Mutations in either gene can cause long QT syndrome, which can lead to fatal arrhythmias.

295 e to mutations or certain medications causes long QT syndrome, which can lead to fatal ventricular ar

296 channel function is a main cause of acquired long QT syndrome, which can lead to ventricular arrhythm

297 side effects of pharmaco-therapy is acquired long QT syndrome, which is characterized by abnormal car

298 A reduction in the hERG current causes long QT syndrome, which predisposes affected individuals

299 RG function is the primary cause of acquired long-QT syndrome, which predisposes affected individuals

300 endent cohort of 82 subjects with congenital long-QT syndrome without an identified genetic cause.