ライフサイエンスコーパス: long QT syndrome

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

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

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

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

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

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

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

8 hmias associated with inherited and acquired long QT syndrome.

9 and the phenotypic expression of congenital long QT syndrome.

10 effects such as a predisposition to acquired long QT syndrome.

11 idate the mechanisms underlying drug-induced long QT syndrome.

12 sinus node dysfunction that is distinct from long QT syndrome.

13 idocaine administration in clinical acquired long QT syndrome.

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

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

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

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

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

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

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

21 trigger cardiac arrhythmias associated with 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 ventricular arrhythmia syndromes other than long-QT syndrome.

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

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

27 ) typical of SCN5A mutations associated with long-QT syndrome.

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

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

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

31 humans with restrictive cardiomyopathies and long QT syndromes.

32 ay provide therapeutic efficacy for treating long QT syndromes.

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

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

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

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

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

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

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

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

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

44 ngation and ventricular arrhythmogenicity in long QT syndrome 5.

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 echanism-based approach for the treatment of long QT syndrome, a disorder of cardiac repolarization a

51 Inherited mutations in the HERG gene cause long QT syndrome, a disorder that predisposes individual

52 Long QT syndrome, a rare genetic disorder associated wit

53 t either had been associated previously with long-QT syndrome (A572D and G615E), had been reported to

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

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

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

57 ertent block of I(Kr), known as the acquired long QT syndrome (aLQTS), is a leading cause for drug wi

58 potentially fatal outcome make drug-induced long QT syndrome an important public health problem.

59 NE1 cause congenital deafness and congenital long QT syndrome, an inherited predisposition to potenti

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

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

62 es of SUD identified pathogenic mutations in long QT syndrome and catecholaminergic polymorphic ventr

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

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

65 the remaining 25% of patients with suspected long QT syndrome and in risk stratification.

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

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

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

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

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

71 comprehensive overview of mouse models with long QT syndrome and to emphasize the advantages and lim

72 Nonetheless, drug-induced long QT syndrome and torsade de pointes pose unique chal

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

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

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

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

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

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

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

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

81 ingly, from no obvious phenotype to manifest long-QT syndrome and sudden death, suggesting that mutan

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

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

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

85 ding the HERG potassium channel cause 30% of long-QT syndrome, and binding to this channel leads to d

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

87 time, known to be altered in the congenital long-QT syndromes, and reflected in the difference betwe

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

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

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

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

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

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

94 Long QT syndrome associated mutations of this site lower

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

117 Long QT syndrome, either inherited or acquired from drug

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

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

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

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

122 ac arrhythmia syndromes including congenital long QT syndrome, familial atrial fibrillation, and sudd

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

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

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

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

127 2000 and December 2009 in the Mayo Clinic's Long QT Syndrome/Genetic Heart Rhythm Clinic, all 24 (16

128 Long QT syndrome has a phenotype ranging from asymptomat

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

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

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

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

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

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

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

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

137 th mutations in the genes (a) known to cause long QT syndrome in humans and (b) specific to cardiac r

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

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

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

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

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

143 Congenital long QT syndrome is a rare inherited condition character

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

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

146 Long QT syndrome is one of the first cardiovascular dise

147 Long QT syndrome is one of the leading causes of sudden

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

149 Long-QT syndrome is an inherited cardiac channelopathy c

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

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

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

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

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

155 tions that disrupt this complex cause type 1 long-QT syndrome (LQT1), one of the potentially lethal h

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

157 epinephrine appears pathognomonic for type 1 long-QT syndrome (LQT1).

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

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

160 Type 2 congenital long-QT syndrome (LQT2) results from KCNH2 mutations tha

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

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

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

164 Long QT syndrome (LQTS) and catecholaminergic polymorphi

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

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

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

168 Long QT syndrome (LQTS) exhibits great phenotype variabi

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

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

171 Long QT syndrome (LQTS) is a disorder of ventricular rep

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

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

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

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

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

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

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

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

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

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

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

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

184 to assess the spectrum and outcome of young long QT syndrome (LQTS) patients, addressing treatment i

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

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

187 Long QT syndrome (LQTS) type 3 (LQT3), typified by the D

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

189 se of mutation-confirmed adult patients with long QT syndrome (LQTS), 2) to study life-threatening ca

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

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

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

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

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

195 to determine the spectrum and prevalence of long QT syndrome (LQTS)-associated mutations in a large

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

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

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

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

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

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

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

203 ograms (ECGs) in patients with the inherited long QT syndrome (LQTS).

204 the yield of genetic testing for congenital long QT syndrome (LQTS).

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

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

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

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

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

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

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

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

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

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

215 f predictors of cardiac events in hereditary long-QT syndrome (LQTS) has primarily considered syncope

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

217 Long-QT syndrome (LQTS) is a potentially lethal cardiac

218 Congenital long-QT syndrome (LQTS) is a primary arrhythmogenic synd

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

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

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

222 Type-1 long-QT syndrome (LQTS) is caused by loss-of-function mu

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

224 KCNQ1 K+ channels, the most commonly mutated long-QT syndrome (LQTS) locus.

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

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

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

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

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

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

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

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

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

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

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

236 ferred for clinical evaluation of congenital long-QT syndrome (LQTS).

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

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

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

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

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

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

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

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

245 control, congenital arrhythmia, drug-induced long-QT syndrome) of different ethnicities to discover u

246 Genetic testing for long QT syndrome, once available only through research l

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

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

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

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

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

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

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

254 ved 2772 participants from the International Long QT Syndrome Registry who were alive at age 10 years

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

282 Long-QT syndrome type 2 (LQT2) is caused by mutations in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 Long QT syndrome without symptoms is increasingly recogn

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