ライフサイエンスコーパス: long QT

1 more frequent in patients with drug-induced long QT.

2 3 but much less so for other common forms of long QT.

3 ssociated with cardiac arrhythmias including long QT.

4 f AVB had a 7-fold higher risk of developing long QT.

5 thmia in females with inherited and acquired long-QT.

6 tly in clinical development for treatment of long QT-3 syndrome (LQT-3), hypertrophic cardiomyopathy

7 ium channel (Nav1.5) are associated with the long-QT-3 (LQT3) syndrome.

8 Drug-induced long QT and arrhythmia propensity substantially increase

9 riants in SCN5A and KCNH2, disease genes for long QT and Brugada syndromes, were assessed for potenti

10 n in humans that is associated with combined long QT and Brugada syndromes.

11 ontraindicated for patients with preexisting long-QT and those with repolarization abnormalities.

12 inpatients, 27.3% had abnormal ECG, 1.6% had long QT, and 0.9% qualified as drug-induced long QT case

13 Long-QT, arrhythmogenic right ventricular cardiomyopathy

14 is a risk factor for inherited and acquired long-QT associated torsade de pointes (TdP) arrhythmias,

15 re temperature have been used to rescue some long QT-associated voltage-gated potassium Kv traffickin

16 to determine the prevalence of drug-induced long QT at admission to a public psychiatric hospital an

17 Channelopathies (short and long QT, Brugada, and catecholaminergic polymorphic vent

18 long QT, and 0.9% qualified as drug-induced long QT case subjects.

19 parison subjects, patients with drug-induced long QT had significantly higher frequencies of hypokale

20 5-year period were reviewed for drug-induced long QT (heart-rate corrected QT >/=500 ms and certain o

21 sed by mutations in KCNQ1, includes, besides long QT, hyperinsulinemia, clinically relevant symptomat

22 The long QT interval of type 1 diabetic hearts was shortened

23 0.009), in a pre-defined set of 7 congenital long QT interval syndrome (cLQTS) genes encoding potassi

24 re variants are associated with drug-induced long QT interval syndrome (diLQTS) and torsades de point

25 n KCNQ1, a gene previously implicated in the long QT interval syndrome.

26 major clinical feature of this syndrome is a long QT interval that results in cardiac arrhythmias.

27 etrospective analysis of an ECG identified a long QT interval, but sequencing of known LQT genes was

28 ivity of the channel are associated with the long QT (interval between the Q and T waves in electroca

29 Genetic long QT (LQT) syndrome is a life-threatening disorder ca

30 m channel (hNav1.5) is associated with fatal long QT (LQT) syndrome.

31 In type-2 long QT (LQT2), adult women and adolescent boys have a h

32 Patients with drug-induced long QT (N=62) were compared with a sample of patients w

33 patient indicated that 85.5% of drug-induced long QT patients had two or more factors, whereas 81.1%

34 el of inherited long QT syndrome rescues the long QT phenotype.

35 s been proposed as an important mechanism in long QT related arrhythmias.

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

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

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

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

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

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

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

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

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

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

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

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

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

49 Long QT syndrome (LQTS) and catecholaminergic polymorphi

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

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

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

53 Long QT syndrome (LQTS) exhibits great phenotype variabi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 Long QT syndrome associated mutations of this site lower

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

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

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

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

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

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

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

117 Long QT syndrome has a phenotype ranging from asymptomat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 5%) families: Brugada syndrome, 13/18 (72%); long QT syndrome, 3/18 (17%); and catecholaminergic poly

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

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

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

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

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

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

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

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

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

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

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

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

156 Long QT syndrome, either inherited or acquired from drug

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 trigger cardiac arrhythmias associated with long QT syndrome.

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

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

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

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

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

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

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

184 hmias associated with inherited and acquired long QT syndrome.

185 idocaine administration in clinical acquired long QT syndrome.

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

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

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

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

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

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

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

193 2000 and December 2009 in the Mayo Clinic's Long QT Syndrome/Genetic Heart Rhythm Clinic, all 24 (16

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

246 Long-QT syndrome is an inherited cardiac channelopathy c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

278 ventricular arrhythmia syndromes other than long-QT syndrome.

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

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

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

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

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

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

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

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

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

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

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

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

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

292 humans with restrictive cardiomyopathies and long QT syndromes.

293 ay provide therapeutic efficacy for treating long QT syndromes.

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

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

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

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

298 otes EADs and is an important determinant of long QT type 2 arrhythmia phenotype, most likely by redu

299 ible to torsade de pointes (TdP) in acquired long QT type 2 than males, in-part due to higher L-type

300 In congenital and acquired long QT type 2, women are more vulnerable than men to to