ライフサイエンスコーパス: QT

1 QT interval prolongation is a heritable risk factor for

2 QT interval-prolonging drug-drug interactions (QT-DDIs)

3 QT prolongation occurred in 49 (3%) patients given nerat

4 llow-up (microscopy, 1.2% vs 8.9% [P < .05]; QT-NASBA, 36.7% vs 63.3% [P < .001]).

5 (r = -0.45, P< 0.05), cardiac output kg(-1) (QT kg(-1) , r = -0.54, P < 0.02), and O2 diffusion capac

6 ges of 7.26 +/- 0.10% TAM and 7.80 +/- 0.12% QT.

7 ges of 6.91 +/- 0.13% TAM and 7.72 +/- 0.15% QT after targeting 10% (w/w) each.

8 e 4 thrombocytopenia [cohort 2], one grade 3 QT prolongation on electrocardiogram [cohort 3], and one

9 nd, placebo-controlled, crossover trial of 3 QT-prolonging drugs with 15 time-matched QT and plasma d

10 m at baseline was 3.6% (microscopy) and 97% (QT-NASBA).

11 reports were mined for signals indicating a QT-DDI.

12 Taken together with the mapping of a QT interval GWAS locus near TTN, our observation of rare

13 her coding variants at these 28 genes affect QT interval in the general population as well.

14 e nucleic acid sequence-based amplification (QT-NASBA) are increasingly used to estimate pathogen den

15 e nucleic acid sequence-based amplification (QT-NASBA).

16 up, n=1 [1%]; imatinib group, n=1 [1%]), and QT prolongation (nilotinib group, n=1 [1%]; imatinib gro

17 on age, sex, heart rate, frontal T axis, and QT interval assesses the risk for CVD and compares favor

18 ns, followed by normalization in mean HR and QT intervals at 26 days post ventricular amputation (dpa

19 populations, appropriate use of ischemia and QT-interval monitoring among select populations, alarm m

20 interval during exercise were measured, and QT/RR-interval slopes were determined by using mixed-eff

21 iness was prolonged, along with both QRS and QT interval.

22 R, and T axes; heart rate; and PR, QRS, and QT intervals from NHANES I.

23 n controls; however, resting heart rates and QT/QTc intervals were similar at baseline.

24 ontaneous beat-to-beat variability of RR and QT intervals from standard 24-h electrocardiogram Holter

25 traditional time and frequency domain RR and QT variability indexes.

26 shed the pressor responses, tachycardia, and QT interval prolongation.

27 manifest on the surface electrocardiogram as QT interval prolongation.

28 ereby causing delayed repolarization seen as QT interval prolongation on the ECG.

29 alpain may contribute to ischemia-associated QT prolongation and sudden cardiac death.

30 ever, innate susceptibility to PM-associated QT prolongation has not been characterized.

31 rize genetic susceptibility to PM-associated QT prolongation in a multi-racial/ethnic, genome-wide as

32 may alter susceptibility to PM10-associated QT prolongation in populations protected by the U.S. Env

33 no therapy other than instructions to avoid QT-prolonging medications.

34 variants previously associated with baseline QT interval to drug-induced QT prolongation and arrhythm

35 se in HRV over 24h at 10 dpa, accompanied by QT prolongation as well as diurnal variations, followed

36 long QT syndrome (LQTS) is characterized by QT prolongation.

37 n of Plasmodium falciparum gametocytaemia by QT-NASBA.

38 erlap known loci associated with the cardiac QT interval and QRS duration.

39 d the association of citalopram with cardiac QT prolongation, use of this agent to treat agitation ma

40 We characterized QT adaptation during exercise in anorexia.

41 Corrected QT interval was measured by surface ECG.

42 ) and >/=120 ms (1.75, 1.17-2.62); corrected QT (QTc) interval >/=450 ms in men or >/=460 ms in women

43 e majority of LQTS patients have a corrected QT interval below this threshold, and a significant mino

44 ients with autoimmune diseases and corrected QT (QTc) prolongation directly target and inhibit the hu

45 rs (QRS voltage, QRS duration, and corrected QT interval [QTc]) were evaluated by using multivariable

46 ity were assessed every 30 min and corrected QT intervals and T-wave morphology every 60 min.

47 of onset of 10 months, an average corrected QT interval of 676 ms, and a high prevalence of cardiac

48 The average corrected QT interval was significantly shorter in people with alt

49 oportion of patients who developed corrected QT-interval prolongation (p = 0.16), extrapyramidal symp

50 In the 1270 (63%) with ECGs, corrected QT intervals were not different in variant carriers vs t

51 rhythmia phenotype, and only 2 had corrected QT interval longer than 500 milliseconds.

52 d with uncorrected QT interval, HR-corrected QT interval or high-density lipoprotein-cholesterol.

53 ected, in TdP patients, many known corrected QT interval-prolonging risk factors were simultaneously

54 Mean corrected QT interval was 403 (standard deviation, 30) ms, and no

55 t electrocardiogram occurrences of corrected QT interval more than 500 ms (an indicator of potential

56 edation and two (2.0% [0.4-8%]) of corrected QT lengthening.

57 Indeed, progressive corrected QT prolongation, arrhythmias, and ischemic changes were

58 rug-induced increase in heart rate-corrected QT (QTc) versus drug concentration.

59 f ethanol) per day with heart rate-corrected QT interval and heart rate assessed from electrocardiogr

60 neither associated with heart rate-corrected QT interval duration (QTc) nor cardiac events in any of

61 T axis, heart rate, and heart rate-corrected QT interval were the most significant ECG factors in the

62 ving essentially identical resting corrected QT interval values.

63 ficant minority has normal resting corrected QT interval values.

64 ies may be effective in shortening corrected QT interval and reducing TdP recurrence risk.

65 morphisms (SNPs) that modulate the corrected QT (QTc)-interval and the occurrence of cardiac events i

66 fficient for diagnosis, unless the corrected QT interval is repeatedly >/=500 ms without an acquired

67 ex was increased (P<0.001) and the corrected QT interval on ECG was prolonged (P<0.001) in HFpEF rats

68 units were not associated with the corrected QT interval, with beta = 1.04 (95% confidence interval:

69 pressure, heart rate variability, corrected QT interval, low density lipoprotein (LDL) cholesterol,

70 are novel and are associated with corrected QT (QTc) prolongation and complex ventricular arrhythmia

71 a newly recognized risk of dosage-dependent QT interval prolongation.

72 normal resting QTc values and only developed QT prolongation and malignant arrhythmias after exposure

73 velop a data-driven pipeline for discovering QT-DDIs.

74 future trans-ethnic and ancestrally diverse QT GWAS.

75 ated with increases in QT interval duration (QT).

76 epolarisation and electrocardiographic (ECG) QT interval, associated with increased age-dependent ris

77 sm (seven [3%]), prolonged electrocardiogram QT (five [2%]), decreased neutrophil count (four [2%]),

78 with early childhood cardiac arrest, extreme QT prolongation, and a negative family history.

79 Herein we present the first QT GWAS of Hispanic/Latinos using data on 15,997 partici

80 In this study, we sought to validate PGS for QT interval in 2 real-world cohorts of European ancestry

81 puter-aided detection/diagnosis platform for QT.

82 utcome was the correlation between a genetic QT score comprising 61 common genetic variants and the s

83 We demonstrate that a genetic QT score comprising 61 common genetic variants explains

84 Among white subjects, genetic QT score explained 30% of the variability in response to

85 Furthermore, the genetic QT score was a significant predictor of drug-induced tor

86 The genetic QT score was correlated with drug-induced QTc prolongati

87 e cause and effect relationships among [Hb], QT, DM, and PCO2 remain to be elucidated.

88 However, QT changed minimally across rs1619661 genotypes at lower

89 ociated systemic and pulmonary hypertension, QT prolongation, arrhythmias, pericardial disease, and r

90 SNPs that mapped to 13 previously identified QT loci.

91 ments is an efficient method for identifying QT-DDIs.

92 ciations between genetic markers and imaging QTs identified by existing bi-multivariate methods may n

93 s among SNPs from AD risk gene APOE, imaging QTs extracted from structural magnetic resonance imaging

94 associations among genetic markers, imaging QTs, and clinical scores of interest.

95 Further study may identify impaired QT dynamics as a risk factor for arrhythmias in anorexia

96 ion of breast tissue image classification in QT imaging.

97 nts (20%) experienced a >/=60-ms increase in QT interval, leading to bedaquiline discontinuation in 2

98 posure has been associated with increases in QT interval duration (QT).

99 vided a significant increase in variation in QT interval explained compared with a model with only no

100 Underlying abnormalities include QT prolongation, delayed repolarization from downregulat

101 Furthermore, glucose ingestion increased QT interval and aggravated the cardiac repolarization di

102 e examined the association of the individual QT-interval components (R-wave onset to R-peak, R-peak t

103 Drug-induced QT interval prolongation, a risk factor for life-threate

104 ed with baseline QT interval to drug-induced QT prolongation and arrhythmias is not known.

105 roportion of the variability in drug-induced QT prolongation and is a significant predictor of drug-i

106 ndicate that whereas the same loci influence QT across populations, population-specific variation exi

107 interval-prolonging drug-drug interactions (QT-DDIs) may increase the risk of life-threatening arrhy

108 Long QT syndrome (LQTS) exhibits great phenotype variability

109 Long QT syndrome (LQTS) is a potentially lethal cardiac chann

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

111 Long QT Syndrome 3 (LQTS3) arises from gain-of-function Nav1.

112 Long QT syndrome type 3 (LQT3) is a lethal disease caused by

113 .0001) with 17 Brugada syndromes and 15 long QT syndromes diagnosed based on pharmacological tests.

114 (25%), including Brugada syndrome (7), long QT syndromes (5), dilated cardiomyopathy (2), and hypert

115 nd is the predominant cause of acquired long QT syndrome that can lead to fatal cardiac arrhythmias.

116 ine administration in clinical acquired long QT syndrome.

117 ociated with increased risk of acquired long QT syndrome.

118 being developed for congenital/acquired long QT syndrome.

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

120 polymorphic ventricular tachycardia and long QT syndrome, especially the RYR2 gene, as well as the mi

121 phic ventricular tachycardia (CPVT) and long QT syndrome.

122 s with restrictive cardiomyopathies and long QT syndromes.

123 Channelopathies (short and long QT, Brugada, and catecholaminergic polymorphic ventricul

124 and treatment of autoimmune-associated long QT syndrome.

125 Cardiac long QT syndrome type 2 is caused by mutations in the human e

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

127 Dysfunction of hERG causes long QT syndrome and sudden death, which occur in patients wi

128 A reduction in the hERG current causes long QT syndrome, which predisposes affected individuals to v

129 Congenital long QT syndrome (LQTS) is characterized by QT prolongation.

130 ene are the leading cause of congenital long QT syndrome (LQTS).

131 hic ventricular tachycardia, congenital long QT syndrome, and hypertrophic cardiomyopathy.

132 physiological analysis of corresponding long QT syndrome mutants suggested impaired PIP2 regulation a

133 mplantable cardioverter-defibrillators (long QT syndrome, 9; Brugada syndrome, 8; catecholaminergic p

134 had a 7-fold higher risk of developing long QT.

135 ble for the cardiac arrhythmia disease, long QT syndrome (LQTS).

136 s in SCN5A and KCNH2, disease genes for long QT and Brugada syndromes, were assessed for potential pa

137 and T-wave, we also analysed data from long QT syndrome type 2 (LQT2) patients, testing the hypothes

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

139 Drug-induced long QT syndrome (diLQTS) and congenital LQTS (cLQTS) share m

140 eloped case of acquired or drug-induced long QT syndrome as an exemplar case.

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

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

143 t in the 'disease setting' of inherited long QT syndrome.

144 t of CaM mutations causing CPVT (N53I), long QT syndrome (D95V and D129G), or both (CaM N97S) on RyR2

145 s are found in 13% of genotype-negative long QT syndrome patients, but the prevalence of CaM mutation

146 ons are associated with severe forms of long QT syndrome and catecholaminergic polymorphic ventricula

147 n clinical development for treatment of long QT-3 syndrome (LQT-3), hypertrophic cardiomyopathy (HCM)

148 ssium current (IKr) blockade to predict long QT syndrome prolongation and arrhythmogenesis.

149 or pharmacological inhibition produces Long QT syndrome and the lethal cardiac arrhythmia torsade de

150 rt these same effects on a prototypical long QT syndrome mutation (delKPQ).

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

152 ormal cells and in cells with simulated long QT syndrome.

153 cardiomyocytes have been used to study long QT syndrome, catecholaminergic polymorphic ventricular t

154 Q1, a gene previously implicated in the long QT interval syndrome.

155 inherited long QT syndrome rescues the long QT phenotype.

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

157 cation is of clinical importance in the long QT syndrome (LQTS), however, little genotype-specific da

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

159 ments for cardiac disorders such as the long QT syndrome.

160 ch harbor pathogenic variants linked to long QT syndrome (LQTS) with early and severe expressivity.

161 sion level of hERG channels, leading to long QT syndrome.

162 future IKs channel activators to treat Long QT syndrome caused by diverse IKs channel mutations.

163 ovide therapeutic efficacy for treating long QT syndromes.

164 anges in hERG channel function underlie long QT syndrome (LQTS) and are associated with cardiac arrhy

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

166 l have been identified in patients with Long QT syndrome and cardiac arrhythmia.

167 All patients diagnosed with long QT syndrome and catecholaminergic polymorphic ventricula

168 Compared with long QT syndrome D96V-CaM, A103V-CaM had significantly less e

169 Long-QT syndrome (LQTS) may result in syncope, seizures, or s

170 Long-QT syndrome could, therefore, benefit from having a stan

171 Long-QT syndrome is a potentially fatal condition for which 3

172 Long-QT syndrome is an inherited cardiac channelopathy charac

173 Long-QT, arrhythmogenic right ventricular cardiomyopathy, and

174 genic/benign status to nsSNVs from 2888 long-QT syndrome cases, 2111 Brugada syndrome cases, and 8975

175 Insight into type 6 long-QT syndrome (LQT6), stemming from mutations in the KCNE2

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

177 settings of both inherited and acquired long-QT syndrome.

178 in females with inherited and acquired long-QT.

179 The Brugada syndrome (BrS) and long-QT syndrome (LQTS) present as congenital or acquired dis

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

181 HCM) or cardiac channelopathies such as long-QT syndrome (LQTS); however, the underlying molecular me

182 sible for a novel autoimmune-associated long-QT syndrome by targeting the hERG potassium channel and

183 voltage-gated potassium channel) cause long-QT syndrome type 2 (LQT2) because of prolonged cardiac r

184 dium channel [NaV1.5]) cause congenital long-QT syndrome type 3 (LQT3).

185 ajor factor in triggering TdP in female long-QT syndrome patients.

186 An emerging standard-of-care for long-QT syndrome uses clinical genetic testing to identify ge

187 uired (drug-induced) forms of the human long-QT syndrome are associated with alterations in Kv11.1 (h

188 sympathetic denervation reduces risk in long-QT syndrome (LQTS) and catecholaminergic polymorphic ven

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

190 In long-QT syndrome, transmembrane segments S3-S5+S6 and the DII

191 or probable diagnosis (17%), including Long-QT syndrome (13%), catecholaminergic polymorphic ventric

192 some drugs that were thought to induce long-QT syndrome by direct block of the rapid delayed rectifi

193 pathway as the cause of a drug-induced long-QT syndrome in which alterations in several ion currents

194 Inherited long-QT syndrome (LQTS) is associated with risk of sudden dea

195 atical models of acquired and inherited long-QT syndrome in male and female ventricular human myocyte

196 A mutational analysis of the major long-QT syndrome-susceptibility genes (KCNQ1, KCNH2, and SCN5

197 Although the hallmark of long-QT syndrome (LQTS) is abnormal cardiac repolarization, t

198 n a patient presenting with symptoms of long-QT syndrome as a proof of principle, we demonstrated tha

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

200 ed arrhythmia clinics and the Rochester long-QT syndrome (LQTS) registry.

201 a syndromes capable of producing severe long-QT syndrome (LQTS) with mutations involving CALM1, CALM2

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

203 ic modifiers of disease severity in the long-QT syndrome (LQTS) as their identification may contribut

204 hannel (Nav1.5) are associated with the long-QT-3 (LQT3) syndrome.

205 enicity of Kir2.1-52V in 1 patient with long-QT syndrome and also supports the use of isogenic human

206 myocardial scar is associated with a longer QT interval.

207 Despite the absence of manifest QT prolongation, adolescent anorexic females have impair

208 f 3 QT-prolonging drugs with 15 time-matched QT and plasma drug concentration measurements.

209 d SNPs and electrocardiographically measured QT were combined using fixed-effects meta-analysis.

210 15 years (interquartile range, 2-17), median QT 330 ms (interquartile range, 280-360), and median QTc

211 ominance was identified, although the median QT interval was significantly shorter in women.

212 e do not know why some patients develop more QT prolongation than others, despite similar bradycardia

213 15.8; 95% confidence interval, 15.3-16.4 ms QT change per 10% change in RR interval; P<0.001) and st

214 , in order to detect complex multi-SNP-multi-QT associations, bi-multivariate techniques such as vari

215 can predict individual response to multiple QT-prolonging drugs.

216 ion-induced syncope since age 10, had normal QT interval, and displayed ventricular ectopy during str

217 ic ventricular tachycardia in the absence of QT prolongation, indicating a novel proarrhythmic syndro

218 reast imaging is an important application of QT and allows non-invasive, non-ionizing imaging of whol

219 st genome-wide association studies (GWAS) of QT were performed in European ancestral populations, lea

220 r action potential (AP) for investigation of QT interval changes and arrhythmia substrates.

221 ed the biological clock and normalization of QT intervals at 26 dpa, providing the first evidence of

222 in clinical settings, such as prediction of QT interval.

223 CDSS have reduced prescriptions of QT-prolonging drugs, but these relatively small changes

224 achycardia but abolished the prolongation of QT interval.

225 sts that shifting the focus from the overall QT interval to its individual components will refine SCD

226 At PM10 concentrations >90th percentile, QT increased 7 ms across the CC and TT genotypes: 397 (9

227 an extend action potential duration, prolong QT intervals, and ultimately contribute to life-threaten

228 diograms (ST-segment elevation and prolonged QT interval, respectively) and increased risk for malign

229 -deficient mice (ST3Gal4(-/-)) had prolonged QT intervals with a concomitant increase in ventricular

230 srupted cardiac function including prolonged QT interval duration.

231 Prolonged-QT commonly coexists in the ECG with left ventricular hy

232 rugs delays cardiac repolarization, prolongs QT interval, and is associated with an increased risk of

233 ificant sinus slowing and increased PR, QRS, QT, and QTc intervals, as seen with azithromycin overdos

234 At high QS/QT with FIO2 more than 0.4, the relationship of PaO2/FIO

235 At higher QS/QT, the relationship is more constant and changes less w

236 ees of increased intrapulmonary shunting (QS/QT), assessing the impact of intra- and extrapulmonary f

237 ries at all shunt fractions but most with QS/QT from 0.1 to 0.3 with FIO2 approximately greater than

238 However, with QS/QT of 0.1-0.3, PaO2/FIO2 changes substantially with FIO2

239 o-loaded with tamoxifen (TAM) and quercetin (QT) to investigate the loading, release and in vitro met

240 lta), associated with shorter repolarization QT intervals (the time interval between the Q and the T

241 The RR/QT slope, best described by a curvilinear relationship,

242 Short QT interval was a rare finding in this pediatric populat

243 Short QT syndrome (SQTS) is a rare and life-threatening arrhyt

244 Short QT syndrome (SQTS) is a rare condition characterized by

245 olymorphic ventricular tachycardia, 3; short QT syndrome, 1; and arrhythmogenic right ventricular car

246 sought to determine the prevalence of short QT interval in a pediatric population and associated cli

247 nnels underlie variant 3 (SQT3) of the short QT syndrome, which is associated with atrial fibrillatio

248 Risk associated with short QT interval has recently received recognition.

249 for this pediatric patient cohort with short QT interval.

250 ondition characterized by abnormally 'short' QT intervals on the ECG and increased susceptibility to

251 to block late sodium current and to shorten QT interval in LQT3 patients.

252 AA) and tested their effects on standardized QT interval residuals.

253 polarization is underscored by evidence that QT interval prolongation in diabetes mellitus also may r

254 The QT interval and its components were measured at baseline

255 The QT-shortening effect of ranolazine remained effective th

256 ontrolling action potential duration and the QT interval.

257 However, the QT interval itself is insufficient for diagnosis, unless

258 Changes in the QT interval during exercise were measured, and QT/RR-int

259 coded allele: T) significantly modified the QT-PM10 association (p=2.11x10(-8)).

260 ed IKs inhibition necessary to normalize the QT interval and terminate re-entry in SQT2 conditions wa

261 We systematically assess the ability of the QT images' features to differentiate between normal brea

262 ients with higher sympathetic control of the QT interval and reduced vagal control of heart rate are

263 The mechanism causing a prolongation of the QT interval during epilepsy remains unknown.

264 ed cardiomyocytes nor any lengthening of the QT interval in vivo.

265 s have demonstrated that prolongation of the QT interval is associated with sudden cardiac death (SCD

266 ally produce exaggerated prolongation of the QT interval on the electrocardiogram and the morphologic

267 Although prolongation of the QT interval was associated with a 49% increased risk of

268 more reactive sympathetic modulation of the QT interval, particularly during daytime when arrhythmia

269 layed repolarization and prolongation of the QT interval.

270 When all of the QT-interval components were included in the same model,

271 primary mechanism by which drugs prolong the QT interval) to evaluate our top candidate.

272 e (a proton-pump inhibitor) will prolong the QT interval.

273 Hydroquinidine (HQ) prolongs the QT interval in SQTS patients, although whether it reduce

274 the SCN5A-D1790G mutation and shortened the QT interval of LQT3 patients.

275 To understand the QT/TdP discordance, we used quantitative profiling and c

276 The risk of SCD with the QT interval is driven by prolongation of the T-wave onse

277 own whether any of the components within the QT interval are responsible for its association with SCD

278 The three QT features were used in Support Vector Machines (SVM) c

279 fects causing hypertension, thromboembolism, QT prolongation, and atrial fibrillation.

280 peak VO2 kg(-1) was primarily attributed to QT, DM, and PCO2 (R(2) = 0.88).

281 menon occurs in the heart and contributes to QT prolongation by altering cardiac sodium current prope

282 n of common genetic variants contributing to QT interval at baseline, identified through genome-wide

283 and malignant arrhythmias after exposure to QT-prolonging stressors, 10 had other LQTS pathogenic mu

284 (SNPs) and neuroimaging quantitative traits (QTs) is one major task in imaging genetics.

285 lymorphisms (SNPs)) and quantitative traits (QTs) such as brain imaging phenotypes.

286 ough V4, with either persistent or transient QT prolongation and severe disease expression of exercis

287 Quantitative Transmission Ultrasound (QT) is a powerful and emerging imaging paradigm which ha

288 es, but were not associated with uncorrected QT interval, HR-corrected QT interval or high-density li

289 Exercise testing is useful in unmasking QT prolongation in disorders associated with abnormal re

290 men is not beneficial for heart function via QT interval or heart rate but could be detrimental.

291 d for NP-4%s and NP-8%s, respectively, while QT metabolism was reduced 3 and 4-fold.

292 loci, AJAP1 was suggestively associated with QT in a prior East Asian GWAS; in contrast BVES and CAP2

293 ed 27 nonsynonymous variants associated with QT interval (FDR 5%), 22 of which were in TTN.

294 rious coding variants in TTN associated with QT interval show that TTN plays a role in regulation of

295 al criteria to identify loci associated with QT interval that do not meet genome-wide significance an

296 Arrhythmias associated with QT prolongation on the ECG often lead to sudden unexpect

297 version to normal rhythm was associated with QT prolongation yet absent proarrhythmia markers for Tor

298 eins are more enriched for associations with QT interval than observed for genome-wide comparisons.

299 Consistent with QT prolongation, epileptic rats had longer ventricular a

300 effect estimates from association tests with QT interval obtained from prior genome-wide association