ライフサイエンスコーパス: QT

1 QT dynamics during exercise and recovery were derived in

2 QT interval dynamics during exercise and recovery are he

3 QT interval prolongation is a heritable risk factor for

4 QT prolongation and TdP are a risk in men receiving enza

5 QT/RR, JTp/RR, and JT50/RR profiles were studied in 523

6 times of (min); 0.63 (GA), 0.97 (RT), 2.00 (QT) and 2.41 (LT).

7 ral loads were monitored by NucliSense HIV-1 QT assay and T cell counts and expression of the activat

8 Grade 3 QT prolongation in the quizartinib group was uncommon (e

9 nts [7%]), sepsis or septic shock (11 [5%]), QT prolongation (five [2%]), and nausea (five [2%]) in t

10 Two patients had a QT interval (Fridericia corrected) of more than 500 ms,

11 Abnormal QT interval responses to heart rate (QT dynamics) is an

12 C showed more phenolics of GA (gallic acid), QT (quercetin), LT (luteolin) in ACE (acetone) and RT (r

13 Sensitivity analyses using alternative QT correction formulas (Hodges and Bazett) yielded overa

14 abnormality in PR interval, QRS complex and QT interval the Coefficient Variation (CV) should be gre

15 ures including PR interval, QRS complex, and QT interval from the continuous ECG waveform using featu

16 normalities in PR interval, QRS complex, and QT interval.

17 d 2 composite, conventional (PR interval and QT interval) interval scale traits and conducted multiva

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

19 (1256 +/- 244 per subject) to measure PQ and QT intervals and P wave durations.

20 (mean heart rate, heart rate variability and QT interval variability) and self-reported measures of c

21 added use of beta-blockers, antidepressants, QT-prolonging drugs, opiates, illicit drugs, and dyslipi

22 Additionally, chronotropic as well as QT-prolongation causing reference compounds were used fo

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

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

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

26 mycin held or discontinued due to an average QT prolongation of 60.5+/-40.5 ms from a baseline QTc of

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

28 The strong overlap between QT dynamics and resting QT interval loci suggests common

29 factors play roles on the progressive brain QT changes is of great importance and meaning.

30 lp understand the genetic basis of the brain QT changes over the time during the disease progression.

31 Brain QTs often change over time while the disorder progresses

32 rphisms (SNPs) play roles on affecting brain QTs over the time.

33 But QT interval is too sensitive a marker and not selective,

34 CCORD trial is not likely to be explained by QT prolongation leading to lethal ventricular arrhythmia

35 Computational (DFT, CASSCF, QT-AIM, ELF) and solid-state CP-MAS (13)C NMR spectrosco

36 acute infections, regardless of concomitant QT-prolonging antimicrobial treatments, QTc was signific

37 Corrected QT interval was measured by surface ECG.

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

39 arrest, acute kidney failure, and corrected QT interval prolongation, were not significantly differe

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

41 with the exception of asymptomatic corrected QT interval prolongation, which was significantly higher

42 Baseline corrected QT interval intervals did not differ between patients tr

43 ine extended the electrocardiogram corrected QT interval (mean increase at 52 h compared with baselin

44 Forty-five ECGs were available for corrected QT interval (QTc) measurement, and levels of hydroxychlo

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

46 The maximum corrected QT interval during treatment was significantly longer in

47 ression identified EMW, heart rate-corrected QT interval (QTc), female sex, and LQTS genotype as univ

48 cterized by a prolonged heart rate-corrected QT interval (QTc).

49 23; range, 0-59, median heart rate-corrected QT interval [QTc] at diagnosis 557 ms (IQR, 529-605) wit

50 EMW outperformed heart rate-corrected QT interval as a predictor of symptomatic status.

51 s diagnosed with severe LQT2 (rate-corrected QT>500 ms).

52 n of either the QT interval or the corrected QT interval (calculated with Fridericia's formula) to 50

53 Prolongation of the corrected QT interval and elevation of liver-enzyme levels were mo

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

55 hat can induce prolongation of the corrected QT interval.

56 uation of these medications due to corrected QT interval prolongation.

57 est were potential liver toxicity, corrected QT prolongation, and adrenal insufficiency.

58 e Doppler, and the electrocardiogram-derived QT interval for the same beat.

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

60 T wave (JT50) were reported to differentiate QT prolonging drugs that are predominant blockers of the

61 future trans-ethnic and ancestrally diverse QT GWAS.

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

63 T axis deviation; PR interval, QRS duration, QT, and QTc interval; P, Q, R, S, and T amplitudes in 12

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

65 hrombocytopenia (13%), and electrocardiogram QT prolongation (13%).

66 syndrome (17%), all-grade electrocardiogram QT prolongation (26%), and grade >= 3 leukocytosis (9%).

67 Electrocardiographic QT interval prolongation is the most widely used risk ma

68 rved value of 0.6% for heart rate and 4% for QT interval.

69 ded but the generic universal correction for QT/RR hysteresis is also applicable to JTp/RR and JT50/R

70 It is not known whether formulas for QT heart rate correction are applicable to JTp and JT50

71 A simplified approach to monitoring for QT prolongation and arrythmia was implemented on April 5

72 Further study of the need for QT interval monitoring is needed before final recommenda

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

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

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

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

77 dual phenolic was, GA (47.06) > RT (26.21) > QT (19.34) > LT (6.18).

78 The heterogeneous QT-prolonging potential of SSRIs may differentially affe

79 ty irrespective of VL status, and (2) higher QT variability if they had detectable, but not with unde

80 sis patients who initiated SSRIs with higher QT-prolonging potential and 34,722 (52.9%) who initiated

81 However, QT changed minimally across rs1619661 genotypes at lower

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

83 SNPs that mapped to 13 previously identified QT loci.

84 cannot only select relevant SNPs and imaging QTs for each diagnostic group alone, but also allows the

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

86 nsistent and time-dependent SNPs and imaging QTs, which further help understand the genetic basis of

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

88 agnostic groups might carry distinct imaging QTs, SNPs and their interactions.

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

90 The differences in QT and JT, and JTp intervals should also be corrected fo

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

92 lthough use of these medications resulted in QT prolongation, clinicians seldomly needed to discontin

93 men have greater beat-to-beat variability in QT interval (QTVI) than HIV- men, especially in the sett

94 ls were used to compare the risk of incident QT prolongation (>460 ms in women or >450 ms in men) in

95 ood pressure control on the risk of incident QT prolongation.

96 Underlying abnormalities include QT prolongation, delayed repolarization from downregulat

97 Secondary outcomes included QT prolongation, the need to prematurely discontinue any

98 Increased QT dynamics during recovery was significantly associated

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

100 ants associated with any of five independent QT interval (QTi)-associated GWAS hits at the SCN5A-SCN1

101 models were used to characterize individual QT/RR, JTp/RR, and JT50/RR profiles both without and wit

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 lethal cardiac consequences of drug-induced QT prolongation because they have a substantial cardiova

107 our molecular understanding of drug-induced QT syndrome.

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

109 Additionally, we examined two known QT interval genes, SCN5A and NOS1AP, in the Atherosclero

110 nt than the PQ interval (9 +/- 10% of linear QT/RR slopes).

111 Long QT syndrome (LQTS) exhibits great phenotype variability

112 Long QT syndrome (LQTS) is a leading cause of sudden cardiac

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

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

115 Long QT syndrome (LQTS) is caused by the abnormal function of

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

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

118 Long QT syndrome has been associated with sudden cardiac deat

119 Long QT syndrome is a potentially lethal yet highly treatable

120 Long QT syndromes (LQTS) arise from many genetic and nongenet

121 .0001) with 17 Brugada syndromes and 15 long QT syndromes diagnosed based on pharmacological tests.

122 nts with sodium channel-mediated type 3 long QT syndrome (LQT3).

123 r effect, quinidine can induce acquired long QT syndrome and torsade de pointes through its interacti

124 el function is a main cause of acquired long QT syndrome, which can lead to ventricular arrhythmias a

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

126 main inherited cardiac arrhythmias are long QT syndrome, short QT syndrome, catecholaminergic polymo

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

128 ntified in 115 (51%) of 225 RSCA cases: long QT syndrome (LQTS) (n = 48 [42%]), hypertrophic cardiomy

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

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

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

132 15 KCNQ1 mutations with known clinical long QT phenotypes, we developed a method to stratify the eff

133 rtant factor in acquired and congenital long QT syndrome.

134 tients with the cardiac rhythm disorder long QT syndrome 3 (LQT3) carrying SCN5A sodium channel varia

135 ents at the highest phenotypic risk for long QT syndrome (LQTS)-associated life-threatening cardiac e

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

137 equence of the KCNH2 gene implicated in Long QT Syndrome (LQTS), which occurred once in 500 whole gen

138 e the reduced repolarization reserve in long QT syndrome and prevent EADs and PVTs.

139 polymorphic ventricular tachycardia in long QT syndrome type 2 (LQT2) has been associated with a cha

140 S967 prevents EADs and abolishes PVT in long QT syndrome type 2 rabbits by counterbalancing the reduc

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

142 e-threatening arrhythmia syndromes like long QT syndrome (LQTS).

143 atients with potassium channel-mediated long QT syndrome (ie, LQT1 and LQT2) has not been investigate

144 t with E-4031 to block I(Kr) (mimicking long QT syndrome 2) or with sea anemone toxin II to impair Na

145 r Na(+) channel inactivation (mimicking long QT syndrome 3) prolonged AP duration (APD); however, usi

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

147 There was stronger clinical evidence of long QT syndrome in carriers (38.6% versus 5.5%, P=0.0006), g

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

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

150 duction in a transgenic rabbit model of long QT syndrome type 2 using intact heart optical mapping, c

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

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

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

154 inherited long QT syndrome rescues the long QT phenotype.

155 led that I(NaL) potentiates EADs in the long QT syndrome type 2 setting through (1) providing additio

156 eolin-3 (Cav3), have been linked to the long QT type 9 inherited arrhythmia syndrome (LQT9) and the c

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

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

159 Patients with long QT syndrome (LQTS) are predisposed to life-threatening a

160 71C>T, p.T224M), a gene associated with long QT syndrome type 1, which can cause syncope and sudden c

161 ially fatal arrhythmias associated with long QT syndrome type 3.

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

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

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

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

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

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

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

169 nction is the primary cause of acquired long-QT syndrome, which predisposes affected individuals to v

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

171 in females with inherited and acquired long-QT.

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

173 such as hypertrophic cardiomyopathy and long-QT syndrome, uncovered large-effect genetic variants tha

174 ave been associated with the congenital long-QT syndrome (LQT9).

175 CNA1C is a bona fide, definite evidence long-QT syndrome susceptibility gene.

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

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

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

179 included genes implicated in mendelian long-QT syndrome.

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

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

182 the experience obtained in the study of long-QT syndrome, Brugada syndrome, and arrhythmogenic cardio

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

184 monogenetic substrate for the patient's long-QT syndrome phenotype.

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

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

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

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

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

190 rhythmogenic phenotypes associated with long-QT syndrome.

191 myocardial scar is associated with a longer QT interval.

192 itiation of an SSRI with higher versus lower QT-prolonging potential was associated with higher risk

193 risk among those initiating SSRIs with lower QT-prolonging potential (fluoxetine, fluvoxamine, paroxe

194 4,722 (52.9%) who initiated SSRIs with lower QT-prolonging potential.

195 eated Holter recordings were used to measure QT, JT, JTp, and Tpe intervals preceded by both stable a

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

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

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

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

200 We also did not observe associations of QT dynamics during exercise and recovery with cardiovasc

201 re hospital discharge in 46 (27%) because of QT prolongation (14%), torsades de pointe or polymorphic

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

203 Heritability of QT dynamics during exercise and recovery were 10.7% and

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

205 ty index (QTVI), defined as a log measure of QT-interval variance indexed to heart rate variance.

206 +/- 220 electrocardiographic measurements of QT, JTp, and JT50 intervals were available including a 5

207 ary python script to identify any mention of QT prolongation, ventricular tachy-arrhythmias and cardi

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

209 74.20, p<0.1) were independent predictors of QT-prolongation.Incidence of LTA during hospitalization

210 ontrol arm did not have an increased risk of QT prolongation.

211 Genome-wide association studies of QT interval identified several single-nucleotide polymor

212 The prognostic value of QT dynamics was evaluated for cardiovascular events (dea

213 al electrocardiogram findings (arrhythmia or QT prolongation).

214 are associated with quantitative traits, or QTs, is the primary focus of quantitative genetics.

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

216 and demographic factors on the pretreatment QT interval.

217 liver function test results (n=1), prolonged QT interval (n=2), and adrenal insufficiency (n=1).

218 vere cardiac decompensation were a prolonged QT interval corrected (462 vs. 443 ms; P = 0.05), an ele

219 srupted cardiac function including prolonged QT interval duration.

220 1C-p.R518C variant associated with prolonged QT intervals, cardiomyopathy, and sudden cardiac death i

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

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

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

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

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

226 bnormal QT interval responses to heart rate (QT dynamics) is an independent risk predictor for cardio

227 avoid misattributing malaria-disease-related QT changes to antimalarial drug effects.

228 tment for malaria and fever-recovery-related QT lengthening is necessary to avoid misattributing mala

229 rong overlap between QT dynamics and resting QT interval loci suggests common biological pathways; ho

230 not overlap with previously reported resting QT interval loci; candidate genes included KCNQ4 and KIA

231 frequent concomitant treatment with several QT-prolonging drugs.

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

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

234 t with GS-967 shortened APD (mimicking short QT syndrome), and E-4031 reverted APD shortening.

235 ir magnitudes can cause either long or short QT syndromes associated with malignant ventricular arrhy

236 diac arrhythmias are long QT syndrome, short QT syndrome, catecholaminergic polymorphic ventricular t

237 The short QT syndrome (SQTS) is an inherited arrhythmogenic syndro

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

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

240 uncomplicated falciparum malaria had shorter QT intervals (-61.77 milliseconds; 95% credible interval

241 ed independently with clinically significant QT shortening of 2.80 milliseconds (95% CI: -3.17 to -2.

242 rders, and those treated with other non-SSRI QT-prolonging medications.

243 ed with prolongation of the QT interval that QT prolongation is an accepted surrogate marker for arrh

244 The QT interval and its components were measured at baseline

245 The QT interval is a recording of cardiac electrical activit

246 The QT interval is an important diagnostic feature on surfac

247 effect of other factors that may affect the QT interval but are not consistently collected in malari

248 he duration of the action potentials and the QT interval were significantly shorter in p.P888L-SAP97

249 Prolongation of either the QT interval or the corrected QT interval (calculated wit

250 gase rififylin (RFFL) and variability in the QT interval.

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

252 identified genetic variants that modify the QT interval upstream of LITAF (lipopolysaccharide-induce

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

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

255 tightly associated with prolongation of the QT interval that QT prolongation is an accepted surrogat

256 to -42.83) and increased sensitivity of the QT interval to heart rate changes.

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

258 Serial assessments of the QT interval were performed.

259 hERG1 block leads to a prolongation of the QT interval, a phase of the cardiac cycle that underlies

260 kinesia, hallucinations, prolongation of the QT interval, and impulse control disorders were infreque

261 mbination, can lead to a prolongation of the QT interval, possibly increasing the risk of Torsade de

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

263 n European Americans, and had effects on the QT interval and TP segment that ranked among the largest

264 laria disease and demographic factors on the QT interval in order to improve assessment of electrocar

265 Omadacycline has no effect on the QT interval, and its affinity for muscarinic M2 receptor

266 er agents, and many others), can prolong the QT interval and provoke torsades de pointes.

267 Is), citalopram and escitalopram prolong the QT interval to the greatest extent.

268 s with a higher potential for prolonging the QT interval (citalopram, escitalopram) versus the risk a

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

270 Although less rate dependent than the QT intervals (36 +/- 19% of linear slopes), PQ intervals

271 corrected for heart rate and similar to the QT interval, the differences in JT, JTp and Tpe interval

272 ricular repolarization lability by using the QT variability index (QTVI), defined as a log measure of

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

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

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

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

277 ly discontinue any of the medications due to QT prolongation, and arrhythmogenic death.

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

279 er by using the imaging quantitative traits (QTs) as endophenotypes is an important task in brain sci

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

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

282 isms (SNPs) and imaging quantitative traits (QTs).

283 wave inversions, and 10 (53%) have transient QT prolongation > 480 ms.

284 ed by extensive T-wave inversions, transient QT prolongation, and severe disease expression of exerci

285 nversions in the precordial leads, transient QT prolongation in some, and recurrent ventricular arrhy

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

287 ternative mechanisms may exist that underlie QT interval dynamics.

288 ylation variance QTs and expression variance QTs.

289 lication to identifying methylation variance QTs and expression variance QTs.

290 The primary outcome was QT prolongation resulting in Torsade de pointes.

291 Average for phenolics (ppm) was, QT (10.91) > GA (7.33) > LT (4.10) > RT (3.90) whereas,

292 icated for other febrile illnesses for which QT-interval-prolonging medications are important therape

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

294 l antimalarial medicines are associated with QT interval prolongation.

295 ntensive glycemic control is associated with QT prolongation, which may lead to ventricular arrhythmi

296 sociation studies that associated LITAF with QT interval variation.

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

298 ority (25%) of these cases were treated with QT-prolonging antimicrobials.

299 ively result from concomitant treatment with QT-prolonging antimicrobials, direct effects of inflamma

300 morphic ventricular tachycardia (VT) without QT prolongation is well described in patients without st