ライフサイエンスコーパス: QT interval

1 ard ECG measures (heart rate, PQ-, QRS-, and QT-intervals).

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

3 hat can induce prolongation of the corrected QT interval.

4 achycardia but abolished the prolongation of QT interval.

5 ontrolling action potential duration and the QT interval.

6 layed repolarization and prolongation of the QT interval.

7 for this pediatric patient cohort with short QT interval.

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

9 ing RING finger protein 207 (RNF207) and the QT interval.

10 s that shorten action potential duration and QT interval.

11 arts with an INaP blocker also shortened the QT interval.

12 hy by voltage and slight prolongation of the QT interval.

13 rtion of patients, most commonly a prolonged QT interval.

14 mia, as measured by the electrocardiographic QT interval.

15 extremely unlikely in the absence of a short QT interval.

16 sted by prolongation of the QRS duration and QT interval.

17 parent risk of prolongation of the corrected QT interval.

18 10 loci explain 5.4-6.5% of the variation in QT interval.

19 ent human genome-wide association studies of QT interval.

20 q21 locus, which is strongly associated with QT interval.

21 the action potential duration and corrected QT interval.

22 and demographic factors on the pretreatment QT interval.

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

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

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

26 myocardial scar is associated with a longer QT interval.

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

28 r exercise duration, and longer PR, QRS, and QT intervals.

29 al treatments for individuals with prolonged QT intervals.

30 10% incidence) were nausea (16%), prolonged QT interval (12%), vomiting (11%), and dysgeusia (11%);

31 is associated with an extremely abbreviated QT interval (200 ms) on ECG and paroxysmal atrial fibril

32 s (84% male; age, 26 +/- 15 years; corrected QT interval, 329 +/- 22 ms) were studied, and 62 were fo

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

34 over, patients with schizophrenia had longer QT-intervals (410.9 versus 393.1 and 401.9 ms; both P<0.

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

36 Prolongation of the electrocardiographic QT interval, a measure of cardiac repolarization, is ass

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

38 ly 24% to 32% of patients had rate-corrected QT intervals above 500 ms.

39 ments predict that, in addition to the short QT interval, absence of inward rectification in the E299

40 Analysis of corrected QT interval among 74 control subjects from our dataset s

41 The QT interval, an electrocardiographic measure reflecting

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

43 Adjustment for QT interval and coronary heart disease risk factors atte

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

45 s, such as palonosetron, does not affect the QT interval and has a half-life of 40 h that should be a

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

47 prognostic association between the baseline QT interval and incident cardiovascular events in indivi

48 hERG1 channels by some drugs can prolong the QT interval and induce arrhythmia.

49 The QT interval and its components were measured at baseline

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

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

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

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

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

55 st that the incidence of prolongation of the QT interval and the occurrence of torsades de pointes is

56 ions in NOS1AP were associated with baseline QT interval and the risk of SCD in white US adults.

57 association between NOS1AP variants and the QT interval and to examine the association with SCD in a

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

59 adverse cardiac events (prolongation of the QT interval and/or development of torsades de pointes).

60 on of p90RSK (p90RSK-Tg) had prolongation of QT intervals and of ventricular myocyte action potential

61 (1256 +/- 244 per subject) to measure PQ and QT intervals and P wave durations.

62 these mice have prolongation of the QRS and QT intervals and spontaneous ventricular arrhythmias, in

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

64 omplexes (PVCs) from 40 patients with normal QT intervals and with PVCs in 24 of the 35 LQTS patients

65 rophysiologically (bradycardia and prolonged QT interval) and functionally (hyperdynamic left ventric

66 arrest (normal left ventricular function and QT interval) and selected family members from the Cardia

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

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

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

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

71 r hypertrophy, prolongation of the corrected QT interval, and repolarization changes (ST/T wave abnor

72 ght ventricular ejection fraction, prolonged QT interval, and total infarct size and resulted in impr

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

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

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

76 nificantly enriched for association with the QT interval, as compared to genome-wide markers.

77 Electrocardiographic parameters, including QT intervals, as well as ventricular action potential wa

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

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

80 Rare variant analysis of 6 new QT interval-associated loci in 298 unrelated probands wi

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

82 diac PI3K signaling in diabetes prolongs the QT interval at least in part by causing an increase in I

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

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

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

86 of the channel are associated with the long QT (interval between the Q and T waves in electrocardiog

87 romes, representing the very extremes of the QT interval, both seem to have a high prevalence of AF.

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

89 dictors for TdP commonly rely on a prolonged QT interval but rarely consider abnormal T-U waves.

90 pective analysis of an ECG identified a long QT interval, but sequencing of known LQT genes was uninf

91 on (APD) of individual myocytes and thus the QT interval by altering multiple ion currents, including

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

93 1C-p.R518C variant associated with prolonged QT intervals, cardiomyopathy, and sudden cardiac death i

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

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

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

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

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

99 mine the association between prolongation of QT interval corrected for heart rate (QTc) with incident

100 .002]) independently of patients' individual QT interval corrected for heart rate (QTc).

101 ed low-frequency HRV and prolongation of the QT interval corrected for heart rate (QTc).

102 QT intervals, corrected for heart rate, >500 ms and abno

103 mice, although action potential duration and QT intervals did not reflect this benefit.

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

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

106 associated with MeanNN, heart-rate-corrected QT interval duration (QTc), deceleration capacity, and w

107 The corrected baseline 12-lead ECG QT interval duration (QTcorr) was determined by adjustme

108 atures that, along with heart rate-corrected QT interval duration, may risk stratify perinatal manage

109 QT interval duration, reflecting myocardial repolarizati

110 srupted cardiac function including prolonged QT interval duration.

111 show that cardiac ion-channel expression and QT-interval duration (an index of myocardial repolarizat

112 e a contributor to population variability in QT-interval duration among men.

113 stosterone levels may explain differences in QT-interval duration between men and women and could be

114 multivariate adjusted differences in average QT-interval duration comparing the highest quartiles wit

115 tween physiologic levels of sex hormones and QT-interval duration in humans was evaluated using data

116 Estradiol levels were not associated with QT-interval duration in men, but there was a marginally

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

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

119 omatic but displaying a marginally prolonged QT interval during exercise.

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

121 QT interval dynamics during exercise and recovery are he

122 ternative mechanisms may exist that underlie QT interval dynamics.

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

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

125 Median corrected QT interval for heart rate was 312 ms (range: 194 to 355

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

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

128 trioventricular block, AZD1305 increased the QT interval from 535+/-28 to 747+/-36 ms (+40%, P<0.0001

129 ericans (n=12,097) and regressed on measured QT interval from ECGs.

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

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

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

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

134 otal of 1,059 LQTS patients with a corrected QT interval > or =450 ms presenting with syncope as a fi

135 A corrected QT interval >500 msecs was considered prolonged.

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

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

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

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

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

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

142 genetic disease characterized by a prolonged QT interval in an electrocardiogram (ECG), leading to hi

143 in one; hypertension and prolonged corrected QT interval in another) occurred in patients initially e

144 as longer than neonatal heart rate-corrected QT interval in both group 2 (491.2+/-27.6; P=0.004) and

145 ant role for propagation variation affecting QT interval in humans, we show that common polymorphisms

146 the strongest SNP previously associated with QT interval in individuals of European ancestry.

147 Heart rate and QT interval in lead II were measured using the Bazett fo

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

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

150 sociation studies (GWAS) of variation in the QT interval in population-based cohorts now report assoc

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

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

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

154 tric oxide synthase, are associated with the QT interval in white adults.

155 were significantly associated with adjusted QT interval in whites (P<0.0001).

156 channel blockers are largely used to shorten QT intervals in carriers of SCN5A mutations.

157 S1AP gene variants play a role in modulating QT intervals in healthy subjects and severity of present

158 However, increased miR-133a levels increased QT intervals in surface electrocardiographic recordings

159 vealed an age-dependent heart rate-corrected QT interval increase (1% per additional 10 years) irresp

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

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

162 ts investigated altered heart rate-corrected QT interval irrespective of mutation status, as well as

163 The QT interval is a recording of cardiac electrical activit

164 The QT interval is an important diagnostic feature on surfac

165 The ECG QT interval is associated with risk of sudden cardiac de

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

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

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

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

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

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

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

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

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

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

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

177 The neonatal heart rate-corrected QT interval (mean+/-SE) of group 1 (664.7+/-24.9) was lo

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

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

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

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

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

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

184 897 polymorphism is predicted to prolong the QT interval of cardiac myocytes.

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

186 essential in control of the duration of the QT interval of the electrocardiogram.

187 The long QT interval of type 1 diabetic hearts was shortened by i

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

189 Prolonged heart rate-corrected QT interval on electrocardiograms (ECGs) is associated w

190 pounds have been identified that prolong the QT interval on the electrocardiogram and cause torsade d

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

192 Prolongation of the QT interval on the electrocardiogram is also a risk fact

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

194 ce of increased risks of prolongation of the QT interval or dysglycemia with the 4-month regimen.

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

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

197 ucleotide polymorphisms in NOS1AP and either QT interval or SCD were observed in blacks.

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

199 h congenital or acquired prolongation of the QT interval, or long QT syndrome (LQTS), are at risk of

200 of association between genetic ancestry and QT interval (P=0.94).

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

202 4991 in meta-analysis: increase in corrected QT interval per C allele: 9.1 +/- 3.2 ms, p = 1.7 x 10(-

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

204 points; 95% CI, -1.97 to -0.13; P = .03) and QT interval prolongation (18.1 ms; 95% CI, 6.1-30.1; P =

205 Here we report a correlation between QT interval prolongation and T-wave notching in LQTS2 pa

206 dentifying hospitalized patients at risk for QT interval prolongation could lead to interventions to

207 in APD and INaP in myocytes translated into QT interval prolongation for both types of diabetic mice

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

209 pport system (CDSS) for reducing the risk of QT interval prolongation in hospitalized patients.

210 QT interval prolongation is a heritable risk factor for

211 QT interval prolongation is common with ATO and can pose

212 QT interval prolongation is common with ATO treatment, b

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

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

215 QT interval prolongation on the surface ECG is the hallm

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

217 hat mutations cause action potential and ECG QT interval prolongation, consistent with clinical pheno

218 icant associations were seen among corrected QT interval prolongation, repolarization changes, and al

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

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

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

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

223 manifest on the surface electrocardiogram as QT interval prolongation.

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

225 KCNH2, which accounts for the side effect of QT interval prolongation.

226 l antimalarial medicines are associated with QT interval prolongation.

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

228 The degree of QT-interval prolongation and the number of breakthrough

229 790 microg/L) was associated with subsequent QT-interval prolongation in women.

230 nt of surrogate markers of TdP-risk, such as QT-interval prolongation or inhibition of the rapid dela

231 ositive for long-QT syndrome if the absolute QT interval prolonged by >/= 30 ms at 0.10 mug/kg per mi

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

233 tween methadone and other drugs that possess QT interval-prolonging properties or slow the eliminatio

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

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

236 All patients developed corrected QT interval (QTc interval) prolongation (median QTc inte

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

238 The corrected QT interval (QTc) should be assessed as a routine when o

239 cohort study, prolongation of the corrected QT interval (QTc) was associated with an independent inc

240 abeling prolongation of heart rate-corrected QT interval (QTc), an arrhythmia risk marker.

241 ts of AKAP9 variants on heart rate-corrected QT interval (QTc), cardiac events, and disease severity.

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

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

244 with exertional syncope and normal corrected QT interval (QTc).

245 electrocardiographically affected (corrected QT interval [QTc] > or = 470 ms), borderline (QTc 440 to

246 23; range, 0-59, median heart rate-corrected QT interval [QTc] at diagnosis 557 ms (IQR, 529-605) wit

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

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

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

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

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

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

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

254 ), in a pre-defined set of 7 congenital long QT interval syndrome (cLQTS) genes encoding potassium ch

255 riants are associated with drug-induced long QT interval syndrome (diLQTS) and torsades de pointes.

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

257 (acLQTS), which is associated with prolonged QT intervals, tachycardias, and sudden cardiac arrest.

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

259 ified 35 common variant loci associated with QT interval that collectively explain approximately 8-10

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

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

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

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

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

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

266 tance and coupling and thereby regulates the QT interval through propagation defects.

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

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

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

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

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

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

273 ving essentially identical resting corrected QT interval values.

274 ficant minority has normal resting corrected QT interval values.

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

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

277 QT interval variation is assumed to arise from variation

278 us are the most common genetic regulators of QT interval variation.

279 sociation studies that associated LITAF with QT interval variation.

280 collectively explain approximately 8-10% of QT-interval variation and highlight the importance of ca

281 from the corresponding common complex trait, QT-interval variation, to identify candidate genes that

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

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

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

285 The QT interval was associated with incident cardiovascular

286 Corrected QT interval was measured by surface ECG.

287 QT interval was measured using a standard 12-lead electr

288 SNPs, and a genome-wide association study of QT interval was performed in 10 cohorts (n=13,105).

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

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

291 which was not correlated with rs16847548 or QT interval, was also independently associated with SCD

292 Serial assessments of the QT interval were performed.

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

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

295 QT intervals were assessed using four different correcti

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

297 the proband, including an exceedingly short QT interval with merging of the QRS and the T wave, abse

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

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

300 on of repolarization and prolongation of the QT interval, yet the mechanisms underlying CO-induced ar