ライフサイエンスコーパス: T wave

1 ve center of gravity x axis (last 25% of the T wave).

2 orphology and amplitude of the ST-segment or T-wave).

3 regions, are important in the genesis of the T wave.

4 the inscription of the electrocardiographic T wave.

5 coincident with the terminal portion of the T wave.

6 anges; LQT1 prolongs QT without widening the T wave.

7 pears on the ST segment or first half of the T wave.

8 es along all anatomic axes contribute to the T wave.

9 ves generated from scaling of the sinus-rate T-wave.

10 he T wave, absence of ST segment, and peaked T waves.

11 zation sequence with simultaneously recorded T waves.

12 tissue level factors, contribute to notched T waves.

13 mean [SD], 69 [39] mm), and deeply inverted T-waves.

14 deeply inverted, or diffusely flat/biphasic, T waves (14% vs. 3% [p < 0.05] and 25% vs. 8% [p < 0.008

15 ing rates (ie, alternans threshold) at which T-wave (369+/-11 bpm), APD (369+/-21 bpm), and Ca2+ (371

16 a higher prevalence of biphasic or inverted T waves (7 of 9 [77.8%] vs. 4 of 14 [29%], p = 0.04); an

17 QT interval, and repolarization changes (ST/T wave abnormalities).

18 third intercostal space and ECG revealed ST-T wave abnormalities.

19 of isolated minor nonspecific ST-segment and T-wave abnormalities (NSSTTAs) in older adults are poorl

20 tant in understanding the cellular causes of T-wave abnormalities found in the electrocardiograms of

21 persion of repolarization and creating other T-wave abnormalities on simulated electrocardiograms.

22 pertension, left ventricular hypertrophy, ST-T-wave abnormalities, and current cigarette smoking.

23 asymmetric repolarization, reflected in ECG T-wave abnormalities, is associated with a greatly incre

24 Abnormalities on resting ECG (ST-segment or T-wave abnormalities, left ventricular hypertrophy, bund

25 ram abnormalities: 25/26 had repolarization (T wave) abnormalities.

26 QT interval with merging of the QRS and the T wave, absence of ST segment, and peaked T waves.

27 Tests such as microwave T wave alternans (repolarization abnormality) and signal

28 In this regard, T wave alternans (TWA) is a heart-rate-dependent measure

29 Microvolt T wave alternans added information on resuscitated cardi

30 False-negative microvolt T wave alternans results were seen in 8% of patients.

31 (MASTER I-Microvolt T Wave Alternans Testing for Risk Stratification of Post

32 inical association of cardiac alternans (eg, T wave alternans) with arrhythmia risk, which may lead t

33 to-normal R-R intervals), exercise microvolt T wave alternans, and signal-averaged ECG, and corrected

34 In the single time point analysis, microvolt T wave alternans, baroreceptor reflex sensitivity, and S

35 repolarization abnormality such as microwave T wave alternans.

36 The combination of abnormal HRT and T-wave alternans (5 cohorts: 1516 patients) increased th

37 trate for ventricular arrhythmia), microvolt T-wave alternans (a marker of electrophysiological vulne

38 ECG T-wave alternans (ECG ALT) and Ca2+ transient alternans

39 This study hypothesized that microvolt T-wave alternans (MTWA) improves selection of patients f

40 ose of this study was to assess if microvolt T-wave alternans (MTWA) is an independent predictor of m

41 his trial was to determine whether microvolt T-wave alternans (MTWA) predicts ventricular tachyarrhyt

42 hypothesis that an "indeterminate" microvolt T-wave alternans (MTWA) test, when due to ectopy, unsust

43 t to determine whether noninvasive microvolt T-wave alternans (MTWA) testing could identify patients

44 nalysis of the predictive value of microvolt T-wave alternans (MTWA) testing for arrhythmic events in

45 d without risk stratification with microvolt T-wave alternans (MTWA) testing in the MADIT-II (Second

46 e (positive and indeterminate) for microvolt T-wave alternans (MTWA).

47 es in the guinea pig model of pacing-induced T-wave alternans (n=7).

48 usses the electrocardiographic phenomenon of T-wave alternans (TWA) (i.e., a beat-to-beat alternation

49 ur aim was to study the relationship between T-wave alternans (TWA) and rate-response (restitution) o

50 othesized that mechanical alternans (MA) and T-wave alternans (TWA) are associated with postdischarge

51 nans and present a perspective on the use of T-wave alternans (TWA) as a risk stratification marker o

52 sessed by second central moment analysis and T-wave alternans (TWA) by modified moving average analys

53 T-wave alternans (TWA) has been implicated in the pathog

54 In this regard, microvolt T-wave alternans (TWA) has emerged as a potentially usef

55 , we tested the predictive values of PRD and T-wave alternans (TWA) in 2,965 patients undergoing clin

56 spectively evaluate the utility of microvolt T-wave alternans (TWA) in predicting arrhythmia-free sur

57 This study sought to determine whether T-wave alternans (TWA) induced by anger in a laboratory

58 Exercise-induced T-wave alternans (TWA) is an established marker of cardi

59 T-wave alternans (TWA) is an important noninvasive measu

60 T-wave alternans (TWA) reflects beat-to-beat fluctuation

61 diograms were monitored for ischemia-induced T-wave alternans (TWA), a marker of electrical instabili

62 T-wave alternans (TWA), an ABAB oscillation, has been po

63 of repolarization instability, manifested by T-wave alternans (TWA), has proved useful for arrhythmia

64 AP) oscillations and cause electrocardiogram T-wave alternans (TWA).

65 HRT power increases in combination with T-wave alternans analysis.

66 We compared the ability of microvolt T-wave alternans and QRS duration to identify groups at

67 istic association of torsade de pointes with T-wave alternans and short-long cardiac sequences is dis

68 T-wave alternans and simultaneous APD alternans always o

69 en implicated in cardiac arrhythmias such as T-wave alternans and various tachycardias.

70 s have suggested that intracellular Ca2+ and T-wave alternans are linked through underlying alternati

71 acteristics and sinus rhythm had a microvolt T-wave alternans exercise test and a 12-lead ECG.

72 Microvolt T-wave alternans has been proposed as an effective tool

73 Microvolt T-wave alternans has been proposed as an effective tool

74 In conclusion, the mechanism underlying T-wave alternans in the intact heart is more closely ass

75 T-wave alternans is a promising predictor of sudden deat

76 Microvolt T-wave alternans is a strong and independent predictor o

77 T-wave alternans is due to alternation of membrane repol

78 Moreover, T-wave alternans is significantly more pronounced in the

79 r discharge studies and ambulatory ECG-based T-wave alternans measurement.

80 ier findings and the clinical observation of T-wave alternans occurring at slower pacing rates in pat

81 Microvolt T-wave alternans represents another promising predictor,

82 lower among patients with a normal microvolt T-wave alternans test (3.8%; 95% confidence interval: 0,

83 Among MADIT II-like patients, a microvolt T-wave alternans test is better than QRS duration at ide

84 compared patients with an abnormal microvolt T-wave alternans test to those with a normal (negative)

85 normal (positive or indeterminate) microvolt T-wave alternans test.

86 Microvolt T-wave alternans testing has been shown to be effective

87 Microvolt T-wave alternans testing has significant value for the p

88 e failed to confirm the utility of microvolt T-wave alternans to predict ventricular arrhythmias in p

89 T-wave alternans was analyzed using time-domain methods.

90 cardiogram, fragmented QRS, QRS-T angle, and T-wave alternans) were included.

91 G techniques (e.g., heart rate turbulence or T-wave alternans), and imaging modalities (computed tomo

92 ical properties of the myocardium, including T-wave alternans, a measure of heterogeneity of repolari

93 T-wave alternans, a powerful marker of arrhythmic events

94 s, both the normal and failing heart develop T-wave alternans, but only the failing heart shows QRS a

95 terogeneity of repolarization as measured by T-wave alternans, known to be associated with arrhythmog

96 effect has been reported in patients whereby T-wave alternans, once induced by rapid heart rate, pers

97 Discordant TWA episodes, with T waves alternating out of phase, were associated with i

98 34 of 35 LQTS patients and were larger than T-wave amplitude (2.8 +/- 0.2 mm) in control patients an

99 gnificant increase in the ratio of U-wave to T-wave amplitude (UTA) occurred before TdP onset in cont

100 T-wave amplitude and downslope were calculated from the

101 x were associated with a smaller decrease in T-wave amplitude in V5 and V6.

102 on between the decrease in Sokolow index and T-wave amplitude in V5 with desaturation at exercise.

103 sted by TWA and beat-to-beat oscillations of T-wave amplitudes at other frequencies, increased before

104 genome-wide association meta-analysis of ST-T-wave amplitudes in up to 37 977 individuals identifyin

105 ral power of the oscillations of consecutive T-wave amplitudes increased nonuniformly, with the great

106 ectral energy of oscillations of consecutive T-wave amplitudes was calculated with the use of the sho

107 The ST-segment and adjacent T-wave (ST-T wave) amplitudes of the electrocardiogram are quantita

108 sis was conducted using a novel, proprietary T wave analysis program that quantitates subtle changes

109 veloped a new method to quantify [K(+)] from T-wave analysis and tested its clinical applicability on

110 evaluate the performance of a morphological T-wave analysis program in defining breakthrough LQTS ar

111 sis was conducted using a novel, proprietary T-wave analysis program.

112 tward (I(to)) potassium current inscribe the T wave and J wave, respectively; T-wave polarity and wid

113 The average interval between the end of the T wave and the aortic valve artifact was 19+/-37 ms.

114 her distinguished by distinct giant negative T waves and a benign clinical course.

115 n 1966 and 1972 for the presence of inverted T waves and followed the subjects for 30 +/- 11 years.

116 rdial fibrosis (67%); inferolateral negative T waves and low QRS voltages on electrocardiography (33%

117 The amplitudes of the R, S, and T waves and the Sokolow index decreased in hypoxia.

118 ntly, the average percent difference between t-wave and drift cell CCS measurements is minimized by c

119 a. 7% between the same lipids measured using t-wave and drift cell IM-MS, while this improves to <0.5

120 eat fluctuations in the electrocardiographic T-wave, and is associated with dispersion of repolarizat

121 In 74 patients, the ST-segment, the T-wave, and the QT-interval were analyzed using the MUSE

122 T-wave axis, polarity, and amplitude on a 12-lead ECG du

123 ss spectrometry coupled with traveling wave (T-Wave)-based ion mobility has been used to filter for p

124 ation, and deeply inverted or diffusely flat T waves by adolescence.

125 Tpeak-Tend interval, T wave left slope, and T wave center of gravity x axis (last 25% of the T wave)

126 (hazard ratio=0.40 [0.24-0.69]; P<0.001) and T-wave center of gravity x axis (last 25% of wave) in le

127 istration, we noted ST segment elevation and T wave changes characteristic of acute myocardial ischae

128 Early complications included transient ST-T wave changes in 5, transient arrhythmias in 4 and sing

129 Short-term cardiac memory is seen as T-wave changes induced by altered ventricular activation

130 QTc interval prolonged in 100% of patients, T-wave changes, STE, and STD (> or =1 mm) occurred in 7%

131 e defined as Q waves, ST-segment depression, T-wave changes, ventricular conduction defects, and left

132 reflected in characteristic QT-interval and T-wave changes; LQT1 prolongs QT without widening the T

133 out of phase, were associated with increased T-wave complexity and fibrillation in 4 of 6 dogs with V

134 This demonstrated increase in T-wave complexity points to a fundamental mechanistic li

135 omplex ventricular ectopy (VE), and abnormal T waves comprise the recently described bileaflet MVP sy

136 pholipid CCS values are used for calibrating t-wave data.

137 A method to calibrate the T-Wave device, to provide estimates of collision cross s

138 Global T-wave distribution was displayed on a 3-dimensional geo

139 T-wave drift-times for the protonated diastereomers beta

140 interval, QRS complex, ST-segment duration, T-wave duration, QTc, and R-R interval (P>0.05).

141 The interval from T-wave peak to T-wave end (TPE interval) is the clinical counterpart of

142 between electrocardiographic T-wave peak to T-wave end interval (TPE) and SCD.

143 gment, T-wave onset to T-peak, and T-peak to T-wave end) with SCD in 12 241 participants (54+/-5.7 ye

144 membrane potential and Ca(i) during shock on T-wave episodes (n=104) and attempted defibrillation epi

145 ions in slope (dV/dt) relative to "expected" T waves generated from scaling of the sinus-rate T-wave.

146 t intervals), TpTe (time from peak to end of T-wave), heart rate turbulence, systolic and diastolic b

147 R-wave heterogeneity (RWH) and T-wave heterogeneity (TWH) were assessed by second centr

148 These results demonstrate the ability of T-wave IM spectrometry to differentiate diastereomers di

149 ile strategies for obtaining CCS values from t-wave IM-MS data remains an active area of research.

150 directly from thin tissue sections by MALDI t-wave IM-MS using CCS calibrants measured by MALDI drif

151 Recently, traveling-wave (t-wave) IM-MS was developed which uses electrodynamic ra

152 correlation between local repolarization and T wave in a pseudo-ECG.

153 zation gradients to the configuration of the T wave in control settings and after the induction of sh

154 e surface ECG were identified: left slope of T wave in lead V6 (hazard ratio=0.40 [0.24-0.69]; P<0.00

155 The deeper T wave in the ECG after induction of memory may be expla

156 513 +/- 54 ms versus 444 +/- 11 ms, and LQT2 T waves in 87% versus 0%.

157 with the long QT (interval between the Q and T waves in electrocardiogram) syndrome that predisposes

158 However, inverted T waves in leads other than V(1) to V(3) were associated

159 ased mortality risk associated with inverted T waves in other leads may reflect the presence of an un

160 epsilon waves (R = 0.39, P = .02), inverted T waves in V1-V3 (R = 0.38, P = .02), and presence of PK

161 unexplained ventricular arrhythmia, inverted T-waves in the right precordial or lateral leads, and/or

162 n, we estimated the signed derivative of the T-wave integral sequence, which allows the classificatio

163 ed with ST segment elevation (n = 19) and/or T wave inversion (n = 20) on admission ECG.

164 Anterior T-wave inversion (ATWI) on electrocardiography (ECG) in

165 y independent predictor for right precordial T-wave inversion (odds ratio, 3.6; 95% confidence interv

166 Pathological T-wave inversion (PTWI) is rarely observed on the ECG of

167 Postpacing precordial T-wave inversion (TWI), known as cardiac memory (CM), mi

168 ercise, including biventricular dilation and T-wave inversion (TWI), may create diagnostic overlap wi

169 Diffuse T-wave inversion and a prolonged QT interval occurred in

170 Most athletes with HCM (96%) exhibited T-wave inversion and had milder LVH (15.8+/-3.4 mm versu

171 gram, as manifested by the strain pattern of T-wave inversion and STdep, are markers for LVH and adve

172 strain pattern of lateral ST depression and T-wave inversion at baseline has been associated with an

173 of children with postpubertal persistence of T-wave inversion at preparticipation screening is warran

174 The prevalence of right precordial T-wave inversion decreased significantly with increasing

175 The prevalence of T-wave inversion decreases significantly after puberty.

176 ATWI was defined as T-wave inversion in >/=2 contiguous anterior leads (V1 t

177 e relation, and underlying cardiomyopathy of T-wave inversion in children undergoing preparticipation

178 e of ECG left ventricular strain (defined as T-wave inversion in leads V(4) through V(6)) and LVH, as

179 T-wave inversion in right precordial leads V(1) to V(3)

180 block pattern with ST-segment elevation and T-wave inversion in the right precordial leads.

181 However, T-wave inversion is a common ECG abnormality of cardiomy

182 The ECG strain pattern of ST depression and T-wave inversion is strongly associated with left ventri

183 T-wave inversion on a 12-lead ECG is usually dismissed i

184 T-wave inversion through V(3) demonstrated optimal sensi

185 ameters that differed were the prevalence of T-wave inversion through V(4) (59% versus 12%, respectiv

186 ked RV enlargement with concomitant anterior T-wave inversion was observed in 3.0% of BAs versus 0.3%

187 T-wave inversion was predominantly confined to leads V1

188 Anterior T-wave inversion was present in 14.3% of BAs versus 3.7%

189 T-wave inversion was recorded in 158 children (5.7%) and

190 ECG criteria for ischemia (ST depression or T-wave inversion), 40% and 97% for peak troponin-I, and

191 Of 158 children with T-wave inversion, 4 (2.5%) had a diagnosis of cardiomyop

192 ncy departments in Ontario, Canada, Q-waves, T-wave inversion, or ST-depression were present in 51.8%

193 ge reduction (QS in V1-V3) and inferolateral T-wave inversion.

194 chest pain with ST-segment elevation and/or T-wave inversion; (2) absence of significant coronary ar

195 onfidence interval, 2.8-22.5; P<0.001), >/=3 T-wave inversions (hazard ratio, 4.2; 95% confidence int

196 nction had higher odds of lateral precordial T-wave inversions (odds ratio, 18.4; 95% confidence inte

197 l, 1.21-4.01; P=0.01) and lateral precordial T-wave inversions (odds ratio, 9.87; 95% confidence inte

198 e majority (52%) of group 2 changes, whereas T-wave inversions constituted 11%.

199 Right precordial T-wave inversions did not predict increased mortality (n

200 All 5 TRDN-null patients displayed extensive T-wave inversions in precordial leads V1 through V4, wit

201 T-wave inversions in right precordial leads are relative

202 T-wave inversions in right precordial leads V(1) to V(3)

203 he prevalence and prognostic significance of T-wave inversions in the middle-aged general population

204 T-wave inversions in V1 through V3 were observed in 85%

205 ular arrhythmias before ICD implantation and T-wave inversions inferiorly.

206 gment depressions, ST-segment elevations, or T-wave inversions on the presenting ECG.

207 lows discrimination from ischemic precordial T-wave inversions regardless of the coronary artery invo

208 T-wave inversions were the most sensitive predictor of L

209 DLTs included reversible, asymptomatic T-wave inversions, without any associated changes in tro

210 In hearts where electrocardiogram T waves involve a well-defined repolarization edge trave

211 of drug-like molecules as a traveling wave (T-wave) ion mobility (IM) calibration sample set, coveri

212 The genesis of the electrocardiographic T wave is incompletely understood and subject to controv

213 The T-wave is a symbol of transmural dispersion of repolariz

214 The top 3 features were Tpeak-Tend interval, T wave left slope, and T wave center of gravity x axis (

215 T-wave loop morphology was quantified by the ratio of th

216 ies of repolarization measured by PCA of the T-wave loop predict CV death in men and women, supportin

217 VER), manifested electrocardiographically as T-wave memory and ultimately as deleterious mechanical r

218 Although T-wave memory is associated with altered expression of s

219 tricle is the electrophysiological basis for T-wave memory.

220 tion, ST segment depression and a pathologic T wave more frequently compared to controls (p < 0.05 fo

221 o develop and validate a novel, quantitative T wave morphological analysis program to differentiate L

222 tered to patients with hypokalemia, abnormal T wave morphology, HCV infection, and HIV infection.

223 , HCV infection, HIV infection, and abnormal T wave morphology, the effects of haloperidol, clotiapin

224 (HCV) infection, HIV infection, and abnormal T wave morphology.

225 s program that quantitates subtle changes in T wave morphology.

226 n the signal-averaged ECG and variability in T-wave morphology (T-wave variability) between baseline

227 In multivariable Cox models, T-wave morphology dispersion and total cosine R-to-T rem

228 e R-to-T remained as predictors of SCD, with T-wave morphology dispersion showing the highest SCD ris

229 -1.7, P=0.001] per 1 SD increase in the loge T-wave morphology dispersion).

230 ameters (principal component analysis ratio, T-wave morphology dispersion, total cosine R-to-T, T-wav

231 every 30 min and corrected QT intervals and T-wave morphology every 60 min.

232 Both QT dispersion and T-wave morphology improved in most subjects.

233 A total of 4 T-wave morphology parameters (principal component analys

234 an association between electrocardiographic T-wave morphology parameters and cardiovascular mortalit

235 the predictive value of electrocardiographic T-wave morphology parameters and TPE for SCD in an adult

236 Electrocardiographic T-wave morphology parameters describing the 3-dimensiona

237 In univariable analyses, all T-wave morphology parameters were associated with an inc

238 Furthermore, the T-wave morphology was assessed in mutation carriers, dou

239 rrected for heart rate, >500 ms and abnormal T-wave morphology were observed during hypoglycemia in s

240 at computes the beat-by-beat integral of the T-wave morphology, over time points within the T-wave wi

241 es the electrocardiogram (ECG), particularly T-wave morphology.

242 , or only 7% the value of those with VF, and T-wave multupling was not observed (0 of 6 versus 5 of 6

243 elation between QT interval prolongation and T-wave notching in LQTS2 patients and use a novel comput

244 ned as the maximum derivative (dV/dt) of the T wave of the shock electrogram, correlates with the mos

245 .005): (1) ST-segment elevation and inverted T wave of unipolar electrograms (2.21+/-0.67 versus 0 mV

246 enomenon (an extrasystole originating on the T-wave of a preceding ventricular beat) is probably due

247 Calibration of these drift-times yields T-wave Omega(N(2)) values of 189.4 and 190.4 A(2), respe

248 The experimental RF-confining drift-tube and T-wave Omega(N(2)) values were also evaluated using a ni

249 es with available ECG, 10 (83%) had inverted T waves on inferior leads, and all had right bundle-bran

250 als (the time interval between the Q and the T waves on the cardiac electrocardiogram), was investiga

251 5% confidence interval, 1.01-2.18), only the T-wave onset to T-peak component (per 1-SD increase: haz

252 QT interval is driven by prolongation of the T-wave onset to T-peak component.

253 components were included in the same model, T-wave onset to T-peak remained the strongest predictor

254 to R-peak, R-peak to R-wave end, ST-segment, T-wave onset to T-peak, and T-peak to T-wave end) with S

255 rogen based trajectory method, optimized for T-wave operating temperature and pressures, incorporatin

256 convex ST segment with inverted asymmetrical T-wave opposite the QRS axis in lead V5 or V6.

257 termination rules, enhancements to minimize T-wave oversensing, and features that restrict therapy t

258 received inappropriate shocks, mainly due to T-wave oversensing, which was mostly solved by a softwar

259 trical angle between the QRS complex and the T-wave; p = 0.0005), wider QRS complex (p = 0.004), long

260 T-Wave parameters have been optimized to maximize the se

261 x), and on exercise ECGs (Ex QTc-max) and by T-wave patterns.

262 The interval from T-wave peak to T-wave end (TPE interval) is the clinical

263 the association between electrocardiographic T-wave peak to T-wave end interval (TPE) and SCD.

264 s method was able to accurately identify the T-wave phase in artificially induced alternans (P<0.0001

265 Calibrating t-wave phospholipid CCS values with drift cell peptide C

266 nscribe the T wave and J wave, respectively; T-wave polarity and width are strongly influenced by the

267 aximal QTc interval prolongation, changes in T-wave polarity, > or =1 mm STE, and ST-segment depressi

268 tion, 76 (0.7%) of the subjects had inverted T waves present only in leads other than V(1) to V(3).

269 Detailed morphological analysis of the T wave provides novel insights into risk of breakthrough

270 V outflow tract ectopy; and exercise-induced T-wave pseudonormalization.

271 T wave quantitative analysis on the 12-lead surface ECG

272 Increased R:T wave ratio in the S-ICD screening ECG (odds ratio, 4.0

273 in complexes can be confined within the Trap T-wave region of a modified Waters Synapt G2S instrument

274 morphology dispersion, total cosine R-to-T, T-wave residuum) as well as TPE were measured from digit

275 The ULV was the weakest T-wave shock that did not induce VF.

276 The system delivered up to 4 T-wave shocks of 18 J.

277 method may be automated in an ICD by timing T-wave shocks relative to TR.

278 The T-wave slope-to-amplitude ratio (TS/A) was used as start

279 The ST-segment and adjacent T-wave (ST-T wave) amplitudes of the electrocardiogram a

280 rs describing the 3-dimensional shape of the T-wave stratify SCD risk in the general population, but

281 ation during hypoglycemia as demonstrated by T-wave symmetry and principal component analysis ratio c

282 nd P- or F-wave duration even when overlying T waves, then prospectively applied them to patients dur

283 margin system was conducted, which measured T-wave timing using an intracardiac electrogram during a

284 ethods have required manual determination of T-wave timing.

285 ific limited time during the upstroke of the T-wave to be the critical time for injury, but specific

286 ogram rather than the latest-peaking surface T wave (Tpeak).

287 red QRS (2.2 ms; 95% CI, -1.4 to 5.9 ms), or T-wave variability (3.0 microV; 95% CI, -4.8 to 10.7 mic

288 ity, the time-domain signal-averaged ECG, or T-wave variability during the first year after myocardia

289 ed ECG and variability in T-wave morphology (T-wave variability) between baseline and 1 year.

290 ysis showed weaker association between these T-wave variables and LQT1-triggered events while these f

291 ac memory' describes an electrocardiographic T wave vector change, recorded during normal sinus rhyth

292 io of the second to first eigenvalues of the T-wave vector (PCA ratio) (>32.0% in women and >24.6% in

293 io of the second to first eigenvalues of the T-wave vector by PCA (PCA ratio); QTd was quantified as

294 T-wave vector displacement (TVD) obtained during VP was

295 r, principal component analysis (PCA) of the T-wave vector loop may more accurately represent repolar

296 d the lead with the highest magnitude of the T wave was selected for analysis.

297 duced decrease in the amplitude of the P/QRS/T waves was observed.

298 o elucidate the mechanism linking [K(+)] and T-wave, we also analysed data from long QT syndrome type

299 (n = 20), tachycardia P or F waves overlying T waves were identified from transitions in slope (dV/dt

300 wave morphology, over time points within the T-wave with positive alternans.