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 es along all anatomic axes contribute to the T wave.

4 anced I(Ca,L) lead to PVCs emerging from the T wave.

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

6 coincident with the terminal portion of the T wave.

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

8 zation sequence with simultaneously recorded T waves.

9 tissue level factors, contribute to notched T waves.

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

11 for QRS complexes, and 0.57 (0.35-0.76) for T waves.

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

13 rolled excitation of a Tollmien-Schlichting (TS) wave.

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

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

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

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

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

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

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

27 Microvolt T wave alternans added information on resuscitated cardi

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

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

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

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

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

33 repolarization abnormality such as microwave T wave alternans.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 T-wave alternans and simultaneous APD alternans always o

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

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

64 ternans in single atrial myocytes and atrial T-wave alternans at the whole heart level.

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

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

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

68 ficantly attenuated or even abolished atrial T-wave alternans in isolated Langendorff perfused hearts

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

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

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

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

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

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

75 Microvolt T-wave alternans represents another promising predictor,

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

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

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

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

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

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

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

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

84 n LQTS type 2 (LQT2) and LQTS type 3 (LQT3), T-wave alternans was observed followed by premature vent

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

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

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

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

89 functional 2 degrees atrioventricular block, T-wave alternans, and torsade de pointes (TdP).

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

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

92 34 of 35 LQTS patients and were larger than T-wave amplitude (2.8 +/- 0.2 mm) in control patients an

93 T-wave amplitude and downslope were calculated from the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 wave, PR segment, QRS interval, ST segment, T wave, and TP segment) and 2 composite, conventional (P

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

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

115 In R-from-T, the PVC and the T wave are causally related, where steep repolarization

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

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

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

119 It was found that the TS wave can be attenuated with scales on the plate which

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

121 (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

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

123 ram showed sinus bradycardia and nonspecific T wave changes.

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

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

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

127 quare of successive differences (RMSSD), and T-wave complexity.

128 nt associations between particle metrics and T-wave complexity.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

149 513 +/- 54 ms versus 444 +/- 11 ms, and LQT2 T waves in 87% versus 0%.

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

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

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

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

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

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

156 T amplitudes in 12 leads; as well as QRS and T wave integrals.

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

158 T wave inversion in infero-lateral and left precordial l

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

175 wed sinus rhythm, right bundle branch block, T-wave inversion in V6, and evidence of right atrial dil

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

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

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

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

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

181 Anterior T-wave inversion was more common in females than males (

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

183 T-wave inversion was predominantly confined to leads V1

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

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

186 ular complex count, and number of leads with T-wave inversion) were associated with LTVA.

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

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

189 hypertrophy voltage criteria, long QTc, and T-wave inversion, all P<0.05) and predicted clinical wor

190 e number of anterior and inferior leads with T-wave inversion, left and right ventricular ejection fr

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

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

193 ith presence of MAD, leaflet redundancy, and T-wave inversion/ST-segment depression (all p < 0.0001)

194 left ventricular end-systolic diameter, and T-wave inversion/ST-segment depression (all p <= 0.001).

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

196 The older patient had anterior T wave inversions, prolonged terminal activation duratio

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

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

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

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

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

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

203 T-wave inversions in right precordial leads are relative

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

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

206 potentially lethal disease characterized by T-wave inversions in the precordial leads, transient QT

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

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

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

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

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

212 the 19 surviving patients, 16 (84%) exhibit T-wave inversions, and 10 (53%) have transient QT prolon

213 Electrocardiography revealed nonspecific T-wave inversions, and a series of cardiac biomarkers we

214 ts, TKOS has been characterized by extensive T-wave inversions, transient QT prolongation, and severe

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

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

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

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

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

220 (JTp) and J to the median of area under the T wave (JT50) were reported to differentiate QT prolongi

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

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

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

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

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

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

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

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

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

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

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

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

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

234 -1.7, P=0.001] per 1 SD increase in the loge T-wave morphology dispersion).

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

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

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

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

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

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

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

242 The T-wave morphology restitution (TMR), an ECG marker quant

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

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

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

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

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

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

249 .005): (1) ST-segment elevation and inverted T wave of unipolar electrograms (2.21+/-0.67 versus 0 mV

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

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

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

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

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

255 5% confidence interval, 1.01-2.18), only the T-wave onset to T-peak component (per 1-SD increase: haz

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

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

258 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

281 isualise which part of the ECG signal (e.g., T-wave, ST-interval) is significantly associated with th

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

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

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

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

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

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

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

289 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

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

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

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

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

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

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

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.