The Effects of Sympathetic Imbalance on the Canine T Wave and QT Interval

The effects of sympathetic imbalance with left dominance on the electrocardiogram was studied in 12 open-chest anesthetized dogs. Heart rate was held constant (80 or 150 bpm) by right vagal stimulation and atrial pacing, To minimize vagai-sympathetic interactions, the intensity of vagal stimulation was well below the threshold for asystole. Electrocardiographic recordings were obtained from three ECC leads (II, X, and Z). Transection of the right stellate increased the T-wave amplitude in lead II (0.12 ± 0.05 mV, P < 0.05) but had no effect on the QT interval in any lead. Left stellate transect ion after right transection decreased the T-wave amplitude in lead II (0.13 ± 0.06 mV, P < 0.05) but did not alter the QT interval in any lead. Electrical stimulation of the decentralized left stellate for periods of 3 or 15 sec prolonged the QT interval by as much as 21 msec, but the average changes were considerably less (± 6.0 msec) and were not significant. Left stellate stimulation for 30 or 60 seconds shortened the QT by as much as 30 msec (P < 0.05). All periods of left stellate stimulation significantly increased the T-wave amplitude in lead II. The electrocardiographic changes induced by sympathetic imbalance were similar at both heart rates. The results do not support the presence of a significant degree of "silent" repolarization after the end of the T wave in the normal canine electrocardiogram.     

Use of intracoronary electrocardiography for detecting ST-T, QTc, and U wave changes during coronary balloon angioplasty

Intracoronary electrocardiography (IC-ECG) is a more sensitive method than surface ECG to detect electrical changes during percutaneous transluminal coronary angioplasty (PTCA). It also provides direct monitoring of ST-T segment, QTc intervals, and U-wave genesis during balloon inflation. These changes are reflective of myocardial ischemia. The authors studied the effect of transient myocardial ischemia on ST-T segment, QTc intervals, and U-wave appearance by comparing standard and perfusion balloon angioplasty. PTCA of left anterior descending artery was performed in 14 patients using the standard balloons and in 11 patients using the perfusion balloons. Patients with perfusion balloon angioplasty had less ST-T elevation (0.15 +/- 0.05 mV versus 1.04 +/- 0.19 mV, P < 0.001), less QTc-shortening intervals (0.01 +/- 0.02 seconds versus -0.05 +/- 0.04 seconds, P < 0.001), and less positive U waves (two versus nine). The authors concluded that balloon angioplasty with perfusion balloons is associated with less ischemia as reflected by ST-T, QTc-shortening intervals, and U-wave changes. There was more positive U-wave appearance with the standard balloon angioplasty, which implies more ischemia. In addition, QTc-shortening intervals are associated with the development of U waves during standard balloon angioplasty. These findings suggest that IC-ECG is a sensitive tool in detecting myocardial ischemia. IC-ECG may also help to clarify the nature of chest pain during PTCA in some patients. Like QT dispersion (QTd), QTc-shortening intervals and new U waves can have prognostic implications and additional studies are needed to define this role.     

Relation between serum digoxin concentration and the electrocardiogram

The relation between serum digoxin concentration and the electrocardiogram was assessed by correlating computerized measurements of electrocardiographic parameters (PR, QRS, QT and QTc intervals, ST segment, and T-wave amplitude) with the serum digoxin concentration in 97 patients on digoxin maintenance therapy and in 40 nondigitalized control subjects. None of the patients had unstable ischemic heart disease, electrolyte disorders, medication known to influence the ST segment, and/or the presence of a bundle-branch block or ventricular hypertrophy. We found a trend toward lengthened PR interval and shortened QT and QTc intervals in digitalized versus nondigitalized patients. Increasing serum digoxin concentrations were associated with progressive depression of the ST segment and decreased T-wave amplitude (p less than 0.001). A normal ST segment in four leads (I, aVF, V5, V6) excluded the presence of a serum digoxin concentration greater than 1.3 ng/ml in our patients, whereas severe ST-segment depression with a J point of greater than or equal to 100 microV was a strong indicator for the presence of a serum digoxin concentration greater than 2.0 ng/ml in our selected patient population (specificity 99%, sensitivity 30%, predictive accuracy 85%). We conclude that computerized electrocardiographic analysis of the ST segment may provide clinically useful information for the management of selected patients on digitalis therapy and may therefore increase the diagnostic yield of the electrocardiogram in predicting the presence of higher serum digoxin concentrations in a small but significant percentage of patients.     

左心交感神经切除术对长QT综合征患者U波的调节作用

目的为进一步理解T波和U波的关系及U波在长QT综合征(LQTS)中的病理生理学意义。方法对11例LQTS患者行左心交感神经切除(LCSD)手术,评价其手术前后及跟踪期间ECG上U波和T波变化。结果术后QTc(校正的QT间期:从0.50±0.05s到0.47±0.03s,P=0.02)、QTp(从QRS波起始到T波顶点的时间间隔:0.37±0.07s到0.33±0.06s,P=0.041)和QTpc(校正的QTp:从0.37±0.07s到0.34±0.05s,P=0.006)均显著缩短。同时QU间期(从QRS波起始到U波结束)、QUc(校正的QU间期)、QUp(从QRS波起始到U波顶点的时间间隔)、QUpc(校正的QUp)却无显著改变。TpTe(同一导联上T波顶点到T波结束点的时间间隔)无显著变化,但TpTe-max(12导联中最早的T波顶点到最晚的T波结束点的时间间隔,代表跨壁复极离散度:0.21±0.09s到0.18±0.07s,P=0.02)显著降低。U波幅度、T波幅度及U/T幅度比值均无显著变化,但TpUp(T波顶点到U波顶点的时间间隔:0.16±0.06s到0.19±0.05s,P=0.041)显著增加。手术后2天内,多数患者U波更明显并叠加于T波之上形成T-U融合现象;但随后融合程度逐渐减轻。结论LQTS患者的U波与T波具有不同的起源机制,因此在诊断LQTS测量QT间期时不应包含U波。     

Morphological algebraic models of the TU-wave patterns/in idiopathic long QT syndrome

A computer-assisted analysis of the TU-complex morphology was employed to characterize repolarization abnormalities in LQTS and to assess arrhythmic risk. Electrocardiograms (ECGs) were collected from 14 idiopathic LQTS patients (seven without symptoms and seven with a history of syncope or cardiac arrest) and from 14 sex- and age-matched normal subjects. Digitized TU-wave patterns from V2-V6 precordial leads were analyzed. The morphologies of the T and U waves were modeled by an algebraic sum of differences between two pairs of action potential-like curves of different shape and duration so that the whole TU complex was approximated by (S1-S2)+(L1-L2). By finding the best fit model of the digitized TU-wave signal, the amplitude and duration of each decomposition curve were determined for each lead. The following 'secondary' parameters were then derived: (a) the ratio between the sum of the amplitudes of the two long (L1 and L2) and the two short (S1 and S2) decomposition curves (A-ratio), (b) the highest A-ratio found in V2 to V6 (A-ratio(max)), and (c) the model-derived durations of the T-wave, U-wave and TU-complex. Conventional measures of RR and QTc intervals and of QT dispersion did not differ between symptomatic and asymptomatic LQTS patients. Modeled QT interval was significantly longer in the symptomatic than in the asymptomatic LQTS patients and in asymptomatic LQTS patients than in the controls. In addition, symptomatic LQTS patients had a longer S2 and T-wave duration in most leads than normal subjects. Conversely, modeled QU interval and U-wave duration did not significantly differ between the three groups. Compared to normal subjects, the amplitudes of S1, S2, L1 and L2 in the LQTS patients were not significantly different in most leads. A-ratio and A-ratio(max) were greater in symptomatic than asymptomatic LQTS patients and in the latter than in controls. A cut-off value of 0.90 of A-ratio(max) separated all symptomatic (1.34+/-0.38) from all asymptomatic patients (0.60+/-0.21). Although the correlation between model parameters and cellular substrate is at present unclear, it is possible that the morphological alterations described by the model are related to the arrhythmogenic mechanism(s) of the idiopathic LQTS.     

Measuring QT dispersion: man versus machine.

OBJECTIVE: To compare manual and computer automated techniques for measuring QT dispersion. DESIGN: Assessment of the ability of manual and automatic measurements of QT dispersion to discriminate between a normal group and two cardiac groups. SUBJECTS: 12 simultaneous electrocardiogram leads were recorded from 25 healthy volunteers, 25 subjects after myocardial infarction, and 25 with cardiac arrhythmias. MAIN OUTCOME MEASURES: For each subject, QT dispersion was measured as the difference between the maximum and minimum QT from all 12 leads and separately for only those leads with T amplitudes of > 100 microV and for those > 250 microV. RESULTS: Manual QT dispersion (T > 100 microV) was greater (P < 0.02) in the arrhythmia patients (mean (SD), 45 (21) ms), but not the infarction patients (54 (36) ms), than in the normal subjects (39 (13) ms). There were no significant differences when all T waves were included. QT dispersion was significantly reduced by an average of 30% when T waves < 100 microV were excluded, and by 51% when those < 250 microV were excluded. Automatic techniques gave different measurements for dispersion in comparison with manual measurements. Three of the four automatic techniques detected significant differences between normal and both patient groups when no leads were excluded (P < 0.01) as well as when T waves < 100 microV were excluded (with increased significance, P < 0.002). CONCLUSIONS: Measurements of QT dispersion from small T waves increases measurement variability and reduces the potential for detecting clinical differences. Automatic measurement of QT dispersion gives different results from manual measurement, but can satisfactorily discriminate between normal and abnormal groups with good quality electrocardiograms.     

Gender Differences in the Effect of Auditory Stimuli on Ventricular Repolarization in Healthy Subjects

Introduction: Gender differences in the incidence of ventricular arrhythmias have been reported and torsade de pointes associated with long-QT syndrome (LQTS) is more common in women than men. Although auditory stimulation has been recognized as an important trigger of torsade de pointes in LQT2 patients, the normal response and gender differences in ventricular repolarization induced by auditory stimuli remained to be evaluated systematically.
Methods: Holter ECGs were recorded in 30 healthy volunteers (14 men aged 25 ± 4 years and 16 women aged 23 ± 2 years). They were awakened by an alarm clock at 5:00 am. The RR and QT (QTc) intervals and the T-wave amplitude were measured before and after alarm ringing.
Results: The morphology of the T-wave changed dynamically and transiently during awakening. The RR interval significantly decreased just after sounding of the alarm in both sexes (P < 0.0001). The QT interval changed little after the alarm ringing and was significantly longer in women than men (P < 0.0001). The QTc intervals were significantly prolonged just after alarm ringing in both sexes (P < 0.0001); QTc prolongation was significantly longer and more sustained in women than men (P < 0.0001). The T-wave amplitude decreased after the alarm and was significantly lower in women than men (P = 0.0001).
Conclusion: Auditory stimulation abruptly and abnormally modulated the dynamics of ventricular repolarization in healthy subjects; the effect was more pronounced in women than men. This gender difference may partially account for the increased susceptibility of women with electrically unstable hearts to arrhythmogenesis.     

Sympathomimetic infusion and cardiac repolarization: the normative effects of epinephrine and isoproterenol in healthy subjects

Introduction: Catecholamines are known to affect cardiac repolarization, and provocation with either isoproterenol or epinephrine has been proposed as a tool for uncovering latent repolarization abnormalities. This study systematically compares the effects of isoproterenol and epinephrine infusions on QT interval (QT), T waves and U waves in normal subjects.
Methods and Results: Twenty-four normal subjects (29 ± 8 years) were evaluated during graded infusions of up to 0.30 μg/kg/minute epinephrine and 5.0 μg/minute isoproterenol. Heart rates at peak doses were 81 ± 13 bpm at 0.28 ± 0.04 μg/kg/minute epinephrine and 104 ± 5 bpm at 2.4 μg/minute isoproterenol. The longest absolute QT increase was 4 ± 5 msec above baseline during isoproterenol (P < 0.001) and 12 ± 23 msec during epinephrine (P = 0.07), while the longest corrected QT interval (QTc) increase was 67 ± 28 msec (P < 0.0001) and 79 ± 40 msec (P < 0.0001) above baseline during isoproterenol and epinephrine, respectively (P = 0.12 for difference). There was a 2-fold increase in U-wave amplitude during each intervention (P < 0.001). The specificity of paradoxical QT prolongation (≥30 msec at 0.05 μg/kg/minute or ≥35 msec at 0.10 μg/kg/minute epinephrine) and an increase in QTc ≥600 msec at any dose epinephrine were 100%. However, the specificity of other proposed criteria that utilized QTc measurement (≥30 msec at 0.10 μg/kg/minute or ≥65 msec at any dose) was poor whether all leads or only lead II were assessed.
Conclusion: Both epinephrine and isoproterenol are associated with QTc prolongation and amplification of the U wave in normal subjects. The specificity of proposed criteria for epinephrine provocation in diagnosis of the long-QT syndrome is variable; however, paradoxical QT prolongation at low-dose epinephrine or a QTc ≥600 msec is highly specific.     

ST-T integral and T-wave amplitude in detection of exercise-induced myocardial ischemia evaluated with body surface potential mapping

Body surface potential mapping is superior to 12-lead electrocardiogram in detection of acute and old myocardial infarctions. We examined the capability of the ST-T integral and T wave to detect exercise-induced ischemia in body surface potential mapping. Body surface potential mapping with 123 channels was recorded in 70 subjects: 45 coronary artery disease (CAD) patients and 25 healthy controls during supine bicycle exercise testing. Of the patients, 18 had anterior, 14 posterior, and 13 inferior ischemia documented by coronary angiography and thallium scintigraphy. The ST-T isointegral area, as well as the positive and negative ST-T area, and the T-wave apex amplitude were determined. Discriminant index analysis was used to find the sites that optimally separated patient subgroups from other patients and controls. In the pooled CAD group, the optimal sites for detecting the decrease in ST-T isointegral, in the positive ST-T area and in the T-wave amplitude were over the left side (ST-T isointegral area: CAD -3.8 +/- 14 microVs and controls 24 +/- 14 microVs; T-wave amplitude: CAD 3 +/- 110 microV and controls 190 +/- 90 microV; P <.001, both). The area under the receiver operating characteristic curve for the decrease in ST-T isointegral, in the positive ST-T area, and in the T-wave amplitude and for the ST depression were 94%, 95%, 92%, and 93%, respectively. T wave performed especially well in patients with multivessel disease. In stepwise logistic regression analysis, using the presence of CAD as the dependent parameter, the decrease in the positive ST-T area and ST depression were the only parameters that entered the model. ST-T area and T-wave amplitude are sensitive and specific markers of transient myocardial ischemia. ST-T area contains information additional to ST depression and has thus independent discriminative value in ischemia detection.     

Scatter in repolarization timing predicts clinical events in post–myocardial infarction patients

BACKGROUND: Increased spatial and temporal dispersion of repolarization contributes to ventricular arrhythmogenesis. Beat-to-beat fluctuations in T-wave timing are thought to represent such dispersion and may predict clinical events. OBJECTIVE: The purpose of this study was to assess whether a novel noninvasive measure of beat-to-beat instability in T-wave timing would provide additive prognostic information in post-myocardial infarction patients. METHODS: We studied 678 patients from 12 hospitals with 32-lead 5-minute electrocardiogram recordings 6-8 weeks after myocardial infarction. Custom software identified R wave-to-T wave intervals (RTIs) and diastolic intervals (DIs). Repolarization scatter (RTI:DI(StdErr)) was then calculated as the standard error about the RTI:DI regression line. In addition, left ventricular ejection fraction (LVEF), short-term heart rate variability (HRV) parameters, and QT variability index were measured. Patients were followed for the composite endpoint of death or life-threatening ventricular arrhythmia. RESULTS: After a mean follow-up of 63 months, 134 patients met the composite endpoint. An RTI:DI(StdErr) >5.50 ms was associated with a 210% increase in arrhythmias or deaths (P <.001). After adjusting for LVEF, RTI:DI(StdErr) remained an independent predictor (P <.001). RTI:DI(StdErr) was also independent of short-term HRV parameters and the QT variability index. CONCLUSIONS: Increased repolarization scatter, a measure of high-frequency, cycle-length-dependent repolarization instability, predicts poor outcomes in patients after myocardial infarction.     

Multiparametric electrocardiographic evaluation of left ventricular hypertrophy in idiopathic and hypertensive cardiomyopathy.

BACKGROUND: Electrophysiological abnormalities underlying the increased arrhythmogenicity of left ventricular hypertrophy (LVH) are still under investigation. The aim of this study was to assess non-invasively the electrophysiologic alterations in two different types of LVH, METHODS: Multiparametric non-invasive ECG analysis (R-R interval, QRS and QT intervals, QT dispersion, T-wave complexity, activation-recovery interval [ARI] dispersion, standard deviation of RR intervals [SDNN], filtered QRS duration [fQRS], root-mean-square voltage of the terminal 40 ms of the fQRS [RMS40] and low amplitude signal duration (< 40 microV) in the terminal portion of the fQRS [LAS]) was performed in 57 patients with hypertensive LVH and hypertrophic cardiomyopathy (HCM), and in 105 healthy subjects. RESULTS: The R-R interval and SDNN were similar in hypertrophic patients and controls. QRS and QT intervals were longer in hypertrophic patients without any differences between hypertensive LVH and HCM. QT dispersion, T-wave complexity and fQRS were greater in hypertrophic patients; QT dispersion was the greatest in HCM. ARI dispersion was lesser in hypertrophic patients without any differences between subgroups of LVH. fQRS showed a trend toward higher values in hypertensive patients. LAS at 25 Hz had a trend toward lower values in HCM patients, while LAS at 40 Hz and RMS40 showed no difference between controls and hypertrophic patients. Left ventricular mass index was not correlated with any of the above-mentioned parameters. CONCLUSIONS: The QT interval and dispersion did not identify the type of hypertrophy. Similarly, ARI dispersion which explores local variations of repolarization duration, and T-wave complexity could not distinguish patients with hypertensive LVH from those with HCM indicating that multiparametric ECG data are affected more by the presence of LVH, than by its type.     

Significance of T-wave amplitude and dynamics at the time of reperfusion in patients with acute ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention

Background

Peri-interventional T-wave changes may reflect the microvascular reperfusion status and potentially carry early independent, prognostic information in patients with ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI).

Methods

The first available electrocardiogram (ECG) (index ECG) and the ECG recorded immediately post-PCI were analyzed for T-wave morphology in 207 patients with STEMI. Absolute T-wave amplitude was recorded and any change in T-wave amplitude from index ECG to post-PCI ECG was calculated. Continuous ST monitoring was performed from hospital arrival until 90 minutes after PCI. Maximum troponin level and left ventricular ejection fraction were evaluated before discharge. Final infarct size was assessed by myocardial perfusion imaging after 1 month.

Results

Large, positive T-wave amplitude in the index ECG and the post-PCI ECG was associated with delayed ST resolution after PCI. In the post-PCI ECG, T-wave amplitude was positively associated with troponin-T value (P < .001) and final infarct size (P = .036), and inversely associated with left ventricular ejection fraction (P < .001). However, T-wave amplitude in the post-PCI ECG was also associated with procedural increase in ST elevation (P < .001) and inversely associated with spontaneous ST resolution (P < .017). A net decrease in T-wave amplitude during reperfusion therapy was associated with faster microvascular reperfusion as evaluated by time to ST resolution.

Conclusion

Large T-wave amplitudes in static pre- and post-PCI ECGs are associated with delayed microvascular reperfusion, whereas the dynamic development of more negative T waves during PCI is associated with earlier microvascular reperfusion. However, in the acute setting, T waves provide little incremental information when compared to ST parameters available in the per-interventional phase.     

Changes in autonomic activity and ventricular repolarization

An increase in sympathetic activity, manifested by shortening of RR intervals (RR1) and changes in RRi variability, precedes and possibly triggers ventricular tachyarrhythmias (VTAs) by altering repolarization. We examined the effects of autonomic activity on the projection of repolarization as detected by body surface potential maps (BSPMs). We recorded 32 lead/192-point BSPMs during passive head-up tilt, tilt + infusion of isoproterenol, rapid atrial pacing, and atrial pacing + infusion of isoproterenol. Changes in QT; recovery time; activation-recovery interval (ARi); T-wave amplitude; and QT, QRST, and ST integrals and their dispersion were analyzed. Autonomic effects on sinus node were inferred from the Fourier transform-derived low and high frequency powers of RRi variability. Patients were divided into those with (SHD) and without structural heart disease (NSHD). Heart rate increased, whereas QT interval and ARi declined with tilt in both groups. RRi variability indices of sympathetic activity increased in NSHD but did not change in SHD. T-wave amplitudes declined in NSHD but did not change in SHD, suggesting altered responsiveness of ventricular repolarization to autonomic stimulation. Tilt and rapid atrial pacing during infusion of isoproterenol resulted in a paradoxical increase in T-wave amplitudes in some patients, similar to that observed before the onset of spontaneous arrhythmias. We conclude that altering autonomic activity by head-up tilt and/or infusion of sympathomimetic agents results in significant changes in the body surface projection of cardiac repolarization, which differ in patients with SHD from those without SHD. Similar paradoxical changes in the T-wave amplitude have been observed before the onset of spontaneous VTA, suggesting that abnormal response of repolarization to autonomic stimulation predisposes to arrhythmogenesis.     

Validation of ECG indices of ventricular repolarization heterogeneity: a computer simulation study

INTRODUCTION: Repolarization heterogeneity (RH) is functionally linked to dispersion in refractoriness and to arrhythmogenicity. In the current study, we validate several proposed electrocardiogram (ECG) indices for RH: T-wave amplitude, -area, -complexity, and -symmetry ratio, QT dispersion, and the Tapex-end interval (the latter being an index of transmural dispersion of the repolarization (TDR)). METHODS AND RESULTS: We used ECGSIM, a mathematical simulation model of ECG genesis in a human thorax, and varied global RH by increasing the standard deviation (SD) of the repolarization instants from 20 (default) to 70 msec in steps of 10 msec. T-wave amplitude, -area, -symmetry, and Tapex-end depended linearly on SD. T-wave amplitude increased from 275 +/- 173 to 881 +/- 456 muV, T-wave area from 34 x 10(3)+/- 21 x 10(3) to 141 x 10(3)+/- 58 x 10(3)muV msec, T-wave symmetry decreased from 1.55 +/- 0.11 to 1.06 +/- 0.23, and Tapex-end increased from 84 +/- 17 to 171 +/- 52 msec. T-wave complexity increased initially but saturated at SD = 50 msec. QT dispersion increased modestly until SD = 40 msec and more rapidly for higher values of SD. TDR increased linearly with SD. Tapex-end increased linearly with TDR, but overestimated it. CONCLUSION: T-wave complexity did not discriminate between differences in larger RH values. QT dispersion had low sensitivity in the transitional zone between normal and abnormal RH. In conclusion, T-wave amplitude, -area, -symmetry, and, with some limitations, Tapex-end and T-wave complexity reliably reflect changes in RH.     

Origin on the electrocardiogram of U-waves and abnormal U-wave inversion.

AIMS: Soon after the initial development of electrocardiography, U-waves were discovered in many normal subjects following the T-wave repolarisation waveform on the electrocardiogram. Various explanations have been offered for their origin, but none is universally accepted. We used our model of left ventricular repolarisation to explore the most common hypotheses for the genesis of U-waves. METHODS: Recently, we have shown that a computer model of left ventricular repolarisation was able to explain the formation of the characteristic shape of the T-wave, and we have now used this model to explore the most common hypotheses for the genesis of U-waves. The repolarisation phase of the action potentials in the model exhibited an after-potential. We investigated separately the effect on the 12-lead electrocardiogram of three different features of the model: the amplitude of the after-potential; dispersion of repolarisation in the left ventricle ranging from 20 to 100 ms; the timing of the after-potential, relative to the end of the principal action potential component, ranging from -100 to 100 ms. RESULTS: We show that delaying repolarisation in different regions of the heart cannot explain the U-wave, but show that the presence of after-potentials on the cardiac action potential do explain the U-wave polarity and other characteristic U-wave features. We also show that abnormal after-potential timing corresponds with abnormal U-wave inversion. CONCLUSION: Our model provides a realistic and simple solution to the problem of U-wave genesis.     

Effects of bepridil on the resting electrocardiogram

We evaluated the effects of bepridil hydrochloride, a long-acting calcium antagonist, on the electrocardiogram of 13 men with exertional angina. The drug decreased sinus rate (P = 0.01), increased the QT (P less than 0.001) and QTc interval (P less than 0.001), and produced T-wave changes in each patient.     

Low QRS voltage and its causes

Electrocardiographic low QRS voltage (LQRSV) has many causes, which can be differentiated into those due to the heart's generated potentials (cardiac) and those due to influences of the passive body volume conductor (extracardiac). Peripheral edema of any conceivable etiology induces reversible LQRSV, reduces the amplitude of the P waves and T waves, decreases the duration of P waves, QRS complexes, and QT intervals, and alters in turn the measurements of the signal-averaged electrocardiogram and T wave alternans, all with enormous clinical implications.     

Autonomic nervous system influences on QT interval in normal subjects

OBJECTIVES: We sought to determine whether the relationship between heart rate (HR) and QT interval (QT) differs as HR increases in response to exercise, atropine and isoproterenol. BACKGROUND: Autonomic nervous system influences on repolarization are poorly understood and may complicate the interpretation of QT measurements. METHODS: Twenty-five normal subjects sequentially underwent graded-intensity bicycle exercise, atropine injection and isoproterenol infusion. Serial 12-lead electrocardiograms were recorded at steady state during each condition and analyzed using interactive computer software. The HR-QT data were modeled linearly and the slopes (quantifying QT adaptation to HR) as well as the QT intervals at 100 beats/min for each intervention were compared by repeated-measures analysis of variance. RESULTS: As HR increased, QT was longer for isoproterenol in comparison to exercise or atropine, which were similar. The HR-QT slope (ms/beats/min) was less steep for isoproterenol (-0.83 +/- 0.53) than for atropine (-1.45 +/- 0.21) or exercise (-1.37 +/- 0.23) (p < 0.0001). In comparison to men, women had more negative HR-QT slopes during all interventions. At 100 beats/min, the QT was 364 ms during isoproterenol, which was significantly longer than that during exercise (330 ms) or atropine (339 ms) (p < 0.0001). Isoproterenol produced a dose-dependent increase in U-wave amplitude that was not observed during exercise or atropine. CONCLUSIONS: In comparison to exercise and atropine, isoproterenol is associated with much less QT shortening for a given increase in HR and, therefore, greater absolute QT intervals. Our findings demonstrate that autonomic conditions directly affect the ventricular myocardium of healthy subjects, causing differences in QT that are independent of HR.     

脑卒中患者出现明显U波的临床分析

目的 探讨脑卒中患者心电图检查出现明显U波(任何导联的U波振幅超过同一导联T波振幅的1/2)的意义。方法 回顾性分析546例明确诊断为脑卒中的患者,并对其分别进行心电图及生化实验检查。结果 脑卒中后心电图出现明显U波者22例,占脑卒中患者总数4.03%;出现明显U波并伴低血钾者2例,占脑卒中患者总数0.366%(χ2值为17,P<0.001)。结论 心电图出现的明显U波未必由低钾血症引起,临床应综合分析。