bluuebunny/crossref_metadata_2025 huggingface dataset:
Late Potentials in Healthy Subjects
Authors: Toft Jens , Rasmussen Verner , Hesse Birger , Au Samir , Carstensen Steen , Jensen Gorm
Published: October 2006

Objective: Criteria for detection of late potentials have not yet been standardized, but the criteria recommended by ESC/AHA/ACC are widely used. In this investigation, the prevalence of late potentials is studied in an age stratified healthy population with likelihood of coronary artery disease < 5%. Relation between signal‐averaged variables and clinical variables was studied.

Methods: Signal‐averaged ECGs were recorded using Butterworth filters at 40 and 250 Hz. The following three time‐domain parameters were evaluated: QRS duration (duration of the amplified, filtered QRS complex); LPD (duration of the late potentials, i.e., duration from the point of time when the magnitude of the main complex becomes lower than 40 μV); and RMS40 (root mean square of the activity within the last 40 ms of the amplified, filtered QRS complex).

Results: QRS duration was significantly longer in men than in women, and was correlated to the mass of the left ventricle (LVM). The combination LPD and RMS40 gave the highest prevalence of late potentials. The prevalence of late potentials was 25%.

Conclusion: Standard criteria should be used with great caution, and normal limits should be established in each laboratory to a preselected noise level. QRSD should be included within the definition of reference limits and should be gender matched. Even though there is correlation between LVM and the QRSD, the upper normal limit of QRSD based on LVM matching is unchanged.
Nonsustained Ventricular Tachycardia
Authors: Daubert James P. , Kim Chee H.
Published: October 2006

Nonsustained ventricular tachycardia (VT) has been an intimidating diagnosis for many physicians because its presence, in general, portends an increased risk of sudden death. The management and approach has been quite diverse and inconsistent in part due to the absence of a large body of literature. There have been major developments, however, over the last two decades in better understanding the mechanism of VPCs and ventricular tachycardia as well as adopting a more systematic approach to diagnosis and management. With the publication of the results of CAST I and II, there has been a movement away from empiric treatment of asymptomatic VPCs and nonsustained VT, and an emphasis on risk stratification on the basis of the underlying heart disease. Coronary artery disease, by far, is the most common etiology for heart disease in the United States, but there are numerous other conditions such as hypertrophic and dilated cardiomyopathies, as well as right ventricular dysplasia and “normal heart” ventricular tachycardias that require a tailored approach. Noninvasive and invasive methods of risk stratification, such as measurement of heart rate variability and signal‐averaged ECG's, as well as electrophysiologic testing, respectively, have enabled us to identify “high risk” patients that may benefit from therapy whether it be antiarrhythmics or implantable defibrillators. Recent and on‐going prospective trials such as the CAMIAT, EMIAT, GESICA, MADIT, MUSTT, and CABG‐PATCH will hopefully further our knowledge base and make the management of VPCs and nonsustained VT a more uniform process.
Cross Spectral Analysis in Assessment of Baroreflex Gain in Patients with Coronary Artery Disease
Authors: Airaksinen K.E. Juhani , Tahvanainen Kari U.O. , Kuusela Tom A. , Huikuri Heikki V. , Niemelä Matti J. , Karjalainen Pasi , Eckberg Dwain L.
Published: October 2006

Background: Interest in determination of baroreflex sensitivity in clinical practice is growing because of its prognostic information in patients with heart disease. The purpose of the present study was to assess the feasibility of cross spectral analysis in the determination of baroreflex gain from spontaneous RR interval and systolic pressure fluctuations, and to compare the results to the traditional pharmacological method in patients with coronary artery disease.

Methods: We measured the gain and time lag between RR interval and systolic pressure variabilities in the frequency domain, and compared baroreflex indexes obtained by this technique with standard phenylephrine tests in 32 patients with coronary artery disease.

Results: Cross spectral analysis by fast Fourier transform techniques yielded acceptable (> 0.5) coherence between systolic pressure and RR interval in the mid‐ (0.07–0.15 Hz) and in the respiratory‐frequency (0.15–0.40 Hz) band fluctuations in 30 patients (94%), with mean coherences of 0.69 and 0.74. The mean phase difference in the mid‐frequency band was greater than in the respiratory‐frequency band (−83 vs −23 degrees, P < 0.001), suggesting that the mid‐frequency fluctuations of RR intervals followed nearly 2 seconds after pressure changes, while respiratory‐frequency fluctuations of RR intervals occurred nearly concomitantly with systolic pressure. The mean baroreflex slope derived from the bolus phenylephrine technique was 6.2 ms/mmHg (range 1.6–16.0), 5 patients had an abnormally low (< 3 ms/mmHg) baroreflex sensitivity. Baroreflex gain determined by cross spectral analysis from the mid‐frequency band correlated significantly (r = 0.60, P < 0.001, n = 27) with the baroreflex gain determined by the phenylephrine test, while the correlation in the respiratory‐frequency band was not significant (r = 0.35, P = 0.09, n = 26).

Conclusions: Baroreflex slopes derived from cross spectral techniques provide reliable (but not perfect) information regarding baroreflex gain derived from the classic phenylephrine technique, even in patients with depressed baroreflex responses. Cross correlation calculation of spontaneous baroreflex slopes should be limited to data in the mid‐frequency range, where the slopes are likely to reflect simple baroreflex physiology.
Effect of Low‐Dose Scopolamine on Autonomic Control of the Heart
Authors: Raeder Ernst A. , Stys Adam , Cohen Richard J.
Published: October 2006

Background: In low doses, scopolamine paradoxically enhances parasympathetic outflow to the heart. The mechanisms which mediate this action are not fully understood. Moreover, there are conflicting data regarding the potential role of sympathetic activity. This study in 17 healthy individuals was designed to characterize the influence of low dose transdermal scopolamine on the gain of the baroreflex and respiratory heart rate reflex and to determine the role of sympathetic activity.

Methods: The effect of scopolamine was analyzed in the time and frequency domain by computing heart rate variability indices. The gains of the respiratory heart rate reflex and the baroreflex were estimated simultaneously by means of a cardiovascular system identification approach using an optimized autoregressive moving average algorithm. Measurements were repeated in the upright posture to assess the influence of enhanced sympathetic activity. In six subjects ambulatory ECGs were recorded to determine whether there are diurnal variations of the effect of scopolamine.

Results: Scopolamine enhances vagal modulation of heart rate through both the respiratory‐heart rate reflex and the baroreflex, as the gains of both were augmented by the drug in the supine and in the upright postures.

Conclusions: Scopolamine increases parasympathetic cardiac control by augmenting the gain of the respiratory‐heart rate and baroreflex. This action is not attenuated in the upright posture when sympathetic tone is increased.
Association Between Parasympathetic Activity and Late Potentials at Low Noise Level
Authors: Christiansen Evald Høj , Frost Lars , Mølgaard Henning , Nielsen Torsten Toftegaard , Pedersen Anders Kirstein
Published: October 2006

Background: Late potentials (LP) in the signal‐averaged ECG represent activation of myocardial areas with slow conduction and predicts re‐entrant malignant ventricular arrhythmias in coronary artery disease. Low heart rate variability, which reflects low vagal and concomitantly elevated sympathetic activation also predicts ventricular arrhythmia. This autonomic profile is associated with the presence of LP (detected at noise level 0.4 μ;V) early after myocardial infarction. In contrast, sympathetic stimulation and diminution of vagal tone influence LP parameters (detected at noise level 0.2 μ;V) in the opposite direction in healthy subjects. The aim of this study was to estimate the possible association between measures of cardiac autonomic function and LP (detected at 0.4 and 0.2 μ;V) in patients with chronic coronary artery disease.

Methods: ECGs of 174 consecutive patients with angiographically documented coronary artery disease and without myocardial infarction during the last 3 months were signal‐averaged to noise level 0.2 and 0.4 μ;V. LP were considered to be present if any two of the following criteria were present: signal‐averaged QRS duration > 120 ms, root‐mean‐square voltage of the terminal 40 ms of the averaged QRS complex < 25 μ;V, and late potential duration > 40 ms. Heart rate variability was measured at rest in 5‐minute ECG recordings as: the standard deviation (SD) of all RR intervals, SD corrected for RR (SD/mean RR), and the power of high frequency (HF) component (0.15–0.40 Hz).

Results: One hundred seven (61%) of the patients had LP at noise level 0.2 μ;V. LPs were more frequently observed in patients with slow heart rate, high heart rate variability, and high levels of vagal activity (mean RR >; 1000 ms, SD >; 60 ms, and HF >; 100 ms2) than in patients with higher heart rate, low heart rate variability and attenuated vagal activity: 73% vs 54% (P = 0.02), 71% vs 53% (P = 0.02), 72% vs 51% (P = 0.005) for mean RR, SD, and HF power, respectively. Adjustment for possible confounding from mean RR level, gender, previous acute myocardial infarction, treatment with betablocker, and left ventricular ejection fraction did not significantly alter these associations. At noise level 0.4 μ;V 26% (45/174) had LP and the diagnosis of LP was not significantly associated with heart rate variability.

Conclusions: At low noise level (0.2 μ;V) higher parasympathetic activity is associated with the diagnosis of LP. The predictive power of presence of LP diagnosed at low noise level for development of sudden cardiac death may be reduced by this association. In order to increase the predictive accuracy of LP we recommend either the use of noise level 0.4 μ;V, or identification of high arrhythmia‐risk patients by a combination of the presence LP and impaired heart rate variability. However, a prognostic study is needed to further clarify this.
Provocative Testing in Children with Suspect Congenital Long QT Syndrome
Authors: Berul Charles I. , Sweeten Tammy L. , Hill Sharon L. , Vetter Victoria L.
Published: October 2006

Objectives

This study was designed to evaluate several alternative ECG measurements and provocative tests in order to identify markers for children with suspect congenital long QT syndrome (LQTS).

Background

A single QTc measurement on a resting ECG does not identify all children with LQTS. Alternative ECG measurements have been established for identification of LQTS patients, with varied degrees of accuracy. Additionally, findings of QT prolongation during exercise or catecholaminergic stimulation have been suggested as indicators for the presence of LQTS and associated arrhythmias.

Methods

The ECGs from 40 children with suspect congenital LQTS were compared with 1000 gender and age matched control patients. Complete exercise ECG studies were performed on 32 of the 40 suspect LQTS patients and compared with 29 controls. ECGs recorded during isoproterenol infusion were obtained in 9 suspect LQTS patients and compared with 44 matched control subjects.

Results

During exercise, the QTc was mildly prolonged in both groups, without a similar increase in JTc, suggesting prolongation of depolarization time. QT and JT dispersion shortened with exercise in control subjects, but not in the suspect LQTS patients. During isoproterenol infusion, the QTc and JTc are prolonged in the suspect LQTS group, without an increase in the control patients.

Conclusions

We describe the ECG findings with provocative testing in patients in whom there is a clinical suspicion of LQTS, yet have a normal or borderline QTc. Exercise or isoproterenol may aid in identification of patients with congenital long QT syndrome.
Relation Between Autonomic Nerve Activity and QT Interval in Patients with Congenital Long QT Syndrome: Analysis Using 24‐Hour Holter ECG Monitoring
Authors: Shimono Mayumi , Fujiki Akira , Inoue Hiroshi
Published: October 2006

Background

The aim of this study was to determine the relation between the autonomic nerve activity and the QT interval in patients with the long QT syndrome (LQTS) using spectral analysis of the heart rate variability from 24‐hour Holter ECG recordings.

Methods

Seven patients with LQTS (QTc interval > 0.46 s) who had had no recent episode of syncope and nine control subjects without QT prolongation were analyzed. Autoregressive spectral analysis was performed to determine spectral power of low (LF: 0.04–0.15 Hz) and high (HF: 0.15–0.40 Hz) frequency components. The QT interval and RR interval were measured from ECGs that were selected from 24‐hour Holter tape at 1‐hour intervals.

Results

In patients with LQTS and control subjects, there was a positive correlation between the QT interval and RR interval (LQTS: r2= 0.76 ± 0.18, Control: r2= 0.90 ± 0.10, mean ± SD). The slope of the linear regression lines (QT/RR) did not differ between LQTS and control subjects (LQTS: 0.18 ± 0.05, Control: 0.18 ± 0.04), but the intercept of the regression lines in LQTS was significantly larger than in control (LQTS: 0.28 ± 0.05, Control: 0.21 ± 0.02). In LQTS, positive correlation between the QT interval and InHF (r2= 0.53 ± 0.09) and inverse correlation between the QT interval and In(L/H) were identified (r2= 0.50 ± 0.14) as in control subjects. There was no significant difference in the slopes of the regression lines of the QT interval with heart rate variability indices (InHF, In[L/H]) between LQTS and control subjects. The correlation coefficient of the QT interval with RR interval was higher than that with heart rate variability indices both in LQTS (P < 0.01) and control subjects (P < 0.05). In three patients with recent syncopal episodes, the prolongation of QT interval was exaggerated at short RR intervals, and the significant correlations of the QT interval with RR interval and heart rate variability indices observed from the recordings without episodes of syncope could not be identified. Both 24‐hour averaged value of InHF and L/H did not show any significant difference between LQTS and control.

Conclusions

These results indicate that in LQTS without having recent episodes of syncope, the QT interval was regulated mainly through the change in RR intervals as in control subjects. Exacerbation of QT prolongation during syncopal episodes may be due to different modulation of the QT interval by autonomic nerve system and heart rate.
T‐Wave Alternans and Torsades de Pointes Associated with Astemizole
Authors: Strasberg Boris , Kusniec Jairo , Mazur Alexander
Published: October 2006

A case of astemizole‐induced QT prolongation, T‐wave alternans, and torsades de pointes is presented. Failed treatment with intravenous magnesium and lidocaine was followed by overdrive pacing, which successfully prevented further recurrences. The possible pathophysiology of acquired QT syndrome and T‐wave alternans after antihistamine use is discussed.
Variability of the Interlead Synchronization of the T Wave: Beat‐to‐Beat ECG Analyses
Authors: Lund Birgit , Lund Kaspar , Christiansen Evald Høj , Pedersen Anders Kirstein
Published: October 2006

Background

The mean intraobserver (two measurements) and interobserver (two observers) errors of dispersion of QT‐end (QTe‐d), corrected for heart rate, are 12 ms and 15 ms, respectively. One possible contribution to the low reproducibility is beat‐to‐beat variations, so we developed a surrogate of these variations, called the variability of the interlead synchronization of T waves (VST).

Methods

VST can be calculated for any pair of digitized leads, by cross‐correlation of the T wave and a substep alignment procedure that increases the precision from 0.5–0.2 ms. The precision of VST is relatively good (≠ 0.4 ms), because it bypasses the uncertain measurement of QT intervals.

Conclusion

The method was applied to Frank orthogonal leads of a small population of subjects (n = 9) with no cardiac history. The mean magnitudes and standard deviations (SD) of the magnitude of VST were in the range (mean ± SD) of 0.37 ± 0.28 to 2.93 ± 2.11 ms. This confirms the existence of a subject‐specific lower physical limit for the precision of QTe‐d in normal subjects. The results indicate that QTe‐d should be measured as a mean value of several beats if measured on the raw signal. This should, however, be verified by measurement of VST on larger populations. The results also indicate that optimal alignment of T waves requires the waves to be aligned individually, lead by lead. Notice, however, that if the mean beat is used for measurement of QTe‐d, then the alignment must be the same for all leads in each beat.
Effects of Beta‐Blockers on the Relation Between QT Interval and Heart Rate in Survivors of Acute Myocardial Infarction
Authors: Hintze Ulrik , Wüpper Finn , Mickley Hans , Mφller Mogens
Published: October 2006

Background

β‐blockade has been found to reduce the heart rate dependency of the QT interval in healthy individuals, but the effect of β‐blockade on the QT/RR relationship in patients suffering from myocardial infarction (Ml) is unknown.

Methods

Patients with a first Ml were enrolled in a double‐blind, placebo‐controlled study. A 24‐hour ambulatory ECG was performed at discharge before study medication was initiated, and repeated after 4 weeks of therapy. QT and RR intervals were assessed beat to beat for all sinus beats by a computer program. For each patient, the mean QT interval duration for every RR value was determined on an hourly basis and the QT/RR relation was described as the best fit linear regression line.

Results

Before randomization, no differences between the groups could be demonstrated. After 4 weeks of drug study (37 patients receiving metoprolol 100 mg per day and 34 patients receiving placebo), the day, night, and 24‐hour regression lines differed significantly between the groups. Metoprolol reduced the QT/RR slope, increased the intercept, and blunted the day‐night difference of the QT/RR slope.

Conclusion

Long‐term β‐blockade in Ml patients results in a reduction of the QT/RR slope with a prolongation of the QT interval at higher heart rates. These effects, which are similar to observations found in healthy individuals, may be related to the decreased susceptibility to life‐threatening arrhythmias in patients treated with beta‐blockers, possibly suggesting the QT/RR relationship as a marker of ventricular autonomic tone.
Dispersion of the QTend, QTpeak and Tpeak‐Tend Interval: Comparison of Reproducibility in Normal Subjects and Patients with Hypertrophic Cardiomyopathy
Authors: Savelieva Irina , Yi Gang , Malik Marek
Published: October 2006

Background

Prolonged QT interval and QT dispersion have been reported to be associated with arrhythmogenesis in patients with cardiac disorders. However, the use of QT dispersion for risk stratification is limited by its low reproducibility. Recently, measurement of the interval between the peak and the end of the T wave (Tp‐Te interval) has been suggested for detection of repolarization abnormalities, but its clinical utility has not been studied in a systematic fashion.

Methods

This study assessed the intrasubject reproducibility of automatic measurements of QTend, QTpeak, and Tp‐Te interval dispersion in 71 normal subjects and 37 patients with hypertrophic Cardiomyopathy (HC). A set of 20 ECGs (10 in supine and 10 in standing position) was evaluated in each subject. Measurements were performed automatically using an advanced commercial computer system.

Results

HC patients showed significantly higher values of QTtend, QTpeak, Tp‐Te intervals, and QTend, QTpeak dispersion compared to normal subjects (42 ± 20 vs 20 ± 12 ms and 45 ± 24 vs 33 ± 12 ms, respectively; P < 0.04), but no significant difference was observed in Tp‐Te dispersion between both groups (32 ± 16 vs 29 ± 8 ms; NS). The reproducibility of QTend, QTpeak, and Tp‐Te dispersion, expressed as coefficients of variation, was poor in both groups (14%‐28% in normal subjects and 18% to 37% in HC patients).

Conclusion

Despite higher values of QTend, QTpeakTp‐Te intervals and QTend, QTpeak dispersion in HC patients than in normal subjects, Tp‐Te dispersion was similar in both groups. The reproducibility of QTend, QTpeak, and Tp‐Te dispersion was low. Automatic measurement of Tp‐Tp dispersion failed to differentiate normal subjects and HC patients.
Reproducibility, Circadian Variability, and Limit Values of Ventricular Late Potentials in Healthy Men
Authors: Schmid Johann‐Jakob , Zuber Michel , Evéquoz Dominique , Erne Paul
Published: October 2006

Objectives: The aim of the study was to examine the reproducibility of late potential parameters over time and to assess the influence of circadian rhythm, type of activity (rest, exercise) and autonomous state on these parameters in healthy subjects.

Background: Late potentials are used as a marker for an elevated arrhythmic risk in patients after myocardial infarction. The method is increasingly used in cardiovascular hospital departments. However, the relatively high percentage of false‐positive results compared to the outcome of electrophysiological testing precludes its more general use.

Methods: In a population of healthy volunteers, the normal values, the reproducibility, and the dependence from a circadian rhythm of ventricular late potentials were examined. The dependence of the late potentials from the type of activity was studied.

Results: The limit values of the late potential parameters found in this study did not differ from the proposed standard limits in the Euro‐American guidelines. Circadian variability of heart rate and duration of QRS and QT‐interval were documented. No circadian variation was found in the late potential parameters in the subjects studied. The values for late potential parameters did not significantly differ in measurements repeated after 24 hours and 7 days, thus resulting in good reproducibility. The heart rate changes induced by ergometry and autonomous blockade had no influence on late potential parameters.

Conclusions: Late potential parameters are reproducible and are not changed significantly by circadian rhythm, type of activity, or autonomous state in these healthy volunteers.
Standard 12‐Lead and 24‐Hour Ambulatory Electrocardiographic Abnormalities in Survivors of Tachyarrhythmic Cardiac Arrest
Authors: Perkiömäki Juha S. , Koistinen M. Juhani , Huikuri Heikki V.
Published: October 2006

Background

The aim of the present work was to compare the accuracies of variables obtained from a standard 12‐lead ECG and a 24‐hour ambulatory ECG in discriminating between patients with and patients without tachyarrhythmic cardiac arrest after a previous myocardial infarction.

Methods

QTc interval and QTc dispersion measured from a 12‐lead ECG and an analysis of ventricular premature depolarization, nonsustained ventricular tachycardia, and heart rate variability from a 24‐hour ECG were compared in survivors of tachyarrhythmic cardiac arrest (n = 57) and in postmyocardial infarction control patients without a history of arrhythmic events and an arrhythmic‐free survival in a 2‐year follow‐up (n = 57). The groups were matched for age, gender, left ventricular ejection fraction, and the usage of beta‐blocking medication.

Results

QTc dispersion (103 ± 44 vs 71 ± 32 ms, P < 0.001) and the QTc interval maximum, defined as the longest QTc interval in any of the 12 leads of ECG (508 ± 52 vs 459 ± 42 ms, P < 0.001), were longer in the cardiac arrest survivors than in the controls. The standard deviation of R‐R intervals, a measure of heart rate variability, was lower in the cardiac arrest survivors (86 ± 38 vs 108 ± 32 ms, P < 0.001), who had also experienced more commonly ≥; 10 ventricular premature depolarizations/hour (61% vs 35%, P < 0.01) on the 24‐hour ECG. In a stepwise multiple regression analysis, the QTc interval maximum and the standard deviation of R‐R intervals were the most significant independent variables that differed between the groups (P = 0.0002, P = 0.0023, respectively). Their combination yielded a high positive predictive accuracy (91%).

Conclusions

Simple measurement of the maximum QTc interval from a standard 12‐lead ECG performs equally well or even better than the other more time‐consuming 12‐lead or 24‐hour ambulatory ECG variables in discriminating between patients with a history of tachyarrhythmic cardiac arrest and patients without a history of ventricular tachyarrhythmias after a remote myocardial infarction.
The Presence of a Q Wave in Lead V5 Excludes Manifest Preexcitation
Authors: Pavri Behzad B. , Coyne Robert F. , Kocovic Dusan Z.
Published: October 2006

Background

The degree of preexcitation in patients with the Wolff‐Parkinson‐White syndrome may vary depending on autonomic tone, heart rate, pathway location, and atrioventricular node conduction. When subtle, preexcitation may be difficult to detect with a 12‐lead electrocardiogram (ECG). Furthermore, the pattern of preexcitation may be mimicked in patients with QRS widening and rapid atrioventricular node conduction.

Methods

We studied 50 patients with manifest accessory pathways who underwent electrophys‐iological study and pathway ablation. Pre‐ and postablation ECGs for the presence or absence of a Q wave in leads V5 and V6 were studied. ECGs from an additional 19 patients were used to validate the observations.

Results

We found that no patient with preexcitation had a Q wave in lead V5 and only 1 of 50 patients had a Q wave in V6. This was a reproducible finding in the 26 patients with multiple ECGs obtained on separate days. The results were validated in an additional 19 patients none of whom had a Q wave in V5, and 1 had a Q wave in V6.

Conclusions

The presence of a Q wave in lead V5 reliably excludes manifest preexcitation.
Silent Myocardial Ischemia and Late Ventricular Repolarization in the Genesis of Ventricular Fibrillation in Humans
Authors: Santinelli Vincenzo , Modano Pasqualina , Ferraiuolo Maria , De Santo Daniela , Oppo Igino , Fornaro Pasquale , Chiariello Massimo
Published: October 2006

Background

We report a well‐documented case of a patient, a 62‐year‐old man, with severe and asymptomatic left main coronary artery disease who had several episodes of silent myocardial ischemia and a syncopal attack during Holter recording.

Methods and Results

Ambulatory monitoring showed isolated giant U waves separated from the T wave 60 minutes before syncope that was due to reversible ventricular fibrillation lasting about 4 minutes and spontaneously reverting to asystole (7 seconds) and then to atrial fibrillation

Conclusion

Our experience suggests that myocardial ischemia may differently affect the repolarization times within the myocardium leading to widely disparate repolarization gradients that may represent the arrhythmogenic substrate for the occurrence of life‐threatening ventricular tachyarrhythmias. A.N.E. 1999; 4(2):250–254
Accuracy of QTc and QTI for Detection of Autonomic Dysfunction
Authors: Whitsel Eric A. , Boyko Edward J. , Siscovick David S.
Published: October 2006

Background:Correlates of QT interval duration have been described although their effects on its ability to identify autonomic neuropathy have not.

Methods:We examined the ability of QTc and QTI to detect pharmacologically simulated autonomic dysfunction (PSAD) in persons without bundle branch block, U waves, or long QT syndrome by reviewing 249 articles published through 1996 describing the influence of adrenergic beta antagonists or atropine on QT duration. Six of the articles described effects of intravenous drug administration on the ECG among 94 individuals in sinus rhythm. Autonomic dysfunction was pharmacologically simulated in a subset of 30 men and women via coadministration of both drugs. We used logistic regression to estimate accuracy of QTc and QTI for PSAD, reported as area under summary receiver operating characteristic curves (AUC [95% Cl]) and sensitivity (95% Cl) of test thresholds with specificity of 0.80.

Results:Sensitivity of QTC > 436 ms1/2 was 0.20 (0.09–0.38) and AUCQTC, 0.54 (0.41–0.66). A QTI < 95% was similarly insensitive, 0.30 (0.16–0.48), and AUCQTI equally low. However, stratum‐specific AUCQTI' was higher than overall AUCQTI, 0.69 (0.64–0.74) when age mean (37.7 years), 0.77 (0.73–0.81) in males, and 0.87 (0.77–0.97) in participants without history of arrhythmia. Sensitivity of QTI thresholds in these strata, range 0.41 to 0.62, was 2.2 to 7.8 times greater than sensitivity, range 0.08 to 0.19, of equally specific QTc thresholds. In a model combining age (y), gender, and arrhythmia, AUCQTI was 0.88 (0.86–0.90).

Conclusions: In isolation, QTc and QTI inaccurately detect PSAD. When confounding is taken into consideration, low QTI identifies PSAD with greater sensitivity and accuracy than high QTc. A.N.E. 1999;4(3):257–266
Coronary Artery Disease May Alter the Spatial Dispersion of the QT Interval at Rest
Authors: Hailer Birgit , Van Leeuwen Peter , Lange Silke , Pilath Martin , Wehr Michael
Published: October 2006

Background:Increases of QT dispersion (QTd) have been observed in patients with coronary artery‐disease (CAD) under stress. In contrast to ECG, multichannel magnetocardiography (MCG) allows the assessment of the spatial distribution of QTd, which may be altered earlier than standard QTd. The aim of this study was the investigation of repolarization patterns in patients with CAD at rest.

Methods:12‐lead ECG and 36‐channel MCG were performed in 20 healthy subjects (N) (6 m; aged 54 ± 7) and 23 patients with CAD (14 m; aged 59 ± 9). QT intervals were determined for each ECG lead and MCG registration site. QTd was calculated as QTmax‐QTmin for both methods. In MCG, QTd was also examined spatially by calculating the difference between QTmin and QT at each registration site and plotting this value relative to its position. Spatial variability was quantified using two indexes: SI, which quantifies the mean dispersion at each registration site and Sin, which normalizes SI by taking the overall spatial dispersion pattern into account.

Results:In contrast to ECG, the MCG QTd values were higher in patients with CAD (P < 0.05). These patients also displayed more QT variability between neighboring sites and an alteration in global pattern. Accordingly, the SI and Sin values differed most clearly between groups (P < 0.001).

Conclusions:CAD may lead to increased heterogeneity of repolarization at rest. Spatial changes are better able to identify patients with CAD than standard QTd based on ECG. Their visualization and quantification is possible on the basis of multichannel magnetocardiography. A.N.E. 1999;4(3):267–273
Reproducibility of Minimum, Maximum and Median QT Intervals in the 12‐Lead Resting ECG
Authors: Lund Kaspar , Arildsen Hanne , Perkiömäki Juha S. , Huikuri Heikki V. , May Ole , Pedersen Anders Kirstein
Published: October 2006

Background: Heterogeneity in the recovery of ventricular refractory periods is an important factor in the development of ventricular arrhythmia. The QT dispersion (QTD) is increasingly used to measure this heterogeneity but its clinical value is limited due to methodological problems. QTD is defined as the maximum minus the minimum QT intervals that are suspected to be the least reproducible of the QT measurements.

Objective: To analyze the reproducibility of the minimum, maximum and median QT intervals.

Material: One database consisted of 356 subjects: 169 with diabetes and 187 nondiabetic control persons. The other database consisted of 110 subjects with remote myocardial infarction: 55 with no history of arrhythmia, and 55 with a recent history of ventricular tachycardia or fibrillation.

Methods: 12‐lead surface ECGs were recorded with an amplification of 10 millimeters per millivolt at a paper speed of 50 mm/s. QT was measured manually by the tangent‐method. The reproducibility was calculated from measurements of QT in successive beats.

Results: The standard deviation (SD) of QTs reproducibility was 9 ms for the arrhythmia data and 8 ms for the diabetes data. The reproducibility of QTmax and QTmin were on average 30% and 15% worse than for QTmedian. The SD of QTmax was significantly higher than for QTmedian in both database (P < 0.001), whereas SD of QTmin was only significantly higher than for QTmedian for the diabetes data (P < 0.001).

Conclusions: The reproducibility of QTmin and in particular QTmax was significantly lower than for QTmedian. This indicates that the QT dispersion is based on the least reproducible of the QT measurements. A.N.E. 2000;5(4):354–357
Computer Detection of Atrial Flutter
Authors: Morrison Steven , Macfarlane Peter W.
Published: October 2006

Background: As part of ongoing research into methods for rhythm analysis in the Glasgow Program, a new algorithm has been developed for the detection of atrial flutter.

Methods: The new algorithm uses two approaches to detect atrial waves. The first approach uses existing methods for “P” wave detection, searching various leads for patterns of positive and negative gradients satisfying amplitude and duration criteria. A threshold crossing technique is applied to the first difference of leads II and VI. Atrial regularity is measured using a scoring method that takes account of undetected waves. This measure of regularity is used, along with the estimated atrial rate, as criteria for atrial flutter. To develop the algorithm, 422 ECGs, including 49 cases of atrial flutter, were used as a training set. Optimization was achieved using a trial and error approach. A further 462 ECGs, including 75 atrial flutters, were used as a test set.

Results: Using the new algorithm, a sensitivity of 72.0% was achieved, with a specificity of 98.4%. This compares favorably to existing flutter detection logic in the Glasgow Program, which had a sensitivity of 26.7% and specificity of 99.7% on the same difficult test set. The combination of the old and the new algorithms gave a sensitivity of 78.7% with a specificity of 98.1%.

Conclusions: The new algorithm is successful in detecting a wide variety of cases of atrial flutter. However, further refinement is required to deal with certain types of atrial flutter, particularly at high ventricular rates. A.N.E. 2000;5(4):358–364
Dispersion of Repolarization: Time to Move Beyond QT Dispersion
Authors: Zareba Wojciech
Published: October 2006

Background: Over the last few years, the concept of dispersion of repolarization, evaluated as interlead variability of QT interval duration in surface ECG, emerged as a possible tool to identify patients at high‐risk for cardiac arrhythmias. Despite substantial progress in understanding of the electrophysiological basis for dispersion of repolarization, the question remains whether interlead differences in ECG‐ recorded T‐wave duration and morphology (QT dispersion) indicate heterogeneity in ventricular recovery time and pattern.

Methods and Results: Several studies investigated the prognostic significance of QT dispersion for predicting all‐cause mortality, sudden cardiac, and arrhythmic deaths. Some of those studies indicated significant and independent predictive value of QT dispersion whereas others negated such an association. Despite these controversial results, there is concern that substantial overlap in QT dispersion values between patients with and without cardiac events limits or even precludes clinical usefulness of QT dispersion for predicting future cardiac events. The methodological and conceptual limitations of QT dispersion measurements further discourage the bedside use of this noninvasive ECG parameter. Ionic channel phenomena determine the voltage and time components of the T‐wave, the T‐loop, and the QT interval duration. Since the ST‐T area is more representative of recovery times than QT interval duration, future efforts should be focused on developing and testing new automatically quantified parameters describing abnormalities of the T‐wave configuration and/or T‐loop morphology. Electrophysiologic meaning and prognostic significance of these ECG parameters remain to be studied.

Conclusion: In light of conceptual and methodological limitations of QT dispersion analysis, bedside use of this method should be discouraged and the time has come to move beyond QT dispersion and focus on evaluating clinical usefulness of repolarization morphology in risk‐stratification. studies. A.N.E. 2000;5(4):373‐381
QT Dispersion as a Marker for Response to Quinidine in Patients with Ventricular Tachyarrhythmias
Authors: Kertland Heather , White C. Michael , Chow Moses S.S. , Kluger Jeffrey
Published: October 2006

Objective:This study was undertaken to measure the effect of quinidine on QT dispersion and to determine whether changes in QT dispersion are associated with the acute response to quinidine in patients with ventricular tachycardia.

Methods:In 36 patients with inducible ventricular tachycardia during programmed electrical stimulation (PES), QT and JT intervals were measured in all 12 leads of electrocardiograms recorded at baseline and after quinidine. QT/JT dispersion was calculated by subtracting the smallest from the largest interval; QTc and JTc dispersion were also calculated. Response to therapy was defined as the inability to induce a ventricular tachyarrhythmia during a repeat PES study.

Results:Quinidine significantly prolonged the QTc and JTc intervals in the patients who responded to quinidine (n = 12) and in the nonresponders (n = 24). At baseline, QTc dispersion was similar in responders and nonresponders. However, quinidine increased QTc dispersion in nonresponders (from 78 ± 28 to 113 ± 40 ms, P < 0.05) but not in responders (from 81 ± 26 to 83 ± 42 ms). A similar pattern was seen for QT dispersion, JT dispersion, and JTc dispersion.

Conclusion:QT dispersion increases in nonresponders, but not in responders to quinidine for ventricular tachycardia. This QT dispersion profile is distinct from the Class III antiarrhythmics and may explain results from large clinical trials and delineate a new safety and efficacy marker.
The Brugada Syndrome
Authors: Brugada Pedro , Brugada Josep , Brugada Ramon
Published: October 2006

The Brugada syndrome is a genetically determined disease caused by mutations of the cardiac sodium channel. The disease affects mainly males in their forties and causes sudden cardiac death because of polymorphic ventricular tachycardia. These patients have a structurally normal heart. The electrocardiogram of this syndrome shows, spontaneously or after Class 1 antiarrhythmic drugs, ST segment elevation in leads V1 to V3 and a pattern resembling a right bundle branch block. Phase 2 reentry between epi‐ and endocardiac layers is responsible for the arrhythmias. The only effective treatment at present is implantation of a cardioverter defibrillator. A.N.E. 2000;5(1):88–91
Rapid Ventricular Response Due to Treatment of Atrial Flutter or Fibrillation with Class IC Antiarrhythmic Drugs
Authors: Mackstaller Lorraine L. , Marcus Frank I.
Published: October 2006

The Class IC antiarrhythmic drugs, propafenone and flecainide, may slow the atrial rate during atrial flutter permitting 1:1 AV conduction. This effect is well known to occur soon after starting treatment for atrial fibrillation or atrial flutter with these Class IC drugs. We report two patients who had adverse effects after prolonged treatment with either propaienone or flecainide. In addition, we illustrate that this adverse effect can occur despite concomitant treatment with drugs that act on the AV node to prevent rapid AV conduction. A.N.E. 2000;5(1):101–104
P‐P Cycle Alternans During Atrial Tachycardia:
Authors: Satullo Gaetano , Donato Antonino , Cavallaro Lucio
Published: October 2006

Background: A‐63 year‐old man complaining of palpitations underwent a 24‐hour ambulatory ECG monitoring that revealed the presence of recurrent episodes of nonsustained supraventricular tachycardia. Analysis of the tracings suggests an atrial origin of the arrhythmia. Tachycardias, quite regular at the beginning, suddenly showed a P‐P cycle alternans, namely, P‐P intervals alternately short and long. The evidence of two separate cycle ranges can be explained by the presence of a longitudinal dissociation within a discrete zone of the atrial circuit.
Dispersion of the QT Interval in Subjects with Frequent Nonsustained Ventricular Arrhythmias and No Underlying Heart Disease: Arrhythmogenic Substrate or Mechanoelectrical Feedback of Arrhythmias?
Authors: Malfatto Gabriella , Ciambellotti Francesca , Chianca Roberto , Bragato Renato , Branzi Giovanna , Leonetti Gastone , Facchini Mario
Published: October 2006

Background: QT dispersion (QTd) on the ECG is thought to reflect the temporal and spatial inhomogeneity of repolarization in the underlying myocardium. In myocardial infarction, ischemia, and long QT syndromes, an increased QTd is associated with a propensity for malignant ventricular arrhythmias and sudden cardiac death. We investigated this feature of the repolarization process in subjects with frequent ventricular arrhythmias and structurally normal hearts.

Methods: Forty‐nine patients referred for frequent, nonsustained ventricular arrhythmias (45 ± 14 years, ×± SD, 61% female) had normal ventricular dimensions and function, no late potentials, and normal ECG. They were compared with 30 controls (42 ± 13 years, 50% female). QTd was measured as the difference between the longest and the shortest QT in the six precordial leads at a paper speed of 50 mm/s.

Results: In patients, QTc was similar to that of controls: 395 ± 21 versus 386 ± 20. However, QTd was greater: 49 ± 20 ms versus 32 ± 14 ms, P < 001. Moreover, 18 patients (36%) had QTd exceeding 60 ms—a value superior to the mean normal value of 2 SD—compared to only 1 control (3%) (P < 0.01). Finally, patients with more frequent ventricular arrhythmias had larger QTd.

Conclusions: In patients with frequent nonsustained ventricular arrhythmias and otherwise normal hearts, QT interval dispersion is increased. We speculate that, instead of representing a specific electrophysiological substrate of arrhythmias, QT dispersion in this specific population could result from arrhythmias themselves through a possible mechanoelectrical feedback.
Nonlinear Analysis of Heart Rate Variability: Fractal and Complexity Measures of Heart Rate Behavior
Authors: Perkiömäki Juha S. , Mäkikallio Timo H. , Huikuri Heikki V.
Published: October 2006

Many new methods of analyzing heart rate (HR) variability have been developed to describe the features in HR behavior that cannot be detected by traditional time‐ and frequency‐domain methods. Some of the new methods, such as analysis of fractal correlation properties and complexity of HR dynamics, have provided clinically useful information in various patient populations. Importantly, some fractal analysis methods are better risk predictors of mortality than traditional HR variability measures, and analysis of complexity of HR dynamics has been shown to predict the spontaneous onset of atrial fibrillation. New analysis methods based on nonlinear dynamics are a promising tool for better understanding of normal and abnormal HR behavior. More work will be needed to establish the clinical applicability of traditional and new analysis methods of HR variability.
Prognostic Significance of Heart Rate Variability During the First 24 Hours of Acute Myocardial Infarction: A 5‐Year Follow‐up Study
Authors: Sánchez Antonio González , García‐Alberola Arcadio , Lázaro Cristina Llamas , Jimenez Pagan Francisco Javier , Bermúdez Eduardo Pinar , Mingorance Guillermo Vignote , Hernandez Juan Martinez , Valdés Mariano
Published: October 2006

Background: The prognostic value of heart rate variability (HRV) measured within the first 24 hours of acute myocardial infarction was assessed in 94 consecutive patients.

Methods: The mean of standard deviation of normal R‐R intervals for all 5‐minute segments (SDNN index), the width of the R‐R interval histogram at 10% and 50% of the peak, and three frequency‐domain measures of HRV (low frequency [LF], high frequency [HF], and LF/HF ratio) were calculated from a continuous ECG recording taken within the first hours of admission and their prognostic value for long‐term events was studied.

Results: During the follow‐up period (56.7 ± 5.9 months) 6 sudden and 7 nonsudden cardiac deaths occurred. Time‐domain measurements of HRV were lower in patients with sudden death (SDNN index: 27.0 ± 20.2 vs 47.5 ± 20.7 ms in survivors, P < 0.001). LF and HF power, but not the LF/HF ratio, were also inversely associated with sudden death. No significant differences were found between survivors and patients with nonsudden cardiac death. After adjustment for other clinical covariates, LF and HF power remained significantly associated with sudden death.

Conclusion: We conclude that heart rate variability measured within the first 24 hours of myocardial infarction is a strong predictor of sudden death during subsequent follow‐up.
Modulation of Electrical Microvolt Level T‐Wave Alternans and Left Ventricular Late Potentials Evaluated by Heart Rate Variability Indices, QT Dispersion, and Plasma Catecholamine Levels
Authors: Kurita Akira , Matsui Takemi , Ishizuka Toshiaki , Takase Bonpei , Satomura Kimio
Published: October 2006

Objective: The purpose of this study was to investigate how the modulation of electrical microvolt level T‐wave alternans (Twa) relates to left ventricular late potentials as evaluated by heart rate variability (HRV), QT dispersion, and plasma catecholamine levels.

Background: The Twa and left ventricular late potentials are promising noninvasive powerful markers for risk prediction in patients with ischemic heart disease (IHD) and/or cardiomyopathy. However, their relation to autonomic activity is unclear.

Methods: In 56 patients with stable IHD‐measured Twa at rest and during controlled bicycle ergometer testing, we simultaneously recorded recent noninvasive electrocardiographic approaches, such as HRV, QT dispersion, and left ventricular late potentials. Plasma norepinephrine (NE) and epinephrine (E) were also measured.

Results: (1) There were no significant differences in clinical findings, NE, and E levels between positive (group A) and negative (group B) Twa. Left ventricular late potentials, LF (low frequency spectra), as well as HF (high frequency spectra) in group A were significantly lower than in group B, but LF/HF did not differ significantly between the two groups. There was a significant inverse correlation between Twa microvoltage and LF/HF that was higher during exercise (r = ‐0.51, P = 0.006) than at rest (r = ‐0.34, P < 0.01). (2) There were no significant differences in clinical findings between positive (group C) and negative (group D) left ventricular late potentials. Plasma NE in group C was significantly higher than in group D (1060 ± 429 pg/mL vs 395 ± 219, P < 0.05). Furthermore, LF/HF in group C was significantly lower than in group D (0.96 ± 0.27 vs 1.1 ± 0.11, P < 0.05). There were no significant correlations between left ventricular late potential parameters and QT or QTc dispersion.

Conclusions: The Twa microvoltage in patients with stable IHD exhibits similar physiologic conditions as in patients with lower HRV indices. The presence of left ventricular late potentials might be affected by sympathetic nerve modulation.