Ventricular tachyarrhythmias in a canine model of LQT3: arrhythmogenic effects of sympathetic activity and therapeutic effects of mexiletine.

The ventricular tachyarrhythmias associated with the LQT3 syndrome are typically bradycardia-dependent. However, some episodes can be associated with exercise or emotional stress, suggesting a different arrhythmogenic mechanism when sympathetic activity predominates. This study examined the potential arrhythmogenic mechanisms during periods of autonomically mediated transient heart rate acceleration in a canine anthopleurin-A model of LQT3 syndrome. Using plunge needle electrodes, transmural unipolar electrograms of the left ventricle were recorded from endocardial (Endo), mid-myocardial (Mid) and epicardial (Epi) sites. The activation-recovery interval (ARI) was measured to estimate local refractoriness. The cardiac cycle length was gradually shortened by cessation of vagal stimulation (vagal stimulation protocol (VSP)), and intramural electrograms and onset mode of ventricular tachyarrhythmias were analyzed in 7 experiments. The VSP was performed 8 times before and 5 times after administration of mexiletine in each experiment. Before mexiletine, vagal stimulation slowed the heart rate and created large transmural ARI dispersion because of a greater ARI prolongation at Mid rather than Epi/Endo sites. After cessation of vagal stimulation, unipolar electrograms started to show ARI alternans and ventricular premature beats developed sporadically. Sustained ventricular tachyarrhythmias were induced in 12 of the 56 trials of the VSP. Initiation of ventricular tachyarrhythmias was associated with delayed conduction at Mid/Endo sites. Mexiletine attenuated transmural ARI dispersion, and neither ARI alternans nor ventricular tachyarrhythmias was observed during all 35 trials of the VSP after mexiletine administration. Heart rate acceleration induced by an abrupt shift to a state of predominant sympathetic activity enhances arrhythmias in this LQT3 model. Mexiletine homogenizes ventricular repolarization, suppresses premature complexes and was antiarrhythmic during ventricular tachyarrhythmias induced by the VSP.     

Mechanism of discordant T wave alternans in the in vivo heart

INTRODUCTION: Compared to concordant T wave alternans (CA), discordant T wave alternans (DA) may be associated with an increased dispersion of repolarization (DR) and a greater propensity to develop reentrant ventricular tachyarrhythmias. The electrophysiologic mechanisms of DA in the in vivo heart are not well understood. METHODS AND RESULTS: The mechanisms of DA were investigated in the canine anthopleurin-A surrogate model of long QT3 syndrome using tridimensional analysis of activation and repolarization patterns from 256 to 384 unipolar electrograms. Cardiac repolarization was evaluated as the activation-recovery interval (ARI) of local electrograms. Two mechanisms for the development of DA were observed. (1) Stepwise shortening of cycle length (CL) superimposed on preexisting DR resulted in different diastolic intervals (DI) at midmyocardial sites compared to epicardial and endocardial sites. The dispersion of DI coupled with different restitution kinetics at those sites induced DA. (2) The dependence of conduction velocity on DI as the CL is abruptly shortened could result in differential conduction delays at mid sites. This enhanced the dispersion of DI between sites and, coupled with the different restitution kinetics, induced DA. The critical step for the development of DA in both mechanisms was the occurrence of short ARI in two consecutive beats either at epicardial sites in the first mechanism or at mid sites in the second mechanism. Sites with DA had significantly more DR compared to sites with concordant T wave alternans, and ventricular tachyarrhythmias developed mainly in the presence of DA. CONCLUSION: In the in vivo heart, DA developed due to critical interaction between dispersion of DI and differences in restitution kinetics at different myocardial sites. The dispersion of DI could result from preexisting DR or differential conduction delay at a critical short CL. DA is critically linked to the development of malignant tachyarrhythmias.     

Effect of bundle branch block on microvolt T-wave alternans and electrophysiologic testing in patients with ischemic cardiomyopathy

BACKGROUND: T-wave alternans (TWA) and electrophysiology study (EPS) are used for risk stratification for sudden death. OBJECTIVE: The purpose of the study was to determine the effect of bundle branch block or intraventricular conduction delay on TWA and EPS. METHODS: 386 patients with coronary artery disease, nonsustained ventricular tachycardia, and left ventricular ejection fraction < or =40% underwent TWA and EPS, and were followed for 40 +/- 19 months. RESULTS: Patients with wide QRS were more likely than narrow QRS patients to have nonnegative TWA (77% vs 63%, P <.01) or positive EPS (60% vs 48%, P = .03). Nonnegative TWA predicted the combined endpoint of ventricular tachyarrhythmia or death in narrow QRS (HR = 1.64, P = .04) but not wide QRS patients (HR = 1.04, P = .91). Similarly, positive EPS predicted the combined endpoint in narrow QRS (HR = 2.28, P <.001) but not wide QRS patients (HR = 0.94, P = .84). In multivariate analysis, QRS width and TWA, as well as QRS width and EPS, were independent predictors of events. There was no TWA- or EPS-based difference in arrhythmia-free survival within any specific wide QRS morphology. CONCLUSION: TWA and EPS are more often abnormal in patients with a wide QRS than in those with a narrow QRS. In patients with narrow QRS, both TWA and EPS stratify patients according to their risk of ventricular tachyarrhythmia or death. However, among patients with a wide QRS, regardless of specific QRS morphology, the risk is high and comparable regardless of TWA or EPS results. Therefore, the only truly low-risk group consists of those patients with negative test results and a narrow QRS.     

Implantable cardioverter-defibrillator shocks increase T-wave alternans

Introduction: While implantable defibrillator shocks save lives, shock can lead to ventricular arrhythmias. However, the mechanism of shock-related proarrhythmia remains unclear. We evaluated the impact of ICD shock on repolarization instability, a factor associated with ventricular arrhythmogenesis.
Methods and Results: Sixty-five patients with ICDs underwent ambulatory ECG monitoring during defibrillation testing 3 months postimplant. TWA was analyzed continuously in the time domain during baseline, sedated, and post-shock states. RR, QRS, and QT intervals and catecholamines were also measured continuously. Adequate pre- and post-shock Holter data were recorded in 55 patients, 48 male, mean 64 ± 12 years, 50 with coronary disease, 48 with prior spontaneous or induced arrhythmia. TWA significantly increased after shock, from 9.6 ± 0.5 to 11.9 ± 0.6 μV, as did QRS duration, epinephrine, and norepinephrine levels, compared with sedated and baseline states. RR intervals decreased minimally. TWA changes with shock were not associated with RR or QRS duration changes, but were associated with changes in epinephrine.
Conclusions: ICD shock, even in the sedated state, increases repolarization instability as measured by TWA, an effect mediated in part by sympathetic stimulation. This association between shock and TWA may have important mechanistic and clinical implications for optimization of defibrillation therapy.     

Microvolt T wave alternans inducibility in normal newborn puppies: effects of development

INTRODUCTION: The cause of sudden infant death syndrome is unknown, but increased cardiac vulnerability due to repolarization instability may be a contributing factor. The QT interval normally is long at birth and increases further during the first few postnatal months. Although excessive QT intervals indicate increased cardiac vulnerability in the long QT syndrome, the impact of less pronounced QT prolongation during this developmental period is unclear. In adults and older children, the ease of inducing microvolt-level T wave alternans (TWA) is used as a measure of repolarization instability and arrhythmia vulnerability. The aim of this study was to determine if TWA is inducible in normal newborn puppies. METHODS AND RESULTS: Atrial pacing was performed in 15 anesthetized beagle puppies 7 to 35 days old. The pacing drive cycle length was systematically decreased in 20-msec steps from baseline until AV conduction blocked. Pacing was performed for 8 minutes at each cycle length. Three-lead ECGs were recorded continuously during the last 5 minutes of pacing at each cycle length. The recordings were analyzed off-line for the presence of microvolt-level TWA using a sensitive spectral analysis technique. Microvolt-level TWA was present in all puppies. TWA was not present at baseline but developed and increased in amplitude as heart rate increased. The threshold heart rate for TWA did not correlate with age. However, due to age-dependent changes in baseline heart rate, the 7- to 14-day-old animals needed a 50% to 78% increase in heart rate to reach threshold heart rate, whereas the oldest animals needed only a 5% to 25% increase. CONCLUSION: These data suggest that developmentally dependent dynamic repolarization instability exists in puppies as manifest by the inducibility of TWA.     

Clinical significance of T-wave alternans in hypertrophic cardiomyopathy.

The clinical significance of T-wave alternans (TWA) in hypertrophic cardiomyopathy (HCM) is unclear, so SV1+RV5 and QT dispersion on 12-lead electrocardiograms (ECG), the parameters of the left ventricle on echocardiography and the family history of HCM and sudden death were investigated in 53 patients with HCM who experienced TWA. The maximal numbers of successive ventricular ectopic beats (max VE) and nonsustained ventricular tachycardia (NSVT) were measured by Holter monitoring. In 13 patients, genetic abnormalities were examined. In 22 patients, the hypertrophy of myocytes, disarray and fibrosis were histopathologically examined using a scoring method. TWA was positive in 27 patients (TWA+ group), negative in 14 (TWA- group) and indeterminate in 12. The ECG and echocardiographic parameters, family history and genetic abnormalities did not significantly differ between the TWA+ and TWA- groups. Max VE, the percentage of patients with NSVT and disarray score in the TWA+ group were significantly higher than those in the TWA- group (3.6+/-3.6 vs 1.3+/-0.7, 37% vs 0%, 1.9+/-1.1 vs 0.7+/-0.5; p<0.05). TWA in HCM correlates with histopathological changes, especially disarray and ventricular tachyarrhythmia, and measuring it may be a noninvasive means of detecting high-risk patients with HCM.     

急性缺血对犬在体心肌跨心室壁复极不均一性的影响

目的：探讨急性缺血对犬在体心肌跨心室壁复极不均一性及与心律失常的关系。方法：健康家犬10只，应用单相动作电位记录技术，同步记录健康家犬在体阻断左前降支主干前后心外膜、中层及心内膜心肌单相动作电位及体表心电图，分析相关参数的变化。结果：3层心肌单相动作电位时程正常供血状态下差异无显著性意义（P＞0．05），急性缺血状态下则均明显缩短，且心外膜、心内膜的缩短程度较中层心肌更为明显，差异有显著性意义（P＜0．05）。3层心肌间跨室壁复极离散度增大。10只犬中正常供血状态下无一例出现心律失常，急性缺血30min内4只出现了室性心动过速或心室颤动死亡，恶性心律失常发生率达40％。结论：急性缺血时犬在体心肌跨心室壁复极离散度增大，可能是导致缺血性室性心律失常的原因之一。     

T-wave alternans testing for ventricular arrhythmias

T-wave alterans (TWA) measures alternate-beat fluctuations in the ECG T-wave, and has been used to predict the risk for life-threatening ventricular arrhythmias in various clinical populations. This work reviews the traditional literature linking repolarization alternans in cellular and tissue-level studies, with clinical studies that TWA can successfully add to existing clinical risk factors in predicting ventricular arrhythmias. We conclude by providing an evidence-based framework integrating TWA with other risk factors to stratify risk for sudden cardiac arrest.     

Influence of QRS duration on the prognostic value of T wave alternans

INTRODUCTION: T wave alternans (TWA) is a promising new noninvasive marker of arrhythmia vulnerability that quantifies beat-to-beat changes in ventricular repolarization. Secondary repolarization abnormalities are common in subjects with wide QRS complexes. However, the relationship between TWA and QRS prolongation has not been evaluated. The goal of this study was to determine if QRS prolongation influences the prevalence or prognostic value of TWA. METHODS AND RESULTS: The study consisted of 108 consecutive patients with coronary artery disease and left ventricular ejection fraction < or = 40% who were referred for electrophysiologic studies. Patients underwent TWA testing using bicycle ergometry in the absence of beta-blockers or antiarrhythmic drugs. The primary endpoint was the combined incidence of death, sustained ventricular arrhythmias, and appropriate implantable cardioverter defibrillator therapy. The prognostic value of TWA was assessed in the entire cohort and in two subgroups: QRS < 120 msec (normal, n = 62) and QRS > or = 120 msec (prolonged, n = 46). TWA (hazard ratio 2.2, P = 0.03) and QRS prolongation (hazard ratio 2.2, P = 0.01) were both significant and independent predictors of arrhythmic events. QRS prolongation had no effect on the prevalence of positive TWA tests (QRS < 120 msec: 48%, QRS > or = 120 msec: 50%, P = NS). TWA was a highly significant predictor of events in patients with a normal QRS (hazard ratio 5.8, P = 0.02). In contrast, TWA was not useful for risk stratification in subjects with QRS prolongation (hazard ratio 1.1, P = 0.8). CONCLUSION: TWA is useful only for risk stratification in the absence of QRS prolongation. The presence of QRS prolongation and left ventricular ejection fraction < or = 40% may be sufficient evidence of an adverse prognosis that additional risk stratification is not useful or necessary.     

Relationship between duration of repolarisation and T wave amplitude in patients with positive or negative T wave alternans

BACKGROUND: Experimental studies documented the relationship between T wave alternans (TWA) and duration of refractoriness. To date, association between TWA and QT interval on standard ECG has not been examined. Aim. To assess the relationship between TWA and QT interval. METHODS: The study group consisted of 70 patients (57 males, mean age 56+/-16 years) with implantable cardioverterdefibrillator (ICD). TWA was measured using a high-resolution ECG obtained from surface orthogonal bipolar XYZ leads and analysed using a Fast Fourier transform. All recordings were performed during ventricular pacing at 100 betas/min. Correlation between T wave amplitude (T max) and QT interval (measured from R wave to T max) was calculated. RESULTS: TWA was found in 18 patients. In this group of patients, there was a significant positive correlation between Tmax and QT (r = 0.766), whereas in patients with negative TWA no such correlation was detected. CONCLUSIONS: (1) Positive correlation between QT and T max probably depicts the relationship between T wave amplitude and duration of repolarisation, which is associated with TWA; (2) methods used for T wave localisation, based on the identification of Q wave (with possible QT-RR correction) overestimate TWA due to periodic changes (with TWA frequency) in location of T wave in the analysed window; and (3) these results provide new insights in the genesis of TWA.     

T wave alternans in idiopathic long QT syndrome

Objectives. The study evaluates the association between T wave alternans and the risk of cardiac events (syncope, aborted cardiac arrest or cardiac death) in a large population of patients with idiopathic long QT syndrome.Background. T wave alternans is an infrequently recorded electrocardiographic (ECG) finding in patients with delayed repolarization, and its clinical significance is not clear.Methods. A total of 4,656 ECG recordings in 2,442 patients enrolled in the International Long QT Syndrome Registry were reviewed for episodes of T wave alternans. To determine the risk associated with T wave alternans, independent of corrected QT interval (QTc) duration, patients with T wave alternans were matched for QTc value (every 0.025 s^1/2) to patients with long QT syndrome without T wave alternans.Results. T wave alternans was identified in 39 patients (25 of whom had a QTc interval >0.50 s^1/2). A strong association between QTc prolongation and T wave alternans was observed (odds ratio 1.23 per 0.01-s^1/2unit increase in QTc, p < 0.0001). Conditional logistic regression analyses with adjustment for age, gender, status and QTc value revealed that T wave alternans did not make a significant independent contribution to the risk of cardiac events. The risk of experiencing a major cardiac event was primarily related to length of QTc.Conclusions. T wave alternans, a marker of electrical instability and regional heterogeneity of repolarization, identifies a high risk subset of patients with prolonged repolarization. Patients with T wave alternans have an increased risk of cardiac events, but this risk is primarily related to the magnitude of repolarization delay (QTc prolongation). T wave alternans does not make an independent contribution to the risk of cardiac events after adjustment for QTc length.     

Secondary and primary repolarization changes in left ventricular hypertrophy: a model study

The contributions of reduced conduction velocity (CV) and prolonged action potential duration (APD) to QT interval prolongation and T wave and T vector loop morphology in left ventricular hypertrophy (LVH) were studied using an analytical computer model. Three types of anatomic LVH were simulated: concentric and eccentric hypertrophy, and left ventricular dilatation. In each LVH type, depolarization changes were simulated by CV slowing and primary repolarization changes by APD prolongation. Both CV slowing and APD prolongation prolonged the QT interval; however, the secondary and primary repolarization changes differed in additional electrocardiogram (ECG) characteristics creating specific vectorcardiographic/ECG patterns. The secondary repolarization changes were characterized by prolonged QT interval, accompanied by pronounced QRS changes, including increased maximum spatial QRS vector magnitude, prolonged QRS duration, QRS morphology consistent with intraventricular conduction delay, lower values of the T/QRS duration ratio, increased maximum spatial T vector magnitude, narrow and prolonged discordant T vector loops, and discordant tall T waves creating a pattern of ST strain in the precordial ECG leads. QT prolongation in primary repolarization changes was accompanied with inconsiderable changes of QRS amplitude and duration, higher values of the T/QRS duration ratio, widened rounded T loops, and notched or bifid T waves in left precordial leads of the 12-lead ECG. These simulation data are consistent with the accumulated evidence suggesting that LVH induces changes in CV and APD. Our results emphasize the need for simultaneous consideration of morphologic QRS and T wave patterns together with QT prolongation in clinical evaluation of LVH.     

Cellular and ionic basis for T-wave alternans under long-QT conditions

BACKGROUND: T-wave alternans (TWA), an ECG phenomenon characterized by beat-to-beat alternation of the morphology, amplitude, and/or polarity of the T wave, is commonly observed in the acquired and congenital long-QT syndromes (LQTS). This study examines the cellular and ionic basis for TWA induced by rapid pacing under conditions mimicking the LQT3 form of the congenital LQTS in an arterially perfused canine left ventricular wedge preparation. METHODS AND RESULTS: Transmembrane action potentials from epicardial, M, and endocardial cells and 6 to 8 intramural unipolar electrograms were simultaneously recorded together with a transmural ECG and isometric tension development. In the presence of sea anemone toxin (ATX-II; 20 nmol/L), an increase in pacing rate (from a cycle length [CL] of 500 to 400 to 250 ms) produced a wide spectrum of T-wave and mechanical alternans. Acceleration to CLs of 400 to 300 ms produced mild to moderate TWA principally due to beat-to-beat alternation of repolarization of cells in the M region. Transmural dispersion of repolarization during alternans was exaggerated during alternate beats. Acceleration to CLs of 300 to 250 ms caused more pronounced beat-to-beat alternation of action potential duration (APD) of the M cell, resulting in a reversal of repolarization sequence across the ventricular wall, leading to alternation in the polarity of the T wave. The peak of the negative T waves coincided with repolarization of the M region, whereas the end of the negative T wave coincided with the repolarization of epicardium. In almost all cases, electrical alternans was concordant with mechanical alternans. Torsade de pointes occurred after an abrupt acceleration of CL, which was associated with marked TWA. Both ryanodine and low [Ca2+]o completely suppressed alternans of the T wave, APD, and contraction, suggesting a critical role for intracellular Ca2+ cycling in the maintenance of TWA. CONCLUSIONS: Our results suggest that TWA observed at rapid rates under long-QT conditions is largely the result of alternation of the M-cell APD, leading to exaggeration of transmural dispersion of repolarization during alternate beats, and thus the potential for development of torsade de pointes. Our data also suggest that unlike transient forms of TWA that damp out quickly and depend on electrical restitution factors, the steady-state electrical and mechanical alternans demonstrated in this study appears to be largely the result of beat-to-beat alternans of [Ca2+]i.     

T-wave alternans and the susceptibility to ventricular arrhythmias.

T-wave alternans (TWA) reflects beat-to-beat fluctuations in the electrocardiographic T-wave, and is associated with dispersion of repolarization and the mechanisms for sudden cardiac arrest (SCA). This review examines the bench-to-bedside literature that, over decades, has linked alternans of repolarization in cellular, whole-heart, and human studies with spatial dispersion of repolarization, alternans of cellular action potential, and fluctuations in ionic currents that may lead to ventricular arrhythmias. Collectively, these studies provide a foundation for the clinical use of TWA to reflect susceptibility to ventricular arrhythmias in several disease states. This review then provides a contemporary evidence-based framework for the use of TWA to enhance risk stratification for SCA, identifying populations for whom TWA is best established, those for whom further studies are required, and areas for additional investigation.     

Utility of implantable cardioverter defibrillator electrograms to estimate repolarization alternans preceding a tachyarrhythmic event

Electrical alternans is a pattern of variation in the shape of the ECG waveform that appears on an every-other-beat basis. In humans, alternation in ventricular repolarization, namely, repolarization alternans, has been associated with increased vulnerability to ventricular tachycardia/ventricular fibrillation and sudden cardiac death. This study investigates the utility of implantable cardioverter defibrillator electrograms to estimate repolarization alternans preceding a tachyarrhythmic event. It is demonstrated that microvolt-level repolarization alternans is present prior to an arrhythmic event, and one can record low-amplitude-noise signals that can be used to obtain reliable estimates of repolarization alternans. This study eventually may lead to new methods that would prevent the onset of malignant tachyarrhythmias.     

Prognostic significance of risk stratifiers of mortality, including T wave alternans, after acute myocardial infarction: results of a prospective follow-up study

INTRODUCTION: Occurrence of sustained microvolt-level T wave alternans (TWA) at a specified heart rate has been suggested to predict life-threatening arrhythmic events, but its prognostic value has not been well established in patients who survived an acute myocardial infarction (AMI). The purpose of this prospective study was to assess the predictive significance of various noninvasive risk indicators of mortality, including TWA, in consecutive post-AMI patients with optimized medical therapy. METHODS AND RESULTS: In addition to a symptom-limited predischarge exercise test with measurement of TWA, mortality risk was assessed using heart rate variability, 24-hour ECG recordings, baroreflex sensitivity, signal-averaged ECG, QTc interval, QT dispersion, and echocardiographic wall-motion index in 379 consecutive patients. Twenty-six patients (6.9%) died during a mean follow-up of 14 +/- 8 months. Sustained TWA was found in 56 patients (14.7%), none of whom died. Several risk variables, e.g., incomplete TWA test (inability to perform the exercise test or reach the required target heart rate of 105 beats/min), increased QRS duration on signal-averaged ECG, increased QT dispersion, long QTc interval, nondiagnostic baroreflex sensitivity result, and low wall-motion index, predicted all-cause mortality in univariate analyses. In multivariate analysis, the incomplete TWA test was the most significant predictor of cardiac death (relative risk 11.1, 95% confidence interval 2.4 to 50.8; P < 0.01). CONCLUSION: Sustained TWA during the predischarge exercise test after AMI does not indicate increased risk for mortality. An incomplete TWA test and several common risk variables provided prognostic information in this post-AMI population.     

T-wave alternans and the susceptibility to ventricular arrhythmias

T-wave alternans (TWA) reflects beat-to-beat fluctuations in the electrocardiographic T-wave, and is associated with dispersion of repolarization and the mechanisms for sudden cardiac arrest (SCA). This review examines the bench-to-bedside literature that, over decades, has linked alternans of repolarization in cellular, whole-heart, and human studies with spatial dispersion of repolarization, alternans of cellular action potential, and fluctuations in ionic currents that may lead to ventricular arrhythmias. Collectively, these studies provide a foundation for the clinical use of TWA to reflect susceptibility to ventricular arrhythmias in several disease states. This review then provides a contemporary evidence-based framework for the use of TWA to enhance risk stratification for SCA, identifying populations for whom TWA is best established, those for whom further studies are required, and areas for additional investigation.     

T-wave alternans: lessons learned from a biophysical ECG model

T-wave alternans (TWA) is an alteration of the ECG T-wave which repeats every other beat. An alternating pattern has been also observed at myocytes level, involving both action potential duration and morphology (mainly in phases 2 and 3). While this might happen in a specific region (i.e., myocardial ischemia), it can also involve the entire myocardium. It is still unclear how alternations at the myocytes level are reflected on surface ECG modification of T-waves, especially when in vivo human hearts are considered. We have recently proposed a simple stochastic model of ventricular repolarization (IEEE Trans. Biomed. Eng., 2011), which takes into account both repolarization heterogeneity across the myocardium as well as random beat-to-beat variations in cells' activity. In this work, we generalized that model incorporating a term which describes myocytes alternans related to T-wave variability. Starting from the model and using the electrophysiological formulation developed by van Oosterom, we derived an analytical formula relating surface ECG to variations at the myocytes' level. Several theoretical results were then obtained. First, temporal small random variations in repolarization heterogeneity affect the precision of TWA estimates in a significant way. Second, TWA theoretically differs across leads, but multilead configuration can be used to reduce the effect of noise. Finally, the dependency between TWA and T-wave amplitude was analyzed.     

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.     

ECG Phenomena: Pseudopreexcitation and Repolarization Disturbances Resembling ST‐Elevation Myocardial Infarction Caused by an Intraatrial Rhabdomyoma in a Newborn

As is known from other reports, a rhabdomyoma or tumor metastasis may alter intracardiac electrical conduction, producing electrical phenomena like pseudopreexcitation or repolarization disturbances resembling ST‐elevation myocardial infarction or Brugada's syndrome. We present a newborn with a giant atrial rhabdomyoma and additionally multiple ventricular rhabdomyomas. He presented with several electrocardiogram (ECG) phenomena due to tumor‐caused atrial depolarization and repolarization disturbances. Except from the cardiac tumors, the physical status was within normal range. Initial ECG showed a rapid atrial tachycardia with a ventricular rate of 230 bpm, which was terminated by electrical cardioversion. Afterwards, the ECG showed atrial rhythm with frequent atrial premature contractions and deformation of the PR interval with large, broad P waves and loss of discret PR segment, imposing as pseudopreexcitation. The following QRS complex was normal, with seemingly abnormal ventricular repolarization resembeling ST‐elevation myocardial infarction. The atrial tumor was resected with consequent vast atrial reconstruction using patch plastic. The ventricular tumors were left without manipulation. After surgery, pseudopreexcitation and repolarization abnormalities vanished entirely and an alternans between sinus rhythm and ectopic atrial rhythm was present. These phenomena were supposably caused by isolated atrial depolarization disturbances due to tumor‐caused heterogenous endocardial activation. The seemingly abnormal ventricular repolarization is probably due to repolarization of the atrial mass, superimposed on the ventricular repolarization. Recognizably, the QRS complex before and after surgical resection of the rhabdomyoma is identical, underlining the atrial origin of the repolarization abnormalities before surgery.