Differences in 12-lead electrocardiogram between symptomatic and asymptomatic Brugada syndrome patients

Introduction: Brugada syndrome (BrS) is an inherited disorder that predisposes some subjects to sudden cardiac death (SCD). It is not well established which BrS patients are at risk of severe arrhythmias. Our aim was to study whether standard 12-lead electrocardiogram (ECG) would give useful information for this purpose.
Methods: This study included 200 BrS probands (142 male, 62%; mean age 42 ± 16 years). Symptoms related to BrS were defined as syncope, documented ventricular tachyarrhythmia, or SCD. We determined PR, QRS, QTc, T_peak, and T_end interval from leads II and V₂ and QRS from lead V₅, R'/S ratio from lead aVR (aVR sign), QRS axis, and J-point elevation amplitude from right precordial leads from the baseline ECGs.
Results: Sixty-six subjects (33%) had experienced symptoms related to BrS. The only significant difference between the symptomatic and asymptomatic BrS subjects was the QRS duration measured from lead II or lead V₂, for example, the mean QRS in V₂ was 115 ± 26 ms in symptomatic versus 104 ± 19 ms in asymptomatic patients (P < 0.001). The optimized cut-off point of V₂ QRS ≥120 ms gave an odds ratio (OR) of 2.5 (95% CI: 1.4–4.6, P = 0.003) for being symptomatic. In a multivariate analysis adjusted with gender, age, and SCN5A mutation, the OR was 2.6 (95% CI: 1.4–4.8, P = 0.004).
Conclusion: Prolonged QRS duration, measured from standard 12-lead ECG, is associated with symptoms and could serve as a simple noninvasive risk marker of vulnerability to life-threatening ventricular arrhythmias in BrS.     

Risk stratification in patients with Brugada syndrome: analysis of daily fluctuations in 12-lead electrocardiogram (ECG) and signal-averaged electrocardiogram (SAECG)

Introduction: Risk stratification between symptomatic and asymptomatic patients with Brugada syndrome is not yet established. We compared daily fluctuations in 12-lead electrocardiogram (ECG) and signal-averaged ECG (SAECG) characteristics between symptomatic and asymptomatic patients with Brugada syndrome to identify new markers for distinguishing between high- and low-risk patients.
Methods and Results: Thirty-five patients with Brugada syndrome underwent ECG and SAECG simultaneously at least 4 times every 3 months. We evaluated daily fluctuations (differences between maximum and minimum values) in ECG and SAECG characteristics and compared them between symptomatic  (N = 11)  , and asymptomatic  (N = 24)  patients. On ECG, the daily fluctuations in r-J interval (interval from QRS onset to J point) in leads V1, V2, and V6 were significantly larger in symptomatic than in asymptomatic patients  (V1; 20 ± 6 vs 10 ± 8 msec, P < 0.01, V2; 22 ± 8 vs 11 ± 4 msec, P < 0.01, and V6; 24 ± 7 vs 14 ± 7 msec, P < 0.01)  . On SAECG, daily fluctuations in filtered QRS (f-QRS) duration and LAS40 were significantly larger in symptomatic than in asymptomatic patients (f-QRS;  15 ± 7 vs 9 ± 4 msec, P < 0.05  , and LAS40;  21 ± 7 vs 10 ± 6 msec, P < 0.05  ).
Conclusions: Instability of depolarization appears to be related to the risk of fatal ventricular arrhythmias in patients with Brugada syndrome. Daily fluctuations in ECG and SAECG characteristics could be useful for distinguishing between high- and low-risk patients with Brugada syndrome.     

Postprandial augmentation of bradycardia-dependent ST elevation in patients with Brugada syndrome

Introduction : In patients with Brugada syndrome, the circadian variation of ST elevation could be modulated by the autonomic nervous activity and RR interval. Recently, glucose-induced insulin secretion was also reported to contribute to fluctuation of ST elevation. Therefore, we assessed the effects of taking meals on the ST-RR relationship in the daily life of patients with Brugada syndrome.
Methods and Results: Twenty-eight patients with Brugada syndrome, who had the type I ST elevation, were categorized into 12 symptomatic and 16 asymptomatic patients. Unipolar lead (V₂) Holter ECG was recorded and ST-RR relationships for a 2-hour period were compared before and after each meal. From ST-RR linear regression lines, ST-RR slope (mm/sec) and ST(mm) at RR intervals of both 0.6 seconds and 1.2 seconds (ST_(0.6) and ST_(1.2)) were determined. The ST-RR slope increased significantly after lunch (2.6 ± 0.4 vs 4.4 ± 1.2, P < 0.05) and dinner (2.1 ± 1.0 vs 5.2 ± 1.9, P < 0.01) in symptomatic patients, but not in asymptomatic patients. In both groups, ST_(0.6) was not different before or after each meal. However, ST_(1.2) increased after each meal in symptomatic patients. After dinner, ST_(1.2) was significantly higher in symptomatic patients than in asymptomatic patients (5.0 ± 2.7 vs 3.6 ± 0.8, P < 0.05). Postprandial increase in both ST-RR slope and ST_(1.2) was greatest at dinner in symptomatic patients; however, this tendency was not seen in asymptomatic patients.
Conclusions: In symptomatic patients with Brugada syndrome, bradycardia-dependent augmentation of ST elevation was enhanced for the postprandial period, especially after dinner. This could be related to occurrence of ventricular fibrillation in the late evening.     

Is the Brugada Syndrome a Distinct Clinical Entity?

The Brugada Syndrome. In 1992, Brugada and Brugada described a syndrome characterized by right bundle branch block pattern with ST elevation in leads V₁ through V₃ and a history of sudden death due to polymorphic ventricular tachycardia or ventricular fibrillation. Since these patients bad no evidence of cardiac disease, these findings were ascribed to a distinct clinical entity. Further experience bas shown that this same pattern may be mimicked by patients with right ventricular dysplasia, acute ischemia of the right ventricle, other infiltrative cardiomyopathies, as well as tricyclic drug overdose. The pathogenesis of these changes may be due to loss of the dome configuration in the transmembrane potential of right ventricular epicardial cells, which would result in a voltage gradient producing ST elevation. Other explanations involve delayed conduction in a dysplastic right ventricle. The clinical importance of this syndrome is that it calls attention to patients at risk for sudden cardiac death. In addition, these observations have sparked the interest of basic electrophysiologists relative to the relationship of these ECG waveforms and malignant ventricular arrhythmias. Finally, the clinician must exclude other organic diseases before diagnosing this entity.     

Clinical characteristics and risk stratification in symptomatic and asymptomatic patients with brugada syndrome: multicenter study in Japan

Background: Neither the clinical characteristics nor risk stratification in Brugada syndrome have been clearly determined. We compared the clinical and ECG characteristics of symptomatic and asymptomatic patients with Brugada syndrome to identify new markers for high-risk patients.
Methods: A total of 188 consecutive individuals with Brugada syndrome (mean age 53 ± 14 years, 178 males) were enrolled in the Japan Idiopathic Ventricular Fibrillation Study (J-IVFS). Clinical and ECG characteristics were evaluated in three groups of patients: Ventricular fibrillation (VF) group: patients with documented VF (N = 33); Syncope (Sy) group: patients with syncope without documented VF (N = 57); and asymptomatic (As) group: subjects without symptoms (N = 98). Their prognostic parameters were evaluated over a 3-year follow-up period.
Results: (1) Clinical characteristics: incidence of past history of atrial fibrillation (AF) was significantly higher in the VF and Sy groups than in the AS group (P = 0.04). (2) On 12-lead ECG, r-J interval in lead V2 and QRS duration in lead V6 were longest in the VF group (P = 0.001, 0.002, respectively). (3) Clinical follow-up: during a mean follow-up period of 37 ± 16 months, incidences of cardiac events (sudden death and/or VF) were higher in the symptomatic (VF/Sy) groups than in the As group (P < 0.0001). The r-J interval in lead V2 ≥ 90 ms and QRS duration in lead V6 ≥ 90 ms were found to be possible predictors of recurrence of cardiac events in symptomatic patients.
Conclusions: Prolonged QRS duration in precordial leads was prominent in symptomatic patients. This ECG marker may be useful for distinguishing high- from low-risk patients with Brugada syndrome.     

Focal atrial tachycardia originating from the left atrial appendage: electrocardiographic and electrophysiologic characterization and long-term outcomes of radiofrequency ablation

Introduction: This study sought to investigate electrophysiologic characteristics and radiofrequency ablation (RFA) in patients with focal atrial tachycardia (AT) arising from the left atrial appendage (LAA).
Methods: This study included seven patients undergoing RFA with focal AT. Activation mapping was performed during tachycardia to identify an earlier activation in the left atria and the LAA. The atrial appendage angiography was performed to identify the origin in the LAA before and after RFA.
Results: AT occurred spontaneously or was induced by isoproterenol infusion rather than programmed extrastimulation and burst atrial pacing in any patient. The tachycardia demonstrated a characteristic P-wave morphology and endocardial activation pattern. The P wave was highly positive in inferior leads in all patients. Lead V₁ showed upright or biphasic (±) component in all patients. Lead V₂–V₆ showed an isoelectric component in five patients or an upright component with low amplitude (<0.1 mV) in two patients. Earliest endocardial activity occurred at the distal coronary sinus (CS) ahead of P wave in all seven patients. Mean tachycardia cycle length was 381 ± 34 msec and the earliest endocardial activation at the successful RFA site occurred 42.3 ± 9.6 msec before the onset of P wave. RFA was acutely successful in all seven patients. Long-term success was achieved in seven of the seven over a mean follow-up of 24 ± 5 months.
Conclusions: The LAA is an uncommon site of origin for focal AT (3%). There were consistent P-wave morphology and endocardial activation associated with this type of AT. The LAA focal ablation is safe and effective. Long-term success was achieved with focal ablation in all patients.     

Electrocardiographic Changes Following Balloon Dilatation of Valvar Pulmonic Stenosis

The purpose of this paper was to study the electrocardiographic changes following balloon pulmonary valvuloplasty for pulmonic stenosis and to see if such changes reflect improvement in pulmonary valve gradient following balloon valvuloplasty. Forty-one patients, ages 7 days to 20 years, underwent balloon valvuloplasty for severe valvar pulmonic stenosis. In 35 of these patients ECGs were available 3 to 34 months (mean 11) following valvuloplasty and were compared with pre-valvu-loplasty electrocardiograms. In 30 children with excellent relief of pulmonic stenosis (group I), frontal plane mean QRS vector moved toward the left from 127 ±25° to 81 ±47°as did the horizontal plane mean QRS vector, 88 ± 36° to 27 ±51°. The amplitude of R wave in V_1, 19 ± 11.6 mm, and V₂, 19.7 ± 12.2 mm, decreased respectively to 9.5 ± 5.9 mm and 11.3 ±6.1 mm. S wave amplitude in V₅ and V₆ also decreased. The improvement in the electrocardiogram is associated with a decrease in pulmonary valve gradient from 95 ± 50 to 29 ± 23 mm Hg. In five children with significant residual pulmonary valve gradient (group II), the electrocardiograms did not show any significant change. Evaluation of the time course of ECG changes in group I revealed that recognizable electrocardiographic improvement was first observed at 6 months following successful balloon pulmonary valvuloplasty. Normal electrocardiogram suggests minimal residual pulmonary valve gradient while right ventricular hypertrophy suggests significant residual obstruction unless the electrocardiogram was recorded at or before six months following balloon valvuloplasty. These data suggest that electrocardiogram is a good indicator of improvement following balloon pulmonary valvuloplasty. (J. Interven Cardiol 1988:1:3)     

Body surface potential mapping in patients with Brugada syndrome: right precordial ST segment variations and reverse changes in left precordial leads

OBJECTIVE: The aim of this study was to perform quantitative signal analysis of high-resolution body surface potential mapping (BSPM) recordings to assess its usefulness for the electrocardiographic characterization of patients with Brugada syndrome. The diagnostic value of the QRS integral and of the gradient of the ST segment have not been elucidated in Brugada syndrome. METHODS: In 27 subjects (16 with Brugada syndrome and 11 healthy subjects), 120-lead BSPMs were recorded at baseline and after pharmacological provocation with intravenous administration of ajmaline (1 mg/kg). The recordings were analyzed for two regions outside the positions of the standard ECG leads: the right precordial leads (RPL) on the second and third intercostal space (high RPL) and the left precordial leads (LPL) between the fifth and seventh intercostal space (low LPL). RESULTS: At baseline, in high RPL regions, patients with Brugada syndrome showed more positive QRS integrals (-5+/-8 vs. -16+/-8 mV ms) and a steeper negative ST segment gradient (-0.62+/-0.41 vs. -0.29+/-0.40 mV/s) compared to healthy subjects, P<0.001. In contrast, in low LPL regions, reduced QRS integrals and positive ST segment gradients were observed. These ECG signs were even more pronounced after intravenous ajmaline and showed a better discrimination for patients with Brugada syndrome than differences in RPL or LPL during baseline, respectively. CONCLUSIONS: In the left precordial leads, patients with Brugada syndrome showed ECG changes which were reversed in relation to the ECG changes observed in right precordial leads. BSPM measurement is a useful tool to improve the understanding of the electrocardiographic changes in the Brugada syndrome.     

ST Segment Elevation Induced by Class IC Antiarrhythmic Agents: Underlying Electrophysiologic Mechanisms and Insights into Drug-Induced Proarrhythmia

Sodium Block-Induced ST Segment Elevation. Three patients in whom Class IC sodium channel blockers induced ST segment elevation in leads V₁ through V₃ are described. The underlying electrophysiologic mechanism, implications for drug-induced proarrhythmia, and the relationship of the finding to the Brugada syndrome type of idiopathic ventricular fibrillation are discussed.     

Epicardial electrogram of the right ventricular outflow tract in patients with the Brugada syndrome: using the epicardial lead

OBJECTIVES: We tried to record an epicardial electrogram directly, and we examined local electrograms before and after administration of a class IC anti-arrhythmic drug in patients with the Brugada syndrome. BACKGROUND: Electrical heterogeneity of the epicardium in the right ventricular outflow tract (RVOT) has been thought to be related to the Brugada syndrome. However, an epicardial abnormality has not been demonstrated in patients with the Brugada syndrome. METHODS: In five patients with a Brugada-type electrocardiogram (ECG), local unipolar electrograms were recorded at the epicardium and endocardium of the RVOT. To record the epicardial electrogram directly, we introduced an electrical guidewire into the conus branch (CB) of the right coronary artery. The duration of the local electrogram after termination of the QRS complex (DP) was measured before and after class IC anti-arrhythmic drug administration. The signal-averaged electrocardiogram (SAECG) was also obtained in all patients. RESULTS: A definite DP was observed at the epicardium, but not at the endocardium. After administration of a class IC anti-arrhythmic drug, the DP at the epicardium was prolonged from 38 +/- 10 ms to 67 +/- 24 ms. The late potential corresponding to the DP at the epicardium was observed in all patients on the SAECG. CONCLUSIONS: An epicardial electrogram can be recorded from the CB. Recording from the CB enables identification of an epicardial abnormality in patients with the Brugada syndrome. These abnormal electrograms may be related to a myocardial abnormality in the epicardium of patients with the Brugada syndrome.     

Focal atrial tachycardias arising from the right atrial appendage: electrocardiographic and electrophysiologic characteristics and radiofrequency ablation

Objective: To characterize the electrocardiographic and electrophysiological features and frequency of focal atrial tachycardia (AT) originating from the right atrial appendage (RAA).
Background: The RAA has been described as a site of origin of AT, but detailed characterization of these tachycardias is limited.
Methods: Ten patients (3.8%) of 261 undergoing radiofrequency ablation (RFA) for focal AT are reported. Endocardial activation maps (EAM) were recorded from catheters at the CS (10 pole), tricuspid annulus (20 pole Halo catheter), and His positions. P waves were classified as negative, positive, isoelectric, or biphasic.
Results: The mean age was 39 ± 20 years, nine males, with symptoms for 4.1 ± 5.1 years. Tachycardia was incessant in seven patients, spontaneous in one patient, and induced by programmed extrastimuli in two patients. These foci had a characteristic P wave morphology. The P wave was negative in lead V₁ in all patients, becoming progressively positive across the precordial leads. The P waves in the inferior leads were low amplitude positive in the majority of patients. Earliest EAM activity occurred on the Halo catheter in all patients. Mean activation time at the successful RFA site =−38 ± 15 msec. Irrigated catheters were used in six patients, due to difficulty achieving adequate power. RFA was acutely successful in all patients. Long-term success was achieved in all patients over a mean follow up of 8 ± 7 months.
Conclusions: The RAA is an uncommon site of origin for focal AT (3.8%). It can be suspected as a potential anatomic site of AT origin from the characteristic P wave and activation timing. Irrigated ablation catheters are often required for successful ablation. Long-term success was achieved with focal ablation in all patients.     

Electrophysiologic characteristics and implications of induced ventricular fibrillation in symptomatic patients with Brugada syndrome

OBJECTIVES: The study examined the electrocardiographic and electrophysiologic characteristics in relation to programmed ventricular stimulation (PVS)-induced ventricular fibrillation (VF), as well as the implications of PVS-induced VF on the recurrence of cardiac events in symptomatic Brugada syndrome. BACKGROUND: Brugada syndrome is characterized by ST-segment elevation in the right precordial leads (V(1)-V(3)) and an episode of VF. METHODS: Thirty-four symptomatic patients with Brugada syndrome (33 men and 1 woman; 44 +/- 12 years old) were classified into two groups according to the inducibility of VF with PVS: 22 patients with induced VF requiring direct cardioversion for termination (Induced VF group) and 12 patients without induced VF (Noninduced VF group). RESULTS: The induced VF group showed a longer QRS duration, a higher incidence of right bundle branch block and late potentials detected on the signal-averaged electrocardiogram, longer His-ventricular intervals and a longer conduction time from the RVOT to the left ventricle at extrastimulation than those in the non-induced VF group. However, there was no significant difference in the recurrence of cardiac events (VF documented by an implantable cardioverter-defibrillator and sudden cardiac death) between the two groups (8 [36%] of 22 patients vs. 7 [58%] of 12 patients) during long-term follow-up (range 1 to 149 months; mean 38). CONCLUSIONS: Our data suggest that induction of VF by PVS depends on the severity of depolarization abnormalities but does not predict the recurrence of cardiac events in symptomatic Brugada syndrome, indicating that both depolarization and repolarization abnormalities are important in the development of VF.     

Familial Sudden Cardiac Death Associated with a Terminal QRS Abnormality on Surface 12-Lead Electrocardiogram in the Index Case

Familial Sudden Death and ECG Abnormalities. A case is presented of an 18-year-old male who had been resuscitated following an episode of sudden death due to ventricular fibrillation. The patient was noted to have an abnormal deflection in the terminal QRS on surface ECG and an abnormal signal-averaged KCG demonstrating a late potential coincident with the terminal QRS abnormality on the ECG. The patient had easily inducible polymorphic ventricular tachycardia during electrophysiologic study, which was suppressed by quinidine but not by procainamide or beta blockers. The surface ECG and signal-averaged ECG also were normalized by quinidine but not by procainamide or beta blockers. The patient had no further arrhythmias on quinidine for 6 years until he inexplicably discontinued his medication and died suddenly shortly thereafter. The present case may represent a unique familial sudden death syndrome or possibly a variant of the sudden death syndrome associated with right bundle branch block and ST elevation in V₁, through V₃, Currently available data suggest that, in such patients, an implantable cardioverter defibrillator may provide better protection from sudden death than does antiarrhythmic drug therapy.     

Electrocardiographic methods for diagnosis and risk stratification in the Brugada syndrome

The Brugada syndrome (BrS) is a malignant, genetically-determined, arrhythmic syndrome manifesting as syncope or sudden cardiac death (SCD) in individuals with structurally normal hearts. The diagnosis of the BrS is mainly based on the presence of a spontaneous or Na + channel blocker induced characteristic, electrocardiographic (ECG) pattern (type 1 or coved Brugada ECG pattern) typically seen in leads V1 and V2 recorded from the 4th to 2nd intercostal (i.c.) spaces. This pattern needs to be distinguished from similar ECG changes due to other causes (Brugada ECG phenocopies). This review focuses mainly on the ECG-based methods for diagnosis and arrhythmia risk assessment in the BrS. Presently, the main unresolved clinical problem is the identification of those patients at high risk of SCD who need implantable cardioverter-defibrillator (ICD), which is the only therapy with proven efficacy. Current guidelines recommend ICD implantation only in patients with spontaneous type 1 ECG pattern, and either history of aborted cardiac arrest or documented sustained VT (class I), or syncope of arrhythmic origin (class IIa) because they are at high risk of recurrent arrhythmic events (up to 10% or more annually for those with aborted cardiac arrest). The majority of BrS patients are asymptomatic when diagnosed and considered to have low risk (around 0.5% annually) and therefore not indicated for ICD. The majority of SCD victims in the BrS, however, had no symptoms prior to the fatal event and therefore were not protected with an ICD. While some ECG markers such as QRS fragmentation, infero-lateral early repolarisation, and abnormal late potentials on signal-averaged ECG are known to be linked to increased arrhythmic risk, they are not sufficiently sensitive or specific. Potential novel ECG-based strategies for risk stratification are discussed based on computerised methods for depolarisation and repolarisation analysis, a composite approach targeting several major components of ventricular arrhythmogenesis, and the collection of large digital ECG databases in genotyped BrS patients and their relatives.Abbreviations: AP, action potential; ARI, activation-recovery intervals; BrS, Brugada syndrome; ECG, electrocardiogram; EPS, electrophysiology study; ICD, implantable cardioverter-defibrillator; IHD, ischaemic heart disease; LBBB, left bundle branch block; MAP, monophasic action potential; MI, myocardial infarction; PCA, principal component analysis; RVOT, right ventricular outflow tract; SAECG, signal-averaged electrocardiogram; SCD, sudden cardiac death; SNP, single-nucleotide polymorphism; VF, ventricular fibrillation; VT, ventricular tachycardia; WT, wavelet transform     

Role of signal-averaged electrocardiograms for predicting the inducibility of ventricular fibrillation in the syndrome consisting of right bundle branch block and ST segment elevation in leads V1-V3

Right bundle branch block and ST segment elevation (RBBB-STE) in the right precordial leads have been reported as a distinct clinical and electrocardiographic syndrome in patients prone to ventricular fibrillation (VF) in the absence of structural heart disease (Brugada syndrome). The purpose of the study was to investigate the role of signal averaged electrocardiogram (SAECG) in identifying patients at high risk among asymptomatic RBBB-STE patients. Thirteen patients with the RBBB-STE ECG were identified. Symptoms were: syncope (n=3, cases 1, 3, and 11), atypical chest pain (n=3, cases 4, 10, and 12) and palpitations (n=2, cases 6, and 7). The other 5 patients were asymptomatic. SAECG and programmed electrical stimulation (PES) were conducted in all patients. Body surface late potentials (LPs) were present in 7 of 13 patients before PES. Vf was induced in 6 of 7 LP positive patients. Vf was induced in 3 of 6 LP negative patients, but LP became positive in 2 of 3 patients in whom Vf was induced. One patient with syncope due to VF (case 1), 1 patient without symptoms who died suddenly during follow up (case 2), and 1 asymptomatic patient (case 9) showed reproducibly positive LP. In a patient (case 9) with positive LP at baseline, LP transiently became negative during follow up. In RBBB-STE patients, reproducibly positive LP is at risk for malignant ventricular arrhythmias and sudden death. Repeated SAECG recording may be useful for screening high-risk patients who should receive electrophysiological study among asymptomatic RBBB-STE patients.     

Does early repolarization in the athlete have analogies with the Brugada syndrome?

AIMS: To re-examine the prevalence and presentation of early repolarization in athletes and to compare it with electrocardiographic abnormalities observed in patients with the Brugada syndrome. METHODS: Electrocardiograms of 155 male athletes and 50 sedentary controls were studied. Early repolarization was considered present if at least two adjacent precordial leads showed elevation of the ST segment > or =1 mm. Amplitude and morphology of ST elevation, the leads where it was present and the lead in which it showed its maximum value were analysed together with QRS duration, the presence of right ventricular activation delay, QT and QTc duration. Data were compared with those obtained by electrocardiograms of 23 patients with the Brugada syndrome. RESULTS: Early repolarization was found in 139 athletes (89%) and 18 controls (36%, P< or =0.025), being limited to right precordial leads in 42 (30%) athletes and 13 (72%) controls (P< or =0.001). Only 12 (8.6%) athletes and one control (5.5%) with early repolarization had an ST elevation 'convex toward the top' in right precordial leads, similar to that seen in the Brugada syndrome. In athletes the maximum ST elevation was greater (2.3+/-0.6 mm) than in the controls (1.2+/-0.8 mm; P< or =0.004) but significantly lower than in patients with the Brugada syndrome (4.4+/-0.7 mm; P< or =0.0001). Patients with the Brugada syndrome also had a greater QRS duration (0.11+/-0.02 s) than athletes (0.090+/-0.011 s; P< or =0.0001) with early repolarization. CONCLUSIONS: Early repolarization is almost always the rule in athletes but it is also frequent in sedentary males. Tracings somewhat simulating the Brugada syndrome were observed in only 8% of athletes without a history of syncope or familial sudden death. Significant differences exist between athletes with early repolarization and patients with the Brugada syndrome as regards the amplitude of ST elevation and QRS duration.     

Avoidance of right ventricular pacing in cardiac resynchronization therapy improves right ventricular hemodynamics in heart failure patients

Background: Cardiac resynchronization therapy (CRT) applied by pacing the left and right ventricles (BiV) has been shown to provide synchronous left ventricular (LV) contraction in heart failure patients. CRT may also be accomplished through synchronization of a properly timed LV pacing impulse with intrinsically conducted activation wave fronts. Elimination of right ventricular (RV) pacing may provide a more physiological RV contraction pattern and reduce device current drain. We evaluated the effects of LV and BiV pacing over a range of atrioventricular intervals on the performance of both ventricles.
Methods: Acute LV and RV hemodynamic data from 17 patients with heart failure (EF = 30 ± 1%) and a wide QRS (138 ± 25 msec) or mechanical dyssynchrony were acquired during intrinsic rhythm, BiV, and LV pacing.
Results: The highest LV dP/dt_max was achieved during LV pre- (LV paced prior to an RV sense) and BiV pacing, followed by that obtained during LV post-pacing (LV paced after an RV sense) and the lowest LV dP/dt_max was recorded during intrinsic rhythm. Compared with BiV pacing, LV pre-pacing significantly improved RV dP/dt_max (378 ± 136 mmHg/second vs 397 ± 136 mmHg/second, P < 0.05) and preserved RV cycle efficiency (61.6 ± 14.6% vs 68.6 ± 11.4%, P < 0.05) and stroke volume (6.6 ± 4.4 mL vs 9.0 ± 6.3 mL, P < 0.05). Based on LV dP/dt_max, the optimal atrioventricular interval could be estimated by subtracting 30 msec from the intrinsic atrial to sensed RV interval.
Conclusions: Synchronized LV pacing produces acute LV and systemic hemodynamic benefits similar to BiV pacing. LV pacing at an appropriate atrioventricular interval prior to the RV sensed impulse provides superior RV hemodynamics compared with BiV pacing.     

Development and Validation of an ECG Algorithm for Identifying Accessory Pathway Ablation Site in Wolff-Parkinson-White Syndrome

ECG Localization of Accessory AV Pathways. Introduction : Delta wave morphology correlates with the site of ventricular insertion of accessory AV pathways. Because lesions due to radiofrequency (RF) current are small and well defined, it may allow precise localization of accessory pathways. The purpose of this study was to use RF catheter ablation to develop an ECG algorithm to predict accessory pathway location.
Methods and Results : An algorithm was developed by correlating a resting 12-lead ECG with the successful RF ablation site in 135 consecutive patients with a single, anterogradely conducting accessory pathway (Retrospective phase). This algorithm was subsequently tested prospectively in 121 consecutive patients (Prospective phase). The ECG findings included the initial 20 msec of the delta wave in leads I, II, aVF, and V₁ [classified as positive (+), negative (-), or isoelectric (±)] and the ratio of R and S wave amplitudes in leads III and V₁ (classified as R ≥ S or R < S). When tested prospectively, the ECG algorithm accurately localized the accessory pathway to 1 of 10 sites around the tricuspid and mitral annuli or at subepicardial locations within the venous system of the heart. Overall sensitivity was 90% and specificity was 99%. The algorithm was particularly useful in correctly localizing anteroseptal (sensitivity 75%, specificity 99%), and mid-septal (sensitivity 100%, specificity 98%) accessory pathways as well as pathways requiring ablation from within ventricular venous branches or anomalies of the coronary sinus (sensitivity 100%, specificity 100%).
Conclusion : A simple ECG algorithm identifies accessory pathway ablation site in Wolff-Parkinson-White syndrome. A truly negative delta wave in lead II predicts ablation within the coronary venous system.     

Further Characterization of the Syndrome of Right Bundle Branch Block, ST Segment Elevation, and Sudden Cardiac Death

RBBB, ST Elevation, and SCD. We recently described a syndrome characterized by an ECG pattern of right bundle branch block and persistent ST segment elevation in leads V₁ to V₃ in patients suffering from aborted sudden cardiac death and not having demonstrable structural heart disease. We present new observations on this syndrome, especially those related to asymptomatic and intermittent forms. Forty-seven patients with the described ECG pattern were identified; 32 were symptomatic with syncope and sudden death aborted by cardiopulmonary resuscitation. Eleven patients received pharmacologic therapy, mainly amiodarone and/or beta-blocking agents, and 21 patients received an implantable defibrillator with or without pharmacologic therapy. Three of the 11 patients on pharmacologic therapy died suddenly during follow-up, while 9 of 21 patients with an implantable defibrillator used the device during follow-up. The remaining 15 patients were asymptomatic when first seen. Three patients died suddenly after 6 years, 3 months, and 2 months of follow-up without treatment. Another patient received an implantable defibrillator after syncope and had subsequent episodes of ventricular fibrillation terminated by the defibrillator. The other 11 patients remain asymptomatic without (6) or with (5) treatment with beta blockers. In 14 of the 47 patients, the ECG normalized momentarily during follow-up but later became abnormal again. During transient normalization of the ECG, administration of ajmaline or procainamide unmasked the described ECG pattern in six patients who received the drug. Long-term follow-up of survivors failed to show progression to any form of right or left ventricular cardiomyopatby.     

Electrocardiographic (ECG) clues to differentiate idiopathic right ventricular outflow tract tachycardia (RVOTT) from arrhythmogenic right ventricular cardiomyopathy (ARVC)

Introduction

Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is a genetic cardiomyopathy that most commonly affects young adults. The most commonly observed reason of death in patients suffering from ARVC/D is sudden cardiac death (SCD). On the other hand, idiopathic right ventricular outflow tract tachycardia (RVOT VT) usually has a benign course. Both of the entities may have ventricular tachycardia (VT) with left bundle branch block (LBBB) pattern and inferior axis. We tried to propose new discriminating electrocardiographic indices for differentiation of foretold entities.

Material and method

This was a retrospective study. We reviewed records of patients admitted between 2003 and 2012 with the diagnosis of either ARVC/D or RVOT VT that presented with VT (LBBB morphology).

Result

A total of fifty nine patients (30 RVOT VT and 29 ARVC/D) were enrolled. In ARVC/D group, men were dominant while the reverse was true of RVOT VT. Palpitation was more common in the RVOT VT group (90% vs. 66.7%), but aborted SCD and sustained VT were more common in ARVC/D group. The new ECG criteria proposed by us mean QRS duration in V1–V3, QRS difference in right and left precordial leads, S wave upstroke duration, JT interval dispersion, QRS and JT interval of right to left precordial leads were all significantly longer in ARVC/D when compared to RVOT VT patients (p < 0.001).

Conclusion

The proposed ECG criteria can be used for non-invasive diagnosis of ARVC/D and incorporation in the future updates of ARVC/D task force criteria.