Interventricular mechanical asynchrony in pulmonary arterial hypertension: left-to-right delay in peak shortening is related to right ventricular overload and left ventricular underfilling.

OBJECTIVES: The purpose of this study was to explore in pulmonary arterial hypertension (PAH) whether the cause of interventricular asynchrony lies in onset of shortening or duration of shortening. BACKGROUND: In PAH, leftward ventricular septal bowing (LVSB) is probably caused by a left-to-right (L-R) delay in myocardial shortening. METHODS: In 21 PAH patients (mean pulmonary arterial pressure 55 +/- 13 mm Hg and electrocardiogram-QRS width 100 +/- 16 ms), magnetic resonance imaging myocardial tagging (14 ms temporal resolution) was applied. For the left ventricular (LV) free wall, septum, and right ventricular (RV) free wall, the onset time (T(onset)) and peak time (T(peak)) of circumferential shortening were calculated. The RV wall tension was estimated by the Laplace law. RESULTS: The T(onset) was 51 +/- 23 ms, 65 +/- 4 ms, and 52 +/- 22 ms for LV, septum, and RV, respectively. The T(peak) was 293 +/- 58 ms, 267 +/- 22 ms, and 387 +/- 50 ms for LV, septum, and RV, respectively. Maximum LVSB was at 395 +/- 45 ms, coinciding with septal overstretch and RV T(peak). The L-R delay in T(onset) was -1 +/- 16 ms (p = 0.84), and the L-R delay in T(peak) was 94 +/- 41 ms (p < 0.001). The L-R delay in T(peak) was not related to the QRS width but was associated with RV wall tension (p < 0.05). The L-R delay in T(peak) correlated with leftward septal curvature (p < 0.05) and correlated negatively with LV end-diastolic volume (p < 0.05) and stroke volume (p < 0.05). CONCLUSIONS: In PAH, the L-R delay in myocardial peak shortening is caused by lengthening of the duration of RV shortening. This L-R delay is related to LVSB, decreased LV filling, and decreased stroke volume.     

Mechanical right ventricular dyssynchrony in patients after atrial switch operation for transposition of the great arteries

Recent data suggest potential benefits of cardiac resynchronization therapy in the management of right ventricular (RV) dysfunction in congenital heart disease. The aim of this study was to determine the nature, prevalence, and functional implications of mechanical RV dyssynchrony in patients after Senning or Mustard procedures for transposition of the great arteries. Twenty-eight patients (mean age 21.1 +/- 3.5 years) at 19.9 +/- 3.2 years after atrial switch operations and 29 healthy controls were studied. The times from the onset of QRS to peak systolic strain (T epsilon) at the base of and the mid RV free wall, the ventricular septum (VS), and the left ventricular (LV) free wall were determined using tissue Doppler echocardiography. Intraventricular mechanical delay was defined as Delta T epsilon(RV-VS) and interventricular mechanical delay as Delta T epsilon(RV-LV). In patients, the magnitude of RV intra- and interventricular mechanical delay was correlated with cardiac magnetic resonance-derived RV volumes and ejection fractions (n = 26) and treadmill exercise testing parameters (n = 20). Compared with controls, patients had significantly longer Delta T epsilon(RV-VS) (48.1 +/- 50.9 vs 17.0 +/- 16.1 ms, p <0.001) and Delta T epsilon(RV-LV) (63.1 +/- 49.5 vs 19.0 +/- 12.9, p <0.001). Nine patients (32%) exhibited RV dyssynchrony (Delta T epsilon(RV-VS) >49 ms, control mean +/- 2SD), and 16 patients (57%) showed interventricular dyssynchrony (Delta T epsilon(RV-LV) >45 ms). In patients, RV intra- and interventricular mechanical delay was correlated negatively with the RV ejection fraction (both r = -0.42, p = 0.03) and percentage predicted maximum oxygen consumption (r = -0.50, p = 0.03, and r = -0.52, p = 0.02, respectively) and positively with minute ventilation/carbon dioxide production slope (r = 0.49, p = 0.03, and r = 0.56, p = 0.01, respectively). In conclusion, RV dyssynchrony is common in young adults after atrial switch operations and is associated with RV systolic dysfunction and impaired exercise performance.     

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.     

Effects of resynchronization therapy on cardiac function in pacemaker patients "upgraded" to biventricular devices

INTRODUCTION: Cardiac resynchronization therapy (CRT) improves echocardiographic measures of cardiac function and has a variable effect on QRS duration in patients with left bundle branch block (LBBB). How CRT affects these indices in patients with right ventricular (RV) pacing-induced LBBB who are "upgraded" with left ventricular (LV) leads for CRT is unknown. We studied the echocardiographic effects of RV pacing and CRT in patients with prior continuous RV pacing after LV lead placement. METHODS AND RESULTS: Fifteen consecutive patients (age 73 +/- 11 years, LV ejection fraction 24 +/- 6%, QRS duration 190 +/- 27 msec) with New York Heart Association class IIIB-IV symptoms and continuous RV pacing underwent LV lead placement for CRT. Echocardiography and ECG were performed sequentially during RV pacing and CRT. CRT was associated with significantly reduced QRS duration (190 +/- 27 msec vs 165 +/- 18 msec, P = 0.005) and reduced LV electromechanical delay (180 +/- 33 msec vs 161+/- 43 msec). Baseline QRS duration correlated with CRT response. After CRT, patients had significant improvements in indices of systolic function, including LV ejection fraction, myocardial performance index (MPI), and LV ejection time. Abnormal baseline MPI was associated with greater improvement after CRT. LV end-diastolic and systolic volumes were similarly decreased with CRT. Mitral valve deceleration time, an index of diastolic function, was not affected by CRT. CONCLUSION: "Upgrading" RV paced patients with advanced heart failure to CRT improves measures of electrical and LV mechanical synchrony and improves systolic function.     

Prolonged QRS duration in lead V2 and risk of life-threatening ventricular Arrhythmia in patients with Brugada syndrome

Brugada syndrome is an inherited disorder that predisposes some patients to sudden cardiac death. It is not well established which Brugada syndrome patients are at risk of life-threatening arrhythmias. We investigated whether standard 12-lead electrocardiograms (ECG) can identify such patients. The subjects were 35 men with Brugada syndrome (mean age, 50.1 ± 12.4 years). Documented ventricular fibrillation or aborted sudden cardiac arrests were judged to be related to the Brugada syndrome. Ten patients (mean age, 49.6 ± 14.9 years) were symptomatic, and 25 (mean age, 50.3 ± 11.5 years) were asymptomatic. We determined the PR interval, QRS duration, and QT interval from baseline 12-lead ECG leads II and V2 as well as the J point elevation amplitude of lead V2. The QRS interval was measured from QRS onset to the J point in leads II and V2. The only significant difference between the symptomatic and asymptomatic patients was the QRS duration measured from lead V2. The mean QRS interval was 129.0 ± 23.9 ms in symptomatic patients versus 108.3 ± 15.9 ms in asymptomatic patients (P = 0.012). A QRS interval in lead V2 ≥ 120 ms was found to be a possible predictor of a life-threatening ventricular arrhythmia and/or syncope (P = 0.012). Prolonged QRS duration as measured on a standard 12-lead ECG is associated with ventricular arrhythmia and could serve as a simple noninvasive marker of vulnerability to life-threatening cardiac events in patients with Brugada syndrome.     

Discrimination of Brugada syndrome patients from individuals with the saddle-back type ST-segment elevation using a marker of the standard 12-lead electrocardiography.

BACKGROUND: In the clinical situation, the saddle-back (S-B) type is more frequently detected than the coved type. In the present study, the discrimination of Brugada syndrome from the S-B type individuals using a marker of the standard 12-lead electrocardiography (ECG) was attempted. METHODS AND RESULTS: The study group consisted of 55 individuals with the S-B type in whom pilsicainide provocation test (PLC test) was carried out. The time from the onset of the QRS wave in lead V(2) (IV (2)) to the peak of the late R-like wave in the QRS wave (PV(2)), and the time from IV(2) to the offset of the QRS wave in lead V(5) (EV(5)) were measured. The coved type was induced by the PLC test in 29 cases (N-C group), but not in the remaining 26 cases (N-N group). The (IV(2) -PV(2)) - (IV(2) - EV(5)) value before the PLS test was greater in the N-C group than in the N-N group. The negative predictive value of ;(IV(2) - PV(2)) - (IV(2) - EV(5)) > or =0' was 76.4% for the prediction of a positive PLC test. CONCLUSIONS: A ;(IV(2) - PV(2)) - (IV(2) - EV(5)) > or =0' is a useful ECG marker for the discrimination of Brugada syndrome in the S-B type individuals.     

QT-interval prolongation in right precordial leads: an additional electrocardiographic hallmark of Brugada syndrome

OBJECTIVES: The aim of this study was to evaluate whether the occurrence of the Brugada Syndrome typical electrocardiogram (ECG) pattern (i.e., right bundle branch block, coved-type ST-segment elevation, and T-wave inversion in the right precordial leads) is characterized by a concomitant lengthening of QT intervals in the right precordial leads. BACKGROUND: It has been suggested that the typical ECG pattern of Brugada syndrome is due to a decreased net inward current during phase 1 of the action potential, which also leads to its prolongation in the right epicardium. METHODS: Thirty-two subjects (19 males) age 37 +/- 15 years with a suspicious baseline ECG, or who were relatives of Brugada syndrome patients, underwent 12-lead ECG before and after the administration of flecainide. RESULTS: The flecainide test was negative in 14 and positive in 18 subjects. After flecainide administration, the positive ECGs were characterized by a greater QT interval corrected for heart rate (QTc) prolongation in the right precordial leads than that in the negative ECGs (78.2 +/- 35.5 ms vs. 22.0 +/- 28.4 ms in V(1) and 107.1 +/- 43.8 ms vs. 26.7 +/- 30.1 ms in V(2); p < 0.01), whereas there was no difference in the QTc prolongation in the left precordial leads (55.2 +/- 25.3 ms vs. 35.1 +/- 28.1 ms in V(5) and 53.1 +/- 32.8 ms vs. 27.3 +/- 22.4 ms in V(6); p = NS). CONCLUSIONS: In accordance with the electrophysiological background, the typical ECG pattern of Brugada syndrome is also characterized by a considerable prolongation of the QT interval in right precordial leads.     

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.     

Conduction Delay in Right Ventricle as a Marker for Identifying High‐Risk Patients With Brugada Syndrome

Conduction Delay as a Marker for Brugada Syndrome. Objectives: To evaluate the significance of conduction delay (CD) in the right ventricle (RV) in Brugada syndrome (BS) as a marker for risk stratification of sudden death. Methods: Twenty‐five patients with BS (7 with documented ventricular fibrillation (VF), 8 with syncope, and 10 without symptoms) and 10 control subjects were paced from the RV apex using 8 beats of drive pacing and a single extra‐stimulus. CDs in the right ventricular outflow tract (RVOT) (CD‐RV) and in the lateral left ventricle (L‐LV) (CD‐LV), and the local electrogram durations at a single extra‐stimulus in RVOT (D‐RV) and L‐LV (D‐LV) were calculated. We also evaluated changes in 12‐lead ECG parameters in 16 patients with BS after pilsicainide challenge test (Pilsicainide‐test). Results: Maximal CD‐RV and maximal D‐RV were significantly larger than maximal CD‐LV and maximal D‐LV in BS (26 ± 10 and 105 ± 15 vs 20 ± 6 and 92 ± 15 ms, P < 0.05, respectively). Maximal CD‐RV and maximal D‐RV in patients with documented VF were the largest among the 3 groups. There was a significant positive correlation between maximal CD‐RV or maximal D‐RV and changes in QRS duration in leads V2 and V5 and in S wave duration in lead II and V5 after Pilsicainide‐test (CD‐RV; r = 0.54, 0.51, 0.56, and 0.53: D‐RV; r = 0.55, 0.5, 0.57, and 0.53, P < 0.05, respectively). In control subjects, there were no significant differences. Conclusions: CD in RV was a useful marker for identifying high‐risk patients with BS. CD in the RV, especially in the RVOT epicardium, may be related to arrhythmias in BS. (J Cardiovasc Electrophysiol, Vol. 21, pp. 688‐696, June 2010)     

A prospective study on spontaneous fluctuations between diagnostic and non-diagnostic ECGs in Brugada syndrome: implications for correct phenotyping and risk stratification.

AIMS: Fluctuations between the diagnostic ECG pattern and non-diagnostic ECGs in patients with Brugada syndrome are known, but systematic studies are lacking. The purpose of this study was to prospectively evaluate the spontaneous ECG changes between diagnostic and non-diagnostic ECG patterns in patients diagnosed with Brugada syndrome. METHODS AND RESULTS: In 43 patients with Brugada syndrome (27 males; mean age 45+/-11 years), 310 resting ECGs were obtained during a median follow-up of 17.7 months. The ECGs were analysed for the presence of coved type, saddle-back type or no, respectively unspecific, changes. A coved-type ECG pattern with more than 2 mm ST-segment elevation in at least two right precordial leads was defined as diagnostic. The patients were compared for different clinical characteristics with respect to the pattern of fluctuations. Out of a total of 310 ECGs, 102 (33%) revealed a coved type, 91 (29%) a saddle-back type, and 117 (38%) a normal ECG. Fifteen patients (35%) initially presented with a diagnostic coved-type ECG. Fourteen patients (33%) with an initially coved-type ECG exhibited intermittently non-diagnostic ECGs during follow-up. Only one patient (2%) presented constantly with a coved-type ECG. Out of 28 patients (65%) with an initially non-diagnostic ECG, eight (19%) patients developed a diagnostic coved-type ECG during follow-up. Twenty patients (47%) revealed a coved-type ECG during ajmaline challenge, but never had a baseline coved-type ECG recorded. No significant differences were found in gender and clinical characteristics among patients with or without fluctuations between diagnostic and non-diagnostic basal ECGs. The rate of inducible ventricular fibrillation was significantly higher in patients with more than 50% coved-type ECGs than in patients with less than 50% diagnostic ECGs. CONCLUSION: The prevalence of fluctuations between diagnostic and non-diagnostic ECGs in patients with Brugada syndrome is high and may have an implication on the correct phenotyping and on the risk stratification in patients with Brugada syndrome without aborted sudden cardiac death. For correct phenotyping and risk stratification, repetitive ECG recordings seem to be mandatory.     

Variable patterns of septal activation in patients with left bundle branch block and heart failure

INTRODUCTION: Little is known about the septal activation pattern in patients with heart failure and left bundle branch block (LBBB-HF). METHODS AND RESULTS: The right ventricular (RV) and left ventricular (LV) activation patterns of 12 patients (mean age 67 +/- 11 years) with LBBB-HF and 5 patients (mean age 45 +/- 14) with normal hearts were studied during sinus rhythm using a three-dimensional mapping system. The etiology of HF was myocardial infarction (n = 4) or idiopathic dilated cardiomyopathy (n = 8). In patients with LBBB-HF, endocardial activation usually started before the onset of the surface QRS complex on the RV free wall. Latest RV activation occurred in the basal region, and total RV activation time was longer than in patients with normal hearts. In patients with LBBB-HF, the left septum was activated via slowly conducting LBB or via right-to-left transseptal conduction. In both patients with LBBB-HF and those with normal hearts, latest LV activation occurred either in the posterior or posterolateral-basal region. Conduction velocity was slower in the peri-scar region, in patients with previous myocardial infarct and globally slow, in patients with idiopathic dilated cardiomyopathy. CONCLUSION: The two types of left septal activation observed in patients with LBBB-HF may have consequences for biventricular hemodynamic performance. Conduction slowing along the LV, regionally or globally, suggests a contribution outside the specific conduction system in the ECG pattern of LBBB.     

Effects of cardiac resynchronization therapy on ventricular repolarization in patients with congestive heart failure

INTRODUCTION: Biventricular pacing has been shown to improve the clinical status of patients with congestive heart failure, but little is known about its influence on ventricular repolarization. The aim of our study was to evaluate the effect of biventricular pacing on ECG markers of ventricular repolarization in patients with congestive heart failure. METHODS AND RESULTS: Twenty-five patients with congestive heart failure, sinus rhythm (SR), and complete LBBB (6 females; age 61 +/- 8 years; NYHA class II-III; echocardiographic ejection fraction 21 +/- 5%; QRS > or = 130 ms) underwent permanent biventricular DDDR pacemaker implantation. A high-resolution 65-lead body-surface ECG recording was performed at baseline and during right-, left-, and biventricular pacing, and the total 65-lead root mean square curve of the QRST complex and the interlead QT dispersion were assessed. The QRS duration was increased during right (RV)- and left ventricular (LV) pacing (127 +/- 26% and 117 +/- 40%; P < 0.05), as compared to SR (100%) and biventricular pacing (93 +/- 16%; ns). The QTc interval was increased during RV and LV pacing (112 +/- 12% and 114 +/- 14%; P < 0.05) as compared to SR (100%) or biventricular pacing (99 +/- 12%). There was no effect on JT interval during all pacing modes. The T(peak-end) interval was increased during right (120 +/- 34%; P < 0.01) and LV pacing (113 +/- 29%; P < 0.05) but decreased during biventricular pacing (81 +/- 19%; P < 0.01). A similar effect was found for the T(peak-end) integral and the T(peak) amplitude. QT dispersion was increased during right ventricular (129 +/- 16 ms; P < 0.05) and decreased during biventricular pacing (90 +/- 12 ms; P < 0.01), as compared to SR (114 +/- 22 ms). CONCLUSIONS: Using a high-resolution surface ECG, biventricular pacing resulted in a significant reduction of ECG markers of ventricular dispersion of repolarization.     

Electrocardiographic optimization of interventricular delay in cardiac resynchronization therapy: a simple method to optimize the device

Introduction: Echocardiography is widely used to optimize CRT programming, but it is time-consuming. This study aimed to correlate the optimal interventricular pacing (V-V) interval obtained by echo with the optimal V-V interval obtained by a simpler method based on the surface ECG.
Methods and Results : Three V-V intervals were tested: LV preactivation at –30 ms, simultaneous biventricular pacing (0 ms), and RV preactivation at +30 ms. The one that achieved the best LV synchrony was chosen as the optimal V-V. This result was then compared with two different ECG measurements. The first ECG method considered the best V-V to be that which achieved the narrowest QRS. The second V-V method consisted in measuring the interval from the pacing spike to the beginning of the fast deflexion of the QRS complex in leads V1, V2, first pacing from the LV (T1), and after from the RV (T2). The T2-T1 interval was considered as a surrogate measurement of interventricular delay and defined as the best V-V. A cohort of 31 consecutive patients treated with CRT was studied. Optimal V-V interval obtained by echo was –30 ms in 25 patients (80%), +30 ms in three patients (10%), and 0 ms in the remaining three patients (10%). Echo results had 32% coincidence with the first ECG method (r = 0.2, P = NS) and 83% coincidence with the second ECG method (r = 0.81 P< 0.001).
Conclusions : The time difference in the fast ventricular depolarization observed between RV and LV stimulation in the surface ECG shows a good correlation with the V-V optimization chosen according to echo.     

Dispersion of repolarization in cardiac resynchronization therapy

BACKGROUND: Proarrhythmic effects of cardiac resynchronization therapy (CRT) as a result of increased transmural dispersion of repolarization (TDR) induced by left ventricular (LV) epicardial pacing in a subset of vulnerable patients have been reported. The possibility of identifying these patients by ECG repolarization indices has been suggested. OBJECTIVES: The purpose of this study was to test whether repolarization indices on the ECG can be used to measure dispersion of repolarization during pacing. METHODS: CRT devices of 28 heart failure patients were switched among biventricular, LV, and right ventricular (RV) pacing. ECG indices proposed to measure dispersion of repolarization were calculated. The effects of CRT on repolarization were simulated in ECGSIM, a mathematical model of electrocardiogram genesis. TDR was calculated as the difference in repolarization time between the epicardial and endocardial nodes of the heart model. RESULTS: Patients: The interval from the apex to the end of the T wave was shorter during biventricular pacing (102 +/- 18 ms) and LV pacing (106 +/- 21 ms) than during RV pacing (117 +/- 22 ms, P < or =.005). T-wave amplitude and area were low during biventricular pacing (287 +/- 125 microV and 56 +/- 22 microV.s, respectively, P = .0006 vs RV pacing). T-wave complexity was high during biventricular pacing (0.42 +/- 0.26, P = .004 vs RV pacing). Simulations: Repolarization patterns were highly similar to the preceding depolarization patterns. The repolarization patterns of different pacing modes explained the observed magnitudes of the ECG repolarization indices. Average and local TDR were not different between pacing modes. CONCLUSION: In patients treated with CRT, ECG repolarization indices are related to pacing-induced activation sequences rather than transmural dispersion. TDR during biventricular and LV pacing is not larger than TDR during conventional RV endocardial pacing.     

Clinical significance of electrocardiography recordings from a higher intercostal space for detection of the brugada sign.

BACKGROUND: The significance of higher intercostal space electrocardiography (HICS ECG) for the detection of the Brugada sign was investigated. METHODS AND RESULTS: The subjects consisted of 113 cases (108 males, 5 females; mean age, 57+/-17 years) with incomplete right bundle branch block type QRS morphology and ST-segment elevation (>0.10 mV) in the right precordial leads. Obvious structural heart disease was not observed in any of the subjects. The V(1-3) leads of the standard 12-lead ECG and the HICS ECG were recorded in the supine position, and the amplitude of the terminal portion of the QRS (J-point) and ST-segment (80 ms from the J-point) were measured. In the HICS ECG, there was an increase in the area in which the Brugada sign was detectable (47 leads to 66 leads), and in cases with the Brugada sign, the amplitude of the J-point increased. CONCLUSIONS: The HICS ECG may be helpful for the detection of the Brugada sign.     

心电图与超声心动图优化VV间期的对比研究

目的 评价心电图在心脏再同步治疗（CRT）患者VV间期优化中的作用.方法 入选30例心功能Ⅲ～Ⅳ级（NYHA分级）CRT患者（男27例,女3例）,年龄42 ～79（63.3±10.6）岁.植入1个月后,分别程控为单独右心室起搏和单独左心室起搏,记录体表心电图.左心室起搏时,记录胸前导联从起搏信号到QRS波起始部假δ波结束之间的间期（T1）;右心室起搏时,记录胸前导联从起搏信号到QRS波开始改变之间的间期（T2）.T1 -T2的值为从心室侧壁与间隔部同步除极左心室所需的时间延迟,为最佳左-右心室激动的间期（Optimal VV间期）.同时采用超声扫描测定不同VV间期时的主动脉速度时间积分（VTI）,产生最大VTI间期为最佳VV间期,对比两种方法结果.结果 超声优化最佳VV间期在左心室领先起搏-30 ms、-70 ms时分别有20例、5例;左、右心室同步起搏（0 ～5 ms）时有3例;右心室领先起搏＋30 ms时有2例.心电图优化最佳VV间期在左心室领先起搏-30 ms、-70 ms时分别有19例和5例;左、右心室同步起搏时有4例;右心室领先起搏＋30 ms时有2例.两种方法相关性良好.结论 采用心电图可计算出CRT患者最佳VV间期,与超声心动图相关性良好.     

Mechanisms underlying increased right ventricular conduction sensitivity to flecainide challenge

AIMS: The cardiac sodium current (I(Na)) is a major determinant of conduction. Mechanisms underlying regionally heterogeneous conduction slowing secondary to reduced I(Na) in diseases such as the Brugada syndrome and heart failure remain incompletely understood. Right precordial electrophysiological manifestations during flecainide challenge suggest a decreased right ventricular depolarization reserve. We hypothesized that heterogeneous cardiac sodium channel (Na(v)1.5) distribution between ventricles causes interventricular depolarization heterogeneities. METHODS AND RESULTS: Western blotting analysis revealed Na(v)1.5, and Kir2.1 protein expressions were 18.2 and 12.0% lower, respectively, in the guinea pig right ventricle (RV) compared with the left ventricle (LV). Conduction velocity (theta) heterogeneities were quantified by optical mapping during LV or RV pacing. Although RV transverse theta((thetaT)) was significantly greater than LV (thetaT) by 33.09 +/- 1.38% under control conditions, there were no differences in longitudinal theta. During partial sodium channel blockade (flecainide, 0.5 microM), RV theta decreased by 35.3 +/- 1.3%, whereas LV theta decreased by 29.2 +/- 1.0%. These data demonstrate that the RV has an increased conduction dependence on sodium channel availability. Partial blockade of the inward rectifier potassium current (I(K1)) by BaCl(2) (10 microm) significantly increased theta in both ventricles under control conditions. However, BaCl(2) only increased conduction dependence on sodium channel availability in the LV. This suggests that the LV may have an increased depolarization reserve compared with the RV, but the larger I(K1) depresses control LV theta. CONCLUSION: Interventricular I(K1) heterogeneities may underlie conduction heterogeneities observed under control conditions. However, under conditions where I(Na) is functionally reduced in disease or during pharmacological sodium channel blockade, the heterogeneity in Na(v)1.5 expression may become a significant determinant of conduction heterogeneities.     

Tpeak-Tend and Tpeak-Tend dispersion as risk factors for ventricular tachycardia/ventricular fibrillation in patients with the Brugada syndrome.

OBJECTIVES: Our objective in this study was to evaluate Tpeak-Tend interval (Tp-e) and other electrocardiographic parameters as risk factors for recurrence of life-threatening cardiac events in patients with the Brugada syndrome (BS). BACKGROUND: The Tp-e interval in the electrocardiogram (ECG) has been reported to predict life-threatening arrhythmias in the long QT syndrome. METHODS: Twenty-nine patients with the ECG pattern of BS and 29 healthy age- and gender-matched controls were studied. The follow-up period was 42.65 +/- 24.42 months (range 11 to 108 months). RESULTS: Upon presentation, five patients had suffered aborted sudden death, five syncope, and two presyncope. Eleven patients with the ECG pattern of BS had a prolonged (>460 ms) QTc in V2 but usually not in inferior or left leads. No patient had abnormally prolonged QT dispersion. Programmed electrical stimulation induced ventricular tachycardia/fibrillation in 5 out of 26 patients. Inducibility did not predict recurrence of events. Cardioverter-defibrillators were implanted in 14 patients (all symptomatic and two asymptomatic). During follow-up, nine symptomatic patients experienced recurrences. Previous cardiac events and a QTc >460 ms in V2 were significant risk factors (p = 0.00002 and p = 0.03, respectively). Tp-e and Tp-e dispersion were significantly prolonged in patients with recurrences versus patients without events (104.4 and 35.6 ms vs. 87.4 and 23.2 ms; p = 0.006 and p = 0.03, respectively) or controls (90.7 and 17.9 ms; p = 0.02 and p = 0.001, respectively). CONCLUSIONS: Our study demonstrates significant correlation between previous events, QTc >460 ms in V2, Tp-e, and Tp-e dispersion and occurrence of life-threatening arrhythmic events, suggesting that these parameters may be useful in risk stratification of patients with the Brugada syndrome.     

Improved left ventricular mechanics from acute VDD pacing in patients with dilated cardiomyopathy and ventricular conduction delay

BACKGROUND: Ventricular pacing can improve hemodynamics in heart failure patients, but direct effects on left ventricular (LV) function from varying pacing site and atrioventricular (AV) delay remain unknown. We hypothesized that the magnitude and location of basal intraventricular conduction delay critically influences pacing responses and that single-site pacing in the delay-activated region yields similar or better responses to biventricular pacing. METHODS AND RESULTS: Aortic and LV pressures were measured in 18 heart failure patients (mean+/-SD: LV ejection fraction, 19+/-7%; LV end-diastolic pressure, 25+/-8 mm Hg; QRS duration, 157+/-36 ms). Data under normal sinus rhythm were compared with ventricular pacing (VDD) at varying sites and AV delays (randomized order). Right ventricular (RV) apical or midseptal pacing had negligible contractile/systolic effects. However, LV free-wall pacing raised dP/dtmax by 23.7+/-19.0% and pulse-pressure by 18.0+/-18.4% (P<0.01). Biventricular pacing yielded less change (+12.8+/-9.3% in dP/dtmax, P<0.05 versus LV). Pressure-volume analysis performed in 11 patients consistently revealed minimal changes with RV pacing but increased stroke work and lower end-systolic volumes with LV pacing. Optimal AV intervals averaged 125+/-49 ms, and within this range, AV delay had less influence on LV function than pacing site. Basal QRS duration positively correlated with %DeltadP/dtmax (P<0.005), but pacing efficacy was not associated with QRS narrowing. Conduction delay pattern generally predicted pacing sites with most effect. CONCLUSIONS: VDD pacing acutely enhances contractile function in heart failure patients with intraventricular conduction delay. Single-site pacing at the site of greatest delay achieves similar or greater benefits to biventricular pacing in such patients. These data clarify pacing-effect mechanisms and should help in candidate identification for future studies.     

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.