The spectrum of inter- and intraventricular conduction abnormalities in patients eligible for cardiac resynchronization therapy

Although cardiac resynchronization therapy (CRT) has clearly demonstrated its clinical benefit in patients with congestive heart failure (CHF) and intraventricular conduction abnormalities, selection of eligible patients and/or optimal pacing site are still a matter of debate. The aim of the study was to analyze the spectrum of conduction abnormalities in CRT candidates. A total of 26 patients (mean age 62 +/- 9 years) with CHF and conduction disturbances (QRS > or = 130 ms) were studied. The underlying heart disease was dilated cardiomyopathy (DCM) (n = 12) or coronary artery disease (CAD) (n = 14). High density, left ventricular endocardial activation maps were constructed using an electroanatomic mapping system (CARTO). Based on endocardial activation patterns, left ventricular conduction abnormalities were classified as left bundle branch block (LBBB) (n = 9), nonspecific intraventricular conduction disturbances (n = 10), and the bifascicular block (n = 7). In DCM patients the endocardial activation sequences corresponded with a 12-lead ECG pattern with a homogeneous spread of activation wavefront and the latest activation laterally (LBBB) or anteriorly (bifascicular block), respectively. CAD patients presented with variable activation patterns that reflected the location of the postinfarct scar, and the 12-lead ECG was less predictive. Although there was a trend for longer QRS durations for DCM subjects (170 +/- 23 vs 156 +/- 23 ms, P = NS), left ventricular activation time was significantly longer in the CAD group (115 +/- 21 ms vs 134 +/- 23 ms, P < 0.05). CRT candidates represent a broad spectrum of conduction abnormality patterns with variable inter- and intraventricular activation delays. CAD subjects have more pronounced intraventricular conduction abnormality. The standard ECG is less reliable in the characterization of complex conduction abnormalities.     

Activation sequence modification during cardiac resynchronization by manipulation of left ventricular epicardial pacing stimulus strength

BACKGROUND: Success of cardiac resynchronization therapy (CRT) depends on altering electrical ventricular activation (VA) to achieve mechanical benefit. That increases in stimulus strength (SS) can affect VA has been demonstrated previously in cardiomyopathy patients undergoing ablation. OBJECTIVE: To determine whether increasing SS can alter VA during CRT. METHODS: In 71 patients with CRT devices, left ventricle (LV) pacing was performed at escalating SS. Timing from pacing stimulus to right ventricular (RV) electrogram, ECG morphology, and maximal QRS duration on 12 lead ECG were recorded. RESULTS: Demographics: Baseline QRS duration 153 +/- 25 ms, ischemic cardiomyopathy 48%, ejection fraction 24%+/- 7%. With increased SS, conduction time from LV to right ventricle (RV) decreased from 125 +/- 56 ms to 111 +/- 59 ms (P = 0.006). QRS duration decreased from 212 +/- 46 ms to 194 +/- 42 ms (P = 0.0002). A marked change in QRS morphology occurred in 11/71 patients (15%). The RV ring was the anode in 6, while the RV coil was the anode in 5. Sites with change in QRS morphology showed decrease in conduction time from LV to RV from 110 +/- 60 ms to 64 +/- 68 ms (P = 0.04). Twelve patients (16%) had diaphragmatic stimulation with increased SS. CONCLUSIONS: Increasing LV SS reduces QRS duration and conduction time from LV to RV. Recognition of significant QRS morphology change is likely clinically important during LV threshold programming to avoid unintended VA change.     

心肌组织速度成像评价慢性心力衰竭患者心室收缩不同步性及其与QRS间期相关性的研究

目的应用心肌组织速度成像（TVI）评价慢性心力衰竭患者左心室收缩不同步性与心电图QRS间期的关系。方法选取心功能NYHAⅢ～1V级的扩张性心肌病（DCM）患者60例作为研究对象，依QRS间期分为DCMI组21例（QRS间期〈120ms）、DCMII组21例（QRS间期120～150ms）和DCMⅢ组18例（QRS间期〉150ms）；对照组为30例健康志愿者。分别测量QRS波起点到主动脉瓣血流频谱起始点时间（Q-AO）和到肺动脉瓣血流频谱起始点时间（Q-Pulm），采用两者的差值即心室间机械延迟参数（IVMD）评价左右心室间的同步性。获取左心室各节段心肌TVI曲线，测量各节段从心电图QRS波起点到TVI曲线S波起点的时间（Q-Sb），取18节段Q-Sb的标准差作为左心室内同步性指数（TSI），取各室壁基底段和心尖段Q-Sb的差值作为各室壁内的同步性指数（RSI）。结果以IVMD〉40ms为判定左右心室间不同步的截点值，在DCM Ⅰ、Ⅱ、Ⅲ组中观察到室间非同步性的患者分别为4、10和13例，发生率差异无统计学意义（P〈0．01），且IVMD与QRS间期密切相关（r=0．73，P〈0．01）。DCM组TSI和RSI较对照组显著延长（P〈0．01），但TSI和RSI与QRS间期无明显相关性。结论DCM患者心室间非同步性和QRS间期相关，左心室各室壁间与各室壁内非同步性和QRS间期无明显相关性。     

Prolonged paced QRS duration as a predictor for congestive heart failure in patients with right ventricular apical pacing

BACKGROUND: The recent studies showed that right ventricular (RV) pacing was associated with worsening of heart failure. The aim of this study is to clarify the clinical significance of paced QRS duration during RV pacing to predict congestive heart failure (CHF) patients. METHODS AND RESULTS: This study enrolled in 92 patients with atrioventricular block who underwent initial pacemaker implantation. The paced QRS duration was automatically obtained by electrocardiography immediately after pacemaker implantation and then by routine attendance at a pacemaker clinic every 3 months. The paced QRS duration was positively correlated with left ventricular end-diastolic dimension (P < 0.05) and left ventricular end-systolic dimension (P < 0.05), and tended to negatively correlate with left ventricular ejection fraction (P = 0.0507). The paced QRS duration immediately after pacemaker implantation was 170.4 +/- 18.9 ms. During a mean follow-up period of 53 +/- 16 months, 16 patients developed CHF. We selected as a cut-off value the nearest whole number (190 ms) that was one standard deviation greater than the mean, and divided into two groups according to baseline paced QRS duration. Patients with a paced QRS duration of <190 ms comprised group A (n = 77, nine of which developed CHF) and the remainder comprised group B (n = 15, seven of which developed CHF). Prolonged paced QRS duration (> or =190 ms) was associated with a significant increase in the overall morbidity of CHF (P < 0.05). Additionally, paced QRS duration significantly prolonged during the follow-up period among group A patients with CHF (P < 0.05), but did not change among patients without CHF. CONCLUSION: We concluded that paced QRS duration can be a useful indicator of impaired left ventricular function in patients with RV pacing. Even in patients whose paced QRS duration is relatively shorter, progressive prolongation of paced QRS duration can predict the development of CHF.     

Ventricular coupling of electrical and mechanical dyssynchronization in heart failure patients

We studied the relationships of electrical and mechanical synchronization in patients with heart failure (CHF) and various degree of ventricular conduction delays. Ninety-two CHF patients (60 +/- 13 years old, LVEF < 45%), NYHA II-III-IV, and 35 age-matched control subjects were studied with angioscintigraphic phase analysis. We measured ejection fractions (LVEF, RVEF) and calculated the total activation time for the left (TtLV) and right ventricle (TtRV), and the synchronization time between right and left ventricle (TRVLV), and between LV apex and base (Tab). Patients were divided into three groups according to QRS duration: group 1 < 120 ms (n = 28), group 2 < 150 ms (n = 23), group 3 > or = 150 ms (n = 41). In group 1: LVEF = 31.1 +/- 10.9%, RVEF = 30.1 +/- 12.6%, TtLV = 204 +/- 70 ms, TtRV = 183 +/- 61 ms, TRVLV = 7 +/- 33 ms, Tab = 29 +/- 23 ms. In group 2, these were: 27.8 +/- 9.1%, 27.8 +/- 8.8%, 227 +/- 95 ms, 248 +/- 137 ms, 35 +/- 42 ms*, and 39 +/- 53 ms respectively. In group 3: LVEF = 20.5 +/- 9.5%t, RVEF = 28.4 +/- 16.1%, TtLV = 304 +/- 155 mst, TtRV = 234 +/- 106 mst, TRVLV = 64 +/- 42 mst, and Tab = 67 +/- 48 ms*, all P < 0.001 versus controls *P < 0.05 versus G1, tP < or = 0.01 versus G1. A significant relation links QRS to both inter- and intraventricular asynchrony (TRVLV: r = 0.65; TtLL: r = 0.70, Tab: r = 0.60), and to LV function (r = 0.72); while LVEF relates more closely to intraventricular asynchrony: TtLV (r = 0.52), TtLL (r = 0.67), than to interventricular asynchrony: TRVLV (r = 0.48); P < 0.01, P < or = 0.001. In CHF patients, electromechanical and contractile alterations are coupled; regional activation may be an early parameter allowing the detection of ventricular dyssynchronization.     

Increasing left ventricular pacing output decreases interventricular conduction time in patients with biventricular pacing systems

OBJECTIVE: To evaluate the effect of increasing LV pacing output on interventricular timing in patients with biventricular pacing systems. BACKGROUND: Clinical improvement with biventricular pacing is likely related to reduction in ventricular dysynchrony in patients with cardiomyopathy. We hypothesized that increasing left ventricular pacing output would reduce interventricular conduction time and could affect ventricular synchrony. METHODS: Forty-two sequential patients with biventricular pacing systems that permitted independent LV pacing were selected at the time of routine device interrogation. The interval between LV pacing stimulus and onset of the RV electrogram was measured during LV pacing at capture threshold and at maximum pacing output for each patient. RESULTS: The average time from LV pacing stimulus to right ventricular electrogram onset was 142.5 +/- 32.5 ms (range 90-230 ms) at threshold and 132.3 +/- 30.4 ms (range 90-220 ms) at maximum pacing output, with a mean decrease in conduction time of 10.2 +/- 10.9 ms (range 0-45 ms). There was significantly greater interventricular conduction shortening with increased pacing output in patients with ischemic cardiomyopathy compared to others (14.9 +/- 11.9 ms vs 4.0 +/- 4.6 ms; P < 0.01). CONCLUSIONS: Conduction time from LV to RV shortens as LV pacing output is increased. This effect is seen to a greater degree in patients with ischemic cardiomyopathy, possibly related to the presence of myocardial scar near the pacing electrode. Further investigation is needed to assess the clinical outcomes related to this new method for optimizing resynchronization therapy.     

Hemodynamic effect of the ventricular pacing site in fetal lambs with complete atrioventricular block

Complete atrioventricular (AV) block in hydrops fetalis is associated with high mortality. Fetal ventricular pacing to restore ventricular rate can be an effective procedure, however, no fetal data has shown an appropriate epicardial ventricular pacing site. To evaluate the hemodynamic effect of right and left ventricular pacing in fetal lambs with complete AV block, a fetal complete AV block model was created. Aortic pressure, central venous pressure, and QRS duration were measured, and right and left ventricular output was estimated in seven fetal lambs. The uterus was opened under maternal anesthesia, and under local anesthesia, catheters were inserted into the fetal superior vena cava and ascending aorta through a neck incision. Pacing leads were then sutured onto the fetal right and left ventricular epicardium via a midline thoracotomy. Complete AV block was created by cryoablation of the AV node. Ventricular output was estimated using echocardiography by a transuterine approach. Fetal hemodynamics were observed before AV block creation (control), and after complete AV block creation with the right and left ventricular pacing set at 150/min. The right ventricular output was 320 +/- 66 mL/kg per minute at control, decreased to 243 +/- 65 mL/kg per minute during right ventricular pacing (P < 0.05), and was 254 +/- 61 mL/kg per minute during left ventricular pacing. The left ventricular output was 224 +/- 98 mL/kg per minute at control, 176 +/- 77 mL/kg minute during right ventricular pacing, and 178 +/- 67 mL/kg per minute during left ventricular pacing. Biventricular (combined ventricular) output was 544 +/- 134 mL/kg per minute at control, 419 +/- 114 mL/kg per minute during right ventricular pacing, and 432 +/- 100 mL/kg minute during left ventricular pacing. Systolic aortic pressure was 62.2 +/- 8.7 mmHg at control, 55.2 +/- 9.5 mmHg during right ventricular pacing, and 53.4 +/- 9.1 mmHg during left ventricular pacing. Central venous pressure (CVP) was 2.6 +/- 0.5 mmHg at control, 4.0 +/- 2.7 mmHg during right ventricular pacing, and 4.4 +/- 2.5 mmHg during left ventricular pacing. The QRS duration was 51 +/- 54 ms at control, but lengthened to 87 +/- 19 ms during right ventricular pacing and to 78 +/- 21 ms during left ventricular pacing (P < 0.05). In conclusion, the right ventricular output decreased during right ventricular pacing in fetal lambs with complete AV block, while it was preserved during the left ventricular pacing. Left ventricular pacing might be superior for treating hydropic fetuses with complete AV block.     

Automatic Beat‐to‐Beat Left Heart AV Normalization:

Programming the right heart AV interval to a normal value may cause a nonphysiological left heart AV due to interatrial and interventricular conduction delays, thus affecting cardiac performance. Since AV normalization at rest and exercise may be invalidated by pacing or sensing (mode) changes, the aim of this study was to (1) study the feasibility of a mode independent pacemaker (PM) algorithm for automatic beat-to-beat left AV normalization, (2) establish normal values for the time between mitral flow A wave (Af) and ventricular activation (Va), the AfVa interval, the mechanical surrogate of left AV, and (C) determine the range of values of the interatrial electromechanical delays (IAEMDs) and the effect of RA pacing. To pace with the proper right AV, the previously reported RV-paced interventricular electromechanical delay and the interatrial electromechanical delay, either P-sensed (IAEMDs) or atrial-paced (IAEMDp) are required inputs. Data were collected during diagnostic echo Doppler studies in 84 subjects divided in three groups: (1) control with narrow QRS and no structural heart disease (n = 33, age 50 +/- 21 years, 42% men); (2) patients in sinus rhythm with diverse cardiac pathologies except LBBB (n = 39, age 69 +/- 14 years, 56% men), and (3) DDD-paced patients (n = 12, mean age 71 +/- 6 years). Normal values of AfVa were established from the control group, while IAEMDs and IAEMDp and active atrial flow time (A-peak), in all subjects. The algorithm was tested by computer simulation under all possible modes with the following calculation: RAV = N + IAEMD - IVD, where RAV is the right AV, N is the desired normal AfVa value, IAEMD is either P-sensed or A-paced, and IVD is close to zero for intrinsic narrow QRS and biventricular pacing, or 79 ms for RV pacing. The results demonstrated (1) Normal (controls) AfVa: 85 +/- 15 ms (range 52-110 ms); (2) IAEMDs (All): 84 +/- 16 ms; (3) atrial pacing prolonged IAEMDs by 57 +/- 18 ms (from 93 +/- 15 to 150 +/- 25 ms, P < 0.0001); and (4) Computer simulation of rate and mode changes validated the normalization algorithm. An automatic, beat-to-beat left AV normalization algorithm to preserve a normal AfVa without a hemodynamic sensor is feasible. The normal value of AfVa is 85 +/- 15 ms.     

心肌病心肺运动负荷研究：室内传导阻滞和舒张充盈功能的影响

目的双心室起搏已经广泛用于心肌病伴有和不伴有QRS间期延长患者,提高运动能力、改善心肺储备功能是双心室起搏的目标。为了提高双心室起搏时QRS间期与舒张功能对PVO2、VE／VCO2斜率等心肺功能的预测性,对心肌病患者静态室内传导阻滞和舒张功能与运动心肺功能相关性变化进行了评价。方法42例心肌病患者（缺血性心肌病11例,扩张型心肌病31例）,其中21例正常组（QRS间期〈120ms）,21例异常组（QRS间期〉120ms）,进行心肺联合运动试验和彩色多普勒超声心动图检查。运动前、运动高峰和运动后分别测定运动耐量、PVO2、AT、VE／VCO2斜率。结果心肌病患者中,异常组短轴内径大于正常组,房室环运动幅度无明显差异,运动PVO2、AT、VE／VCO2斜率明显改变,舒张时间缩短,心电图QRS间期和舒张充盈时间与PVO2、AT及VE／VCO2斜率有显著相关性（P〈0．05）。结论心电图QRS间期和彩色多普勒超声心动图测定的舒张功能与运动PVO2和AT及VE／VCO2斜率相关,心电图QRS间期和舒张功能有助于预测心肌病患者心脏再同步时心肺储备功能。因此,运动心肺功能不但与QRS间期有关,而且与舒张充盈功能有关。当双心室起搏无反应时,改善舒张功能是另一有效途径。     

Optimization of Ventricular Function by Improving the Activation Sequence During Ventricular Pacing

Abnormal electrical activation occurring during ventricular pacing reduces left ventricular (LV) pump function. Two strategies were compared to optimize LV function using ventricular pacing, minimal asynchrony and optimal sequence of electrical activation. ECG and hemodynamics aortic flowpmbe, thermodilution cardiac output, LV pressure and its maximal rates of rise (LVdP/dtpos) and fall (LVdP/dtneg) were measured in anesthetized open-chest dogs (n = 7) with healthy hearts. The QRS duration (a measure of asynchrony of activation) was 47 ± 5 ms during sinus rhythm and increased to 110 ± 12 ms during DDD pacing at the right ventricular (RV) apex with a short AV interval. During pacing at the LV apex and LV base, the QRS duration was 8%± 7% and 15%± 7% (P < 0.05) longer than during RV apex pacing, respectively. Stroke volumes, LVdP/dtpos and LVdP/dtneg, however, were higher during LV apex(15%± 16%, 10%± 12% [P<0.05], and 15%± 10%, respectively) and LV base pacing (11%± 12% [P<0.05], 3%± 12%, and 3%± 11%, respectively) than during RV apex pacing. Systolic LV pressure was not influenced significantly by the site of pacing. Biventricular pacing (RV apex together with one or two LV sites) decreased the QRS duration by approximately 20% as compared with RV apex pacing, however, it did not improve stroke volumes, LVdP/dtpos and LVdP/dtneg beyond those during pacing at the LV apex alone. In conclusion, the sequence of electrical activation is a stronger determinant of ventricular function than the synchrony of activation. For optimal LV function the selection of an optimal single pacing site, like the LV apex, is more important than pacing from multiple sites.     

右心室间隔部起搏对血流动力学的影响

目的 评价在房室顺序起搏治疗中,右心室间隔部起搏对血流动力学的影响.方法 20例植入双腔起搏器的患者,高度房室传导阻滞6例,完全性房室传导阻滞14例,按照心室电极的位置分为右心室心尖部起搏(RVA)组和右心室间隔部起搏(RVS)组.对2组患者术前、术后3个月随访时的QRS波形态和宽度、左心室射血分数(LVEF)、心室间机械运动延迟(IVMD)和血脑钠肽(BNP)水平进行比较.结果与术前相比,RVA组起搏心电图QRS时限增宽[(187.00±15.67)ms与(94.00±9.17)ms,t=15.98,P＜0.05],LVEF下降[(53.70±1.34)%与(58.60±1.65)%,t=7.30,P＜0.05],IVMD延长[(43.20±6.79)ms与(15.00±4.08)ms,t=7.75,P＜0.05],BNP升高[(89.70±8.30)ng/L与(40.00±4.73)ng/L,t=16.44,P＜0.05],而RVS组无明显变化(P均＞0.05);术后和RVA组相比,RVS组QRS时限缩短[(119.00±7.38)ms与(187.00±15.67)ms,t=12.42,P＜0.05],LVEF增加[(57.00±2.00)%与(53.70±1.34)%,t=4.09,P＜0.05],而IVMD缩短[(19.00±4.59)ms与(43.20±6.79)ms,t=7.94,P＜0.05],BNP降低[(44.加±9.18)ng/L与(89.70±8.30)ng/L,t=11.62,P＜0.05].结论 和传统的RVA起搏相比,RVS起搏尽可能地维持了双心室的正常激动顺序和双心室的同步性,对血流动力学的影响较小,RVS起搏比RVA起搏更接近生理性起搏.     

Evolution of paced QRS and QTc intervals in children with epicardial pacing leads

AIMS : Permanent ventricular pacing in children is associated with ventricular dysfunction due to asynchronous activation. It is unclear whether paced QRS intervals increase disproportionately over time, which could potentially cause ventricular dysfunction. METHODS : A total of 52 children, with bipolar steroideluting epicardial leads implanted at a median age of 5.6 years (0.0-17.4), was analyzed and followed up to 12.2 years (median 3.7). Patients were subdivided in two groups: right (RV, n = 21) and left (LV, n = 31) ventricular pacing. To correct for age, standard deviation scores (Z-scores) for paced QRS and QTc intervals were calculated from published standard-ECG norm-values. As a measure for individual paced QRS and QTc interval changes, a regression slope coefficient (incline(i)) was calculated for each patient's course. RESULTS : Mean Z-scores for paced QRS intervals at first and last follow-up were 4.7 +/- 1.2 and 4.9 +/- 0.9 for group RV, 4.4 +/- 1.1 and 4.8 +/- 1.1 for group LV. Incline(i) of paced QRS (group RV: 0.038 [-0.27-0.12], group LV: 0.147 [-0.05-0.30]; p = 0.07) and QTc intervals (group RV: 0.026 [-0.08-0.06], group LV: 0.023 [-0.04-0.09]; p = 0.63) did not differ between both groups and indicated limited interval changes over time. CONCLUSION : Neither epicardial pacing of the right nor left ventricle caused disproportionate paced QRS or QTc interval increases over time. An age-related prolongation of the electrical activation unlikely causes ventricular dysfunction.     

Basal asynchrony and resynchronization with biventricular pacing predict long-term improvement of LV function in heart failure patients

Biventricular pacing (BiV) is emerging for patients with dilated cardiomyopathy (DCM) and asynchrony. We measured basal asynchrony and early resynchronization by radionuclide angioscintigraphy (RNA) in order to predict long-term evolution of ventricular function after BiV. Thirty-four patients (NYHA Class III-IV,65.4 +/- 11 years) with large QRS(179 +/- 18 ms)were implanted with BiV and studied by RNA before (D0), at day 8 (D8), and during follow-up(20 +/- 7 months). We calculated left and right ejection fractions, the interventricular dyssynchrony (TRVLV), and the apicobasal dyssynchrony (Tab). LVEF improved from 20.2 +/- 8.1%(D0) to27.1%+/- 12.6%(follow-up,P < 0.003 vs D0) and RVEF from 28.6%+/- 13%(D0) to 34.3 +/- 11.5%(follow-up,P < 0.03 vs D0). Inter- (DeltaTRVLV) and intraventricular resynchronization was immediate and remained stable: TRVLV decreased from 68.3 +/- 38 ms(D0) to 13.4 +/- 48.5 ms(D8) and1.8 +/- 39.2 ms(follow-up,P < 0.0001 vs D0); and Tab from 45.8 +/- 64.1 msto-18 +/- 68(D8) and-28.3 +/- 53.6 ms(follow-up,P < 0.0001 vs D0). Early inter- and intraventricular resynchronization (DeltaTab) at D8 were related to late LVEF and RVEF improvement. Together, an LVEF > 15% and a significant interventricular dyssynchrony (TRVLV > 60 ms) at D0 have a sensitivity of 79% and a positive predictive value of 83% to predict an improvement of LVEF superior to 5% at follow-up. In DCM patients, BiV resynchronizes ventricles early and in the long-term, while RVEF and LVEF improve progressively. Patients with large electromechanical dyssynchrony benefit most from BiV.     

The effect of anodal stimulation on V-V timing at varying V-V intervals

We studied the effect of anodal capture at the ring electrode of the right ventricular (RV) lead on interventricular (V-V) timing during biventricular (BiV) pacing, in which left ventricular (LV) pacing was preceding RV pacing. The V-V interval was programmed from 80 to 4 ms (LV first) in the LV unipolar (LV tip--generator can) followed by the LV tip-RV ring pacing configuration. In the LV unipolar configuration, V-V programming leads to a continuous change in morphology of the QRS complex according to a change in collision of both activation fronts. When using the LV tip-RV ring configuration with anodal capture at the RV ring electrode no change in QRS morphology was recorded varying the V-V interval from 80 to 60 and 40 ms. However, at V-V intervals between 20 and 4 ms a change in morphology of the QRS complex was recorded, which was due to additional cathodal stimulation of the RV tip electrode during RV stimulation.     

A Comparison of Ventricular Function During High Right Ventricular Septal and Apical Pacing after His-Bundle Ablation for Refractory Atrial Fibrillation

This study compares LV performance during high right ventricular septal (RVS) and apical (RVA) pacing in patients with LV dysfunction who underwent His-bundle ablation for chronic AF. We inserted a passive fixation pacing electrode into the RVA and an active fixation electrode in the RVS. A dual chamber, rate responsive pulse generator stimulated the RVA through the ventricular port and the RVS via the atrial port. Patients were randomized to initial RVA (VVIR) or RVS (AAIR) pacing for 2 months. The pacing site was reversed during the next 2 months. At the 2 and 4 month follow-up visit, each patient underwent a transthoracic echocardiographical study and a rest/exercise first pass radionuclide ventriculogram. We studied nine men and three women (mean age of 68 +/- 7 years) with congestive heart failure functional Class (NYHA Classification): I (3 patients), II (7 patients), and III (2 patients). The QRS duration was shorter during RVS stimulation (158 +/- 10 vs 170 +/- 11 ms, P < 0.001). Chronic capture threshold and lead impedance did not significantly differ. LV fractional shortening improved during RVS pacing (0.31 +/- 0.05 vs 0.26 +/- 0.07, P < 0.01). RVS activation increased the resting first pass LV ejection fraction (0.51 +/- 0.14 vs 0.43 +/- 0.10, P < 0.01). No significant difference was observed during RVS and RVA pacing in the exercise time (5.6 +/- 3.2 vs 5.4 +/- 3.1, P = 0.6) or the exercise first pass LV ejection fraction (0.58 +/- 0.15 vs 0.55 +/- 0.16, P = 0.2). The relative changes in QRS duration and LV ejection fraction at both pacing sites showed a significant correlation (P < 0.01). We conclude that RVS pacing produces shorter QRS duration and better chronic LV function than RVA pacing in patients with mild to moderate LV dysfunction and chronic AF after His-bundle ablation.     

Localization of the ventricular insertion site of concealed left-sided accessory pathways using ventricular pace mapping

The aim of the present study was to localize the ventricular insertion site of concealed accessory pathway (APs) by using the ventricular pace mapping and examined if the analysis of the timing of retrograde atrial electrogram recorded at the ventricular side of the mitral annulus is useful in identifying the ventricular insertion site of the AP. In 39 patients with concealed left-sided APs, ventricular pacing was delivered along the mitral annulus at a cycle length of 500 ms while measuring the conduction interval from the pacing stimulus to the earliest retrograde atrial electrogram recorded in the coronary sinus (St-A). The ventricular insertion site of the AP was localized by identifying the shortest St-A. Also the interval between the onsets of QRS and atrial electrograms (QRS-A) and presence of continuous electrical activity (CEA) between the ventricular and atrial electrograms were evaluated at each mapping site during atrioventricular reciprocating tachycardia. Initial radiofrequency energy application to the site with the shortest St-A (46 +/- 15 ms) eliminated the AP conduction in all patients, suggesting the accurate localization of the ventricular insertion site by ventricular pace mapping. The QRS-A and the percentage of the presence of CEA at the shortest St-A site were 79 +/- 19 ms and 64%, respectively. However, the earliest retrograde atrial activation site did not coincide with the shortest St-A site in 19 of 39 patients, suggesting an oblique course of AP. Thus, in these 19 patients, there was a significant difference in St-A (47 +/- 16 vs 59 +/- 15 ms, P < 0.0001), QRS-A (83 +/- 13 vs 72 +/- 12 ms, P < 0.0001) and the presence of CEA (32 vs 74%, P < 0.01) between the shortest St-A site and the earliest retrograde atrial activation site, respectively. These indicate that the earliest retrograde atrial activation is not necessarily indicative of the ventricular insertion site of AP. However, ventricular pace mapping was considered to be useful for identifying and ablating the ventricular insertion site of AP, irrespective of the course of AP.     

慢性心力衰竭患者左右心室收缩同步性与心电图关系研究

目的 观察窦性心律慢性心力衰竭患者左右心室收缩同步性差异,以及窦性心律慢性心力衰竭患者心电图、左心室收缩功能的变化.探讨双心室收缩差异的发生率、双心室收缩差异的预测指标、双心室收缩不同步与左心室收缩功能的关系.方法 选择26例慢性心力衰竭患者和16例健康对照者.首先进行心电图检查获得QRS间期,P-R间期.再进行平衡状放射性核素心室造影检查,获得左、右心室射血分数及其他功能参数,在相位直方图上计算左右心室的相角程、半高宽.结果 两组间心电图参数QRS间期、P-R间期差异有统计学意义,(117.64±33.16)ms vs(91.87±9.16)ms,(191.43±55.25)ms vs(161.75±22.17)ms(均P<0.05).位相分析中左右心室相角程及半高宽差异有统计学意义,(86.56±21.88)°vs(223.81±101.41)°,(26.44±8.21)°vs(57.90±42.72)°(均P<0.01).慢性心力衰竭患者左右心室相角程(PS)与LVEF呈相关(r=-0.709,P<0.001);左右心室相角程(PS)与心电图QRS间期无相关性(r＝0.310,P>0.05).病例组76.9%的患者存在室间不同步收缩,存在室间不同步收缩患者与无室间不同步收缩患者相比,左、右心室射血分数差异有统计学意义(P<0.01);心电图、参数差异无统计学意义(P>0.05).这些患者室间不同步收缩PS与LVEF(r＝-0.55,P<0.05);而与心电图的QRS间期无明显相关关系(r=0.090,P>0.05).结论 慢性心力衰竭患者的心电图、功能参数、位相分析参数存在着明显异常;76.9%心力衰竭患者存在着室间非同步收缩,这些患者具有较低的射血分数;室间非同步收缩与左心功能呈明显负相关,与QRS间期无明显相关关系.室间非同步收缩的形成可能是导致心功能下降的原因之一. 缩患者相比,左、右心室射血分数差异有统计学意义(P<0.01);心电图、参数差异无统计学意义(P>0.05).这些患者室间不同步收缩PS与LVEF(r＝-0.55,P<0.05);而与心电图的QRS问期无明显相关关系(r=0.090,P>0.05).结论 慢性心力衰竭患者的心电图、功能参数、位相分析参数存在着明显异常;76.9%心力衰竭患者存在着室间非同步收缩,这些患者具有较低的射血分数;室间非同步收缩与左心功能呈明显负相关,与QRS间期 明显相关关系.室间非同步收缩的形成可能是导致心功能下降的原因之一. 缩患者相比,左、右心室射血分数差异有统计学意义(P<0.01);心电图、参数差异无统计学意义(P>0.05).这些患者室间不同步收缩PS与LVEF(r＝-0.55,P<0.05);而与心电图的QRS问期无明显相关关系(r=0.090,P>0.05).结论 慢性心力衰竭患者的心电图、功能参数、位相分析参数存在着明显异常;76.9%心力衰竭患者存在着室间非同步收缩,这些患者具有较低的射血分数;室间非同步收缩与左心功能呈明显负相关,与QRS间期 明显相关关系.室间非同步收缩的形成可能是导致心功

Abstract：

Objective To observe contraction desynchronization of entire ventricle, alterations of electrocardiography and left ventricular systolic function in patients with chronic congestive heart failure in sinus rhythm. To explore the incidence of interventricular desynchronizition in patients with chronic congestive heart failure,predictive factors of interventricular dyssynchrony, and the correlation between biventricular contractile desynchronization and left ventricular function. Methods Twenty-six patients with chronic congestive heart failure and 16 control subjects were studied by standard 12-lead electrocardiography,and gated equilibrium blood pool scintigraphy.Firstly,QRS duration, P-R duration were obtained by electrocardiography. Finally, these subjects were examined by radionuclide angioscintigraphy. Left ventricular ejection fraction, right ventricular ejection fraction and other functional parameters were obtained. Phase angles and full width half the maximal on phase histogram expressed interventricular contractile synchrony were computed in sinus rhythm. Results There were significant differences between ECGparameters (QRS duration, P-R duration), (117.64±33.16) ms vs (91.87±9.16) ms, (191.43±55.25) ms vs (161.75±22.17) ms (both P <0.05) ,phase angles of phase image analysis, (86.56±21.88)° vs (223. 81±101.41)°,(26.44±8.21)° vs (57.90±42.72)°(both P＜0. 01). In patients with heart failure,significantly negative correlation was found between phase angles and LVEF(r = -0. 709, P <0. 001). No correlation was found between phase angles and QRS duration. In patients with heart failure, 76.9% patients had interventricular contractile desynchrony. These patients also had lower left ventricular ejection fraction. In these patients, significantly negative correlation was found between phase angles and LVEF(r = -0. 55, P ,(0.05), what is more,no correlation was found between phase angles and QRS duration. Conclusion The patients with chronic heart failure have significantly abnormal electrocardiography,left ventricular systolic function, and parameters of phase image analysis. 76.9% patients with heart failure had interventricular contractile dyssynchrony who had lower left ventricular ejection fraction compared with patients without interventricular contractile dyssynchrony. A significant negative correlation is found between phase angles and LVEF. This study shows that interventricular contractile desynchronization may be one of causes decreasing left ventricular function.     

The Importance of the Left Atrioventricular Interval during Atrioventricular Sequential Pacing

During atrioventricular (AV) sequential pacing from the right heart, the interval between the left atrium and ventricle may vary from the programmed AV interval depending on the position of the atrial and ventricular electrodes and interatrial and interventricular conduction. The aim of this study was to determine the hemodynamic effects of altering the left AV interval while keeping the programmed AV interval constant. Four male and 17 female patients, aged 49 ± 15 years were studied. The left AV interval was measured by a catheter in the coronary sinus. Stroke volume and mitral flow were measured by simultaneous echo Doppler during AV sequential pacing from the right atrial appendage and right ventricular apex at programmed AV intervals of 100. 60, and 6 ms. The atrial catheter was then positioned on the atrial septum and the measurements repeated. With the atrial catheter in the right atrial appendage, interatrial activation time (118 ± 20 ms) was similar to interventricular activation time (125 ± 21 ms) and the left AV interval was almost identical to the programmed right AV interval. There was a significant correlation between interatrial and interventricular activation times (r = 0.8; P < 0.001). Positioning the atrial electrode on the septum decreased interatrial activation time by 39 ± 12 ms and increased the left AV interval by a similar amount. At a programmed AV interval of 60 ms, the left AV interval increased from 67 ± 15 ms to 105 ± 17 ms after the atrial catheter was repositioned from the appendage to the septum (P < 0.001). Compared to pacing from the right atrial appendage, atrial septal pacing increased mitral A wave velocity integral (2.8 ± 1.4 vs 4.4 ±1.7 cm at a programmed AV interval of 60 ms, P < 0.01), decreased E wave velocity integral (8.1 ± 2.2 vs 6.1 ± 2.4 cm, P < 0.001) but did not alter stroke volume (44.8 ± 10.6 vs 44.9 ± 10.1 mL). In contrast, a 40 ms decrease in the programmed right AV interval from 100 to 60 ms decreased stroke volume from 48.0 ± 10.0 to 44.9 ± 10.2 mL (P < 0.001). There was a strong relationship between interatrial and interventricular conduction so that patients with prolonged interatrial conduction still had equivalent left and right AV intervals during atrioventricular sequential pacing from the right atrial appendage and right ventricular apex. Positioning the atrial electrode on the septum decreases interatrial activation time and increases the left AV interval by about 40 ms but has minimal hemodynamic effect in patients without heart failure.     

Electrical remodeling and cardiac dimensions in patients treated by cardiac resynchronization and heart failure controls

BACKGROUND: Cardiac resynchronization therapy (CRT) reduces the left ventricular diameter (LVEDD) in heart failure (HF) patients with left bundle branch block (LBBB). The study compares structural and electrical remodeling in HF patients on CRT and matched HF controls without LBBB. METHODS: In 42 patients (64 +/- 9 years left ventricular ejection fraction [LVEF] 25 +/- 8%, 16 coronary artery disease, 26 nonischemic cardiomyopathy, 21 with LBBB and CRT indication vs 21 controls [matched for gender, age, LVEF, and underlying disease]) an unpaced electrocardiogram (ECG) and echocardiogram were recorded at baseline (bl) and after 20.6 +/- 13.8 months (fup). LVEDD, left atrial (LA) width, mitral regurgitation (MR), P-wave, PR interval, QRS width, QRS vector, and QT interval were analyzed. RESULTS: LVEDD diminished with CRT (bl 68.7 +/- 10.3 vs fup 62.0 +/- 7.7 mm, P = 0.002). Controls showed no change (bl 64.1 +/- 9.4 vs fup 64.8 +/- 8.4 mm, P = n.s.). MR improved with CRT (bl 1.2 +/- 0.6 vs fup 0.8 +/- 0.7, P = 0.02), but not among controls. LA width tended to decrease on CRT (CRT bl 48.9 +/- 4.4 vs fup 46.9 +/- 7.2 mm, P = 0.17, controls bl 48.5 +/- 5.1 vs fup 47.5 +/- 6.5 mm, P = 0.49). PR interval lengthened in both groups (CRT bl 175 +/- 29 vs fup 188 +/- 30 ms, P = 0.03, controls bl 177+/-25 vs fup 187 +/- 19 ms, P = 0.27). QRS increased in both groups (CRT bl 165 +/- 22 vs fup 171 +/- 20 ms, P = 0.07, controls bl 111 +/- 17 vs fup 118 +/- 19 ms, P = 0.01). Analyses revealed no significant association of echocardiographic and ECG parameters. CONCLUSIONS: Despite LVEDD reduction with CRT, electrical activation does not recover. Electrical remodeling does not differ between LBBB patients under CRT and matched controls without CRT indication.     

Evaluation of Asynchronous Left Ventricular Relaxation by Doppler Echocardiography During Ventricular Pacing with AV Synchrony (VDD): Comparison with Atrial Pacing (AAI)

The effect of right ventricular pacing on left ventricular relaxation was studied in 13 patients (age 62 ± 3 years), with the atrial sensing ventricular pacing mode (VDD). A control group of similar age (64 ± 4 years) consisted of 11 patients with atrial pacing (AAI). The timing of events was determined in both groups at similar R-R intervals (921 ± 77 ms vs 967 ± 37 ms). The loading conditions as estimated by peak systolic wall stress (afterload) and end-diastolic left ventricular dimensions (preload) were approximately the same in both groups. The ratio of late to early filling velocities were similar in both groups. Dominant changes were: increased preejection period (142 ± 13 ms vs 95 ± 15 ms); and higher velocities of isovolumic relaxation flow (60 ± 34 cm/s vs 25 ± 4 cm/s) in patients with ventricular pacing. The isovolumic relaxation time was longer in patients with VDD pacing (127 ± 14 ms vs 108 ± 12 ms). Anterior systolic interventricular septal motion (paradoxal motion) was recorded in nine patients with VDD pacing and in none of the patients with AAI pacing. Isovolumic relaxation flow was detected during atrial pacing in five (45%) patients and in 13 (100%) patients during atrial sensing ventricular pacing, indicating asynchronous left ventricular relaxation. This data shows that VDD pacing compared to atrial pacing resulted in an altered activation pattern of the left ventricle, associated with delayed onset, asynchronous contraction with interventricular septal motion abnormalities and prolonged asynchronous left ventricular relaxation with abnormal motion manifested by the presence of isovolumic relaxation flow.