左室和双心室起搏对心肌病晚期心衰患者的血流动力学研究

目的　对心电图呈左束支阻滞的晚期心肌病患者行左室和双心室起搏 ,了解左室和双心室起搏的急性期血流动力学效应。方法　对 16例心电图呈左束支阻滞的晚期心肌病患者行左室游离壁和双心室起搏 ,记录左室、双心室和基础状态下的左室腔内dP/dtmax、主动脉根部压力和心电图QRS波宽度。结果　左室和双心室起搏分别使左室dP/dtmax提高 2 1%和 18% (P <0 0 1) ,而左室和双心室起搏组无显著差异 (P >0 0 5 ) ;左室起搏和双心室起搏使主动脉收缩压较基础状态升高 6 %和 5 % (P <0 0 1) ,左室和双心室起搏组间差异不显著 (P >0 0 5 ) ;左室起搏心电图QRS间期缩短不明显 (P >0 0 5 ) ,而双心室起搏QRS间期明显缩短(P <0 0 5 )。结论　对于心电图呈LBBB型的心肌病终末期心衰患者 ,行双心室起搏和左室游离壁起搏均使患者的急性期血流动力学得到显著改善 ,两者的效果相当     

左室和双室起搏对心肌病晚期心力衰竭患者的血流动力学研究

对心电图呈左束支阻滞的晚期心肌病患者行左室和双室起搏,了解左室和双室起搏的急性期血流动力学效应.对16例心电图呈左束支阻滞的晚期心肌病患者行左室游离壁和双室起搏,记录左室、双室和基础状态下的左室腔内最大压力上升速度(dP/dtmax)、主动脉根部压力和心电图QRS波时限.结果:左室和双室起搏分别使左室dP/dtmax提高21%和18%(P＜0.01),而左室和双室起搏组间无显著差异(P＞0.05);左室起搏和双室起搏使主动脉收缩压较基础状态升高6%和5%(P＜0.01),左室和双室起搏组间差异不显著(P＞0.05);左室起搏心电图QRS间期缩短不明显(P＞0.05),而双室起搏QRS间期明显缩短(P＜0.05).结论:对于心电图呈左束支阻滞型的心肌病终末期心力衰竭患者,行双室起搏和左室游离壁起搏均使患者的急性期血流动力学得到显著改善,两者的效果相当.     

窄QRS波充血性心力衰竭双室同步起搏疗效的初步观察

为进一步探讨心电图窄QRS波的充血性心力衰竭 (简称心衰 )患者双室同步起搏治疗的疗效。 9例男性患者 ,年龄 5 9.16± 10 .3 5岁 ,QRS波≤ 13 0ms,其中扩张性心肌病 5例 ,缺血性心肌病 2例 ,高血压性心脏病 2例。行双室再同步起搏治疗 ,于治疗前及治疗后6个月行心功能 (HYNA分级 )、6min步行试验、心脏超声测量左室舒张期末径 (LVEDD)及左室射血分数 (LVEF)评估。结果 :术后 6个月心功能较术前明显改善 ,平均改善一级 (P <0 .0 0 1)。 6min步行距离平均延长约 2 0 0m(P <0 .0 1)。LVEDD术后 6个月较术前平均缩小约 5mm(P <0 .0 5 )。LVEF术后 6个月较术前平均提高约 9% (P <0 .0 0 5 )。结论 :充血性心衰患者无论是否伴LBBB ,若存在着心室间或心室内收缩的不同步 ,给予双室同步起搏治疗后可使患者的运动耐量及血流动力学均有一定程度的改善。     

心室同步化重建治疗扩张型心肌病

目的　观察心室同步化重建起搏对扩张型心肌病顽固性充血性心衰的治疗效果。方法　对 12例临床表现为顽固性心衰 ,合并左束支阻滞的扩张型心肌病患者行双心室同步起搏治疗。观察术中、术后 3个月、6个月左室电极的起搏参数 ,以及术前、术后 3个月的 QRS波时限、左室射血分数、左室舒张末内径 (L VDD)、二尖瓣反流量、最大氧摄取量 (VO2 max)与临床症状变化。结果　随访 3～ 2 0个月 ,患者左室电极的起搏阈值、阻抗及感知各参数值稳定 ,起搏功能良好。与术前相比 ,术后 3个月心功能指标均明显改善 (P <0 .0 5 ) ,且随着时间的延长持续改善。随访期间猝死 1例 ,接受心脏移植 1例。结论　心室同步化重建是治疗室间传导异常充血性心衰的有效新方法。三腔起搏器可改善扩张型心肌病患者的血流动力学、心功能和心衰症状。左室电极植入成功率高 ,性能稳定 ,安全可靠。三腔双心室同步房室顺序起搏心脏自动复律除颤器 (ICD)不仅可治疗心衰 ,同时具有良好的抗室性心律失常、预防猝死的作用     

不同心脏起搏方式对犬急性血液动力学及心肌力学的影响

通过采用 5种不同的心脏起搏方式 ,观察房室同步和心室激动顺序对犬急性血液动力学和心肌力学的影响。方法 :选用健康犬 10只 ,随机顺序进行右心房起搏 (RAP)、右房 His束顺序起搏 (AHSP)、右房 右室顺序起搏(AVSP)、His束近端起搏 (HBP)和右心室起搏 (RVP) ,在每种起搏稳定 5min后测定有关血液动力学和心肌力学参数。结果 :RAP和AHSP对血液动力学和心肌力学无显著影响 ;AVSP时心输出量 (CO)、等容收缩期左室压力最大上升速率 (+dp/dtmax)和等容舒张期左室压力最大下降速率 (-dp/dtmax)分别降低了 16 .32 % ,15 .0 1% ,15 .19% ;HBP时平均肺动脉压 (mPAP)、肺毛细血管楔压 (PCWP)、左室舒张末压 (LVEDP)均升高 ,而CO降低了 14.93 % ;RVP时mPAP、PCWP、LVEDP均明显升高 ,CO、+dp/dtmax和 -dp/dtmax分别降低了 2 3.95 % ,2 2 .2 8% ,19.74%。结论 :丧失房室同步活动引起左室前负荷变化 ,影响整体收缩功能 ;而心室激动顺序异常既影响左室收缩功能 ,也影响左室舒张功能     

不同起搏部位对正常人体心肌复极离散的影响

目的 :观察正常人心脏不同部位或 2个部位同时起搏时的电生理及心室肌复极差异的变化。方法 :15例接受射频消融术后的患者 ,常规检查排除器质性心脏病。经冠状静脉窦将 1根标测电极送至左心室表面静脉分支 ,另 1根Pacing MAP电极送达右室心尖部 ,记录局部单向动作电位 (MAP)。分别起搏左心室心外膜、右心室心内膜及上述两部位同时起搏 ,行S1S1、S1S2 程序刺激。记录测量QRS波时限、QT间期、Tp Te 间期、MAP时程 (MAPD)等指标及心律失常事件。结果 :体表心电图上QT间期、Tp Te 间期在左室心外膜起搏 (376 .2 6ms、12 2 .5 9ms)、双心室起搏 (36 6 .4 2ms、12 4 .2 3ms)明显较右心室心内膜起搏 (349.33ms、10 4 .14ms)延长 (P <0 .0 1) ,伴有右室心尖部局部MAPD的相应变化。在相同总阵次的程序刺激中 ,左室心外膜起搏与双心室起搏时的室性心律失常多于右室心内膜起搏时 (P <0 .0 5 )。结论 :左室心外膜参与起搏后可能会增大心室肌的跨室壁复极差异 ,伴有复极时间的延长 ,从而使室性心律失常易于发生。     

快速右房起搏致猪心动过速性心肌病

目的通过快速右房起搏建立心动过速性心肌病模型,观察该病不同时期血流动力学改变和心肌重构情况。方法将15头滇南小耳猪,按随机区组的方法分为起搏1周组、起搏4周组、假手术组,分别采用240次/分快速起搏右房1周、4周和只手术不起搏。运用超声心动图和左心导管检查测量窦性心律下的血流动力学参数并观察心脏大体结构变化。经Masson染色检测心肌纤维化,测定心肌胶原容积分数(CVF),比较房、室重塑差异。结果起搏1周组左室射血分数、左室收缩末压、左室压力上升最大速率、左室压力下降高峰速率均较假手术组降低(P<0.01);起搏4周组上述血流动力学指标继续恶化,且腔室扩大、室壁变薄,(P<0.01)。心房、心室CVF随起搏时间的延长逐渐增加(P<0.01)。结论采用快速右房起搏成功制作了心动过速性心肌病模型,证实该病是以严重的左、右室舒缩功能障碍,腔室扩大,室壁变薄,心肌重塑为特征。     

右心室流出道主动固定电极和心尖部被动固定电极体表起搏心电图的研究

目的 观察右心室流出道主动固定电极和右心室心尖部被动电极体表起搏心电图的变化. 方法 比较右心室流出道主动固定电极(游离壁12例,间隔部16例)和右心室心尖部被动固定电极(20例)起搏心电图的QRS波群主波方向及时间,比较6个肢体导联上起搏和自主QRS波形态的相似性. 结果 QRS时间间隔部起搏(0.113±0.020)S较游离壁(0.135±0.027)S和右心室心尖部10.151±0.032)s起搏短,差异有显著性或非常显著性意义(P<0.05、0.01);后两者之间无显著性差异.6个肢体导联上,间隔部起搏QRS形态较接近自主QRS形态.间隔部起搏Ⅰ和aVL QRS波群主波向下的比例显著高于游离壁起搏(P<0.05).游离壁起搏ORS波群切迹比例显著高于间隔部起搏(P<0.05). 结论 右心室流出道间隔部起搏可以改善患者血流动力学.心电图特征性改变可指导起搏器起搏位置的选择.     

右室起搏出现右束支阻滞图形的探讨(附二例报告)

<正> 经静脉右室人工起搏,如电极导管位置确在右室而非冠状静脉窦,体表心电图应呈左束支传导阻滞(LBBB)图形,这和起源于一侧心室的过早搏动或室性心动过速时,心电图出现对侧束支传导阻滞图形的规律类似。我们最近遇到2例经静脉埋置ⅤⅥ型起搏器行右室起搏的冠心病患者,起搏信号激发的QRS波群呈右束支阻滞图形(RBBB),X线胸片证实导管未穿透室壁亦非插入窦状静脉窦。右室起搏呈现RBBB图形甚为罕见,     

普通心室电极在双室右房三心腔起搏治疗充血性心力衰竭中的初步应用

目的 观察普通心室电极起搏治疗扩张性心肌病（DCM）伴充血性心力衰竭（CHF）的疗效。方法患者,男,2例,女2例,平均年龄62.6岁±7.7岁（52岁～70岁）,均为扩张性心肌病伴充血性心衰,且有完全性左束支传导阻滞或左前分支传导阻滞,行双室右房三心腔起搏治疗。左心室起搏通过冠状静脉窦植入剪去一部分尖端羽翼的普通心室电极,置于冠状静脉窦的分支静脉起搏左心室,左右心室电极导线通过Y形转换器与双腔起搏器心室孔相连接。结果 以普通心室电极起搏并辅以合适的房室间期（AVP）,患者心力衰竭的症状明显改善,NY-HA心功能分级从Ⅲ～Ⅳ级提高到Ⅰ～Ⅱ级,超声心动图示心功能指标改善,起搏后心电图QRS时限缩短,其中一例患者已基本上停止服药数月。结论 初步临床应用表明,普通心室电极实行双心室同步起搏治疗心力衰竭既行之有效,又价廉物美。     

Area of left ventricular regional conduction delay and preserved myocardium predict responses to cardiac resynchronization therapy

Cardiac resynchronization therapy. BACKGROUND: A significant proportion of patients with dilated cardiomyopathy and left bundle branch block (LBBB) do not respond to cardiac resynchronization therapy (CRT). The purpose of this study was to investigate whether the electromechanical properties of the myocardium would predict acute hemodynamic improvement during left ventricular (LV) pacing. METHODS AND RESULTS: We studied 10 patients with idiopathic dilated cardiomyopathy and LBBB (ejection fraction (EF): 27%+/-7%; QRS duration: 166+/-16 msec) using three-dimensional electromechanical endocardial mapping technique to assess endocardial activation time (Endo-AT), unipolar voltage, and local linear shortening during sinus rhythm. LV stimulation was performed in VDD mode at five different sites and three atrioventricular delays within the coronary sinus. LV+dP/dtmax changes from baseline were measured during LV stimulation at each site (%DeltadP/dtmax). There was no significant relationship between maximum %DeltadP/dtmax during LV stimulation at the best coronary sinus site and LV EF, baseline LV+dP/dtmax, total LV Endo-AT, baseline QRS duration nor changes in QRS duration during LV pacing. However, the maximum %DeltadP/dtmax was significantly positively correlated with percentage area of late Endo-AT (r=0.97, P<0.001) and preserved LV myocardium (r=0.81, P=0.005), respectively. Patients with >20% of LV area with late Endo-AT and >30% of preserved LV myocardium had five times better acute hemodynamic response with LV stimulation. Multivariate analysis showed that only percentage area of late Endo-AT was independently correlated with %DeltadP/dtmax (P<0.05). CONCLUSION: The presence of a larger amount of LV area with late Endo-AT and preserved LV myocardium measured by electromechanical mapping could identify patients who have better acute improvement in systolic performance during LV stimulation.     

Simultaneous vs. sequential biventricular pacing in dilated cardiomyopathy: an acute hemodynamic study

AIMS: Simultaneous biventricular pacing improves left ventricular (LV) systolic performance in patients with dilated cardiomyopathy and intraventricular conduction delay. We tested the hypothesis that further improvements can be obtained using sequential biventricular pacing by optimizing both atrioventricular and interventricular delays. METHODS AND RESULTS: In 12 patients, LV pressure, right ventricular (RV) pressure and respective rates of change of pressure (dP/dt) were acutely measured during biventricular pacing with different atrioventricular and interventricular (VVi) intervals ranging from -60 to +40 ms. The average increase vs. baseline in maximum LV dP/dt was higher for sequential than for simultaneous biventricular pacing (VDD mode: 35+/-20 vs. 29+/-18%, P<0.01; DDD mode: 38+/-23 vs. 34+/-25%, P<0.01), with a minority of patients accounting for most of the difference. The mean optimal VVi was -25+/-21 ms in VDD mode and -25+/-26 ms in DDD mode. With these settings, RV dP/dt was not significantly different from baseline. QRS shortening was not predictive of LV dP/dt increase. CONCLUSION: A significant increase of LV dP/dt with no change in RV dP/dt can be obtained by sequential biventricular pacing as compared to simultaneous biventricular pacing. The highest LV dP/dt is achieved when LV is stimulated before RV. The hemodynamic advantage might be of clinical significance in selected cases.     

Effect of optimizing the VV interval on left ventricular contractility in cardiac resynchronization therapy

Simultaneous biventricular pacing improves left ventricular (LV) function in patients with heart failure and LV asynchrony. Proper timing of the interventricular pacing interval (VV interval) may further optimize LV function. We investigated the acute hemodynamic response of changing the VV interval using maximum LV dP/dt (LV dP/dt_max) as a parameter for LV function. A biventricular pacemaker was implanted in 53 patients with severely impaired LV function, New York Heart Association class III and IV heart failure, left bundle branch block, LV asynchrony, and a QRS interval >150 ms. Optimization of the atrioventricular and VV intervals was based on measurement of LV dP/dt_max by a 0.014-in sensor-tipped pressure guidewire. Measurement of LV dP/dt_max was obtained without complications in all patients. In patients in sinus rhythm with ischemic cardiomyopathy or idiopathic dilated cardiomyopathy, mean improvements by simultaneous biventricular pacing were 17% and 18%, respectively. Patients in atrial fibrillation showed an improvement of 21%. Optimizing the VV interval resulted in further absolute increases of 8%, 7%, and 3%, respectively, in dP/dt_max in the 3 groups. Maximum dP/dt was achieved with LV pacing first in 44 patients, simultaneous right and left ventricular pacing in 6 patients, and right ventricular pacing first in 3 patients. The mean optimal VV intervals were 37 ± 32 ms in the atrial fibrillation group, 28 ± 30 ms in the idiopathic dilated cardiomyopathy group, and 52 ± 31 ms in the ischemic cardiomyopathy group. Optimization of the VV interval significantly increased LV dP/dt_max compared with simultaneous biventricular pacing, and such optimization could be easily, accurately, and reliably evaluated by a 0.014-in sensor-tipped pressure guidewire.     

Nonexcitatory stimulus delivery improves left ventricular function in hearts with left bundle branch block

INTRODUCTION: Preliminary data in a heart failure animal model and isolated muscle preparation have suggested that nonexcitatory stimulation (NES) improves left ventricular (LV) function. METHODS AND RESULTS: We compared biventricular (BV) pacing with NES in an animal model with left bundle branch block (LBBB). The left bundle branch (LBB) was ablated in eight normal heart pigs and led to >50% increase in QRS duration (mean 100 +/- 15 msec). End-diastolic LV pressure, end-systolic LV pressure, LV pressure (LV dP/dtmax), aortic pulse pressure, and LV ejection fraction were measured before pre-LBB ablation and compared with post-LBB ablation (AAI pacing), BV pacing, NES delivery, and BV+NES. Moreover, to evaluate LV diastolic function, we measured the early (E wave) and late flows (A wave) through the mitral valve using spectral Doppler. Compared with post-LBB ablation, NES led to a significant increase in LV dP/dtmax (1,047 +/- 224 mmHg/sec vs 897 +/- 116 mmHg/sec; P < 0.05), LV ejection fraction (64% +/- 18% vs 49% +/- 17%; P < 0.05), and aortic pulse pressure (18 +/- 3.6 mmHg vs 16 +/- 2.8 mmHg; P < 0.05). Moreover, improvement in LV hemodynamic parameters was significantly higher during NES delivery when compared with BV pacing. No significant changes in E wave, A wave, and E/A were recorded during NES, NES+BV, and BV pacing. CONCLUSION: Our preliminary data demonstrate that NES is superior to BV pacing in improving LV function in an animal model with LBBB. Moreover, we demonstrated that NES does not affect transmitral valve flow and subsequently LV diastolic function.     

Hemodynamic effects of atrial septal pacing in cardiac resynchronization therapy patients

INTRODUCTION: Spontaneous or pacing-induced interatrial conduction delay may affect the outcome of heart failure patients treated with cardiac resynchronization therapy (CRT). The objective of this study was to evaluate the impact of the atrial pacing site (right atrial appendage, RAA; and low interatrial septum, LIS) during biventricular (BV) pacing on the left ventricular (LV) systolic function in candidates for CRT. METHODS AND RESULTS: Fifteen heart failure patients with left bundle branch block and LV ejection fraction < or =35% were enrolled. Electrodes were placed at the RAA, LIS, right ventricular apex, and LV free wall. A DDD protocol was tested, which consisted of 50 beats in AAI mode from the RAA followed by 50 beats in BV DDD mode with atrial pacing at the RAA (DDD_RAA) or at the LIS (DDD_LIS) at four AV delays. The average (+/-SD)%LV+dP/dtmax increase during DDD_RAA and DDD_LIS pacing with respect to baseline was 24 +/- 16% and 21 +/- 15%, respectively (P < 0.01), and average percentage change in aortic pulse pressure during DDD_RAA and DDD_LIS with respect to baseline (%PP) was 13 +/- 8% and 13 +/- 7% (ns). CONCLUSIONS: Our results show a significant hemodynamic improvement with both DDD_RAA and DDD_LIS biventricular pacing compared to AAI pacing. However DDD_LIS pacing was not superior to DDD_RAA pacing in acute hemodynamic responses.     

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.     

Acute hemodynamic effects of biventricular and left ventricular pacing in chronic pacemaker-dependent patients with advanced heart failure

The beneficial hemodynamic effects of cardiac resynchronization in patients with intraventricular conduction delay have been demonstrated. The potential hemodynamic effects of cardiac resynchronization to compensate the pacing-induced left ventricular conduction delay in chronically paced heart failure patients are not as well established. The aim of the study was to evaluate the acute hemodynamic effects of biventricular and left ventricular pacing in chronically paced patients with advanced heart failure.Fourteen consecutive pacemaker or defibrillator patients with permanent atrial fibrillation and AV block (11 male, 3 woman, mean age: 68 +/- 7 years) were enrolled in this study. There were 5 ischemic (36%) and 9 nonischemic (64%) patients (mean left ventricular ejection fraction: 19 +/- 5%; mean end-diastolic left ventricular diameter: 71 +/- 11 mm). In all patients a right ventricular and left ventricular (via coronary sinus) pacing lead was placed. The aortic and left ventricular hemodynamic measurements were performed using a two-channel micro-tip catheter. The measurements of the aortic pulse pressure (APP) and (dP/ dtmax) were performed during right ventricular apical pacing (RVP), left ventricular (LVP), and biventricular pacing (BVP) (70 bpm).Compared to RVP, LVP and BVP increased APP and dP/dtmax (35.8 +/- 4.2 vs 43.3 +/- 4.5 and 41.2 +/- 4 mmHg; p < 0.001) and (758 +/- 56 vs 967 +/- 60 and 961 +/- 62 mmHg/s; p < 0.001). LVP and BVP showed a comparable hemodynamic response. The hemodynamic effects were not related to the width of the paced QRS complex. Every patient showed improved hemodynamics during LVP and BVP unrelated to the underlying heart disease and to the baseline level of left ventricular dysfunction. BVP and LVP pacing acutely improve contractile left ventricular function in chronically paced patients with advanced heart failure.     

Mechanical dyssynchrony by 3D echo correlates with acute haemodynamic response to biventricular pacing in heart failure patients.

AIMS: One-third of dilated cardiomyopathy patients receiving a biventricular pacing-device do not respond to this form of therapy. Therefore, the utility of mechanical dyssynchrony by real-time 3D echocardiography (RT3DE) for predicting systolic response to biventricular pacing, of which maximal rate of pressure rise (dP/dt(max)) served as the gold-standard, was evaluated. METHODS AND RESULTS: Seventeen consecutive heart failure patients (aged 64 +/- 10 years, 8 male, 6 ischaemic cardiomyopathy, mean QRS duration 136 +/- 32 ms) underwent RT3DE and biventricular pacing. Post-processing software provided data of global left ventricular (LV) function and the systolic dyssynchrony index of 17 LV segments (SDI(17), %) for mechanical dyssynchrony. During biventricular pacing, percentual change in dP/dt(max) compared to the non-pacing mode, DeltadP/dt(max) was measured invasively with conductance catheters. LV ejection fraction was 31 +/- 10%, SDI(17) was 10.2 +/- 4.2% and percentual DeltadP/dt(max) during biventricular pacing was 14.5 +/- 12.4. A significant correlation (r = 0.729, P = 0.001) was found between SDI(17) and percentual DeltadP/dt(max), and between QRS duration and percentual DeltadP/dt(max) (r = 0.721, P = 0.001). CONCLUSION: The present study suggests that mechanical dyssynchrony measured by RT3DE shows a good correlation with invasively determined acute haemodynamic response to biventricular pacing in patients with symptomatic dilated cardiomyopathy. Future studies are needed to further define the clinical utility of RT3DE in identifying patients who are most likely to respond to cardiac resynchronization therapy.     

Ventricular pacing lead location alters systemic hemodynamics and left ventricular function in patients with and without reduced ejection fraction.

OBJECTIVES: We compared left ventricular (LV) systolic and diastolic function during right ventricular (RV), LV, and biventricular (BiV) pacing in patients with narrow QRS duration with and without LV dysfunction. BACKGROUND: The optimal RV pacing lead location for patients with a standard indication for ventricular pacing remains controversial. METHODS: Left ventricular pressure and volume data were determined via conductance catheter during electrophysiology study in 31 patients divided into groups with ejection fraction (EF) > or =40% (n = 17) or EF <40% (n = 14). QRS duration was 91 +/- 18 versus 106 +/- 25 ms, respectively (p = NS). Hemodynamic data were recorded during atrial and dual chamber pacing from the RV apex, RV free wall, RV septum, LV free wall, and BiV. RESULTS: In patients with EF > or =40%, RV pacing at 1 or more sites, but not LV free wall or BiV pacing, significantly (p < 0.05) impaired cardiac output (CO), stroke work (SW), EF, and LV relaxation compared with atrial overdrive pacing. Right ventricular pacing also impaired hemodynamics and LV function in patients with EF <40%. However, LV and BiV pacing increased CO, SW, EF, and LV +dP/dt(MAX) in patients with LV dysfunction. Left ventricular and BiV pacing enhanced an index of global LV cycle efficiency in patients with depressed EF. The detrimental hemodynamic effects of RV pacing were attenuated by selecting the optimal RV pacing site. CONCLUSIONS: Right ventricular pacing worsens LV function in patients with and without LV dysfunction unless the RV pacing site is optimized. Left ventricular and BiV pacing preserve LV function in patients with EF >40% and improve function in patients with EF <40% despite no clinical indication for BiV pacing.