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.     

Right heart failure due to loss of right ventricular capture in a patient with atrioventricular junction ablation and biventricular pacing

We describe the case of a patient with atrioventricular (AV) junction ablation and chronic biventricular pacing in which intermittent dysfunction of the right ventricular (RV) lead resulted in left ventricular (LV) stimulation alone and onset of severe right heart failure. Restoration of biventricular pacing by increasing device output and then performing lead revision resolved the issue. This case provides evidence that LV pacing alone in patients with AV junction ablation may lead to severe right heart failure, most likely as a result of iatrogenic mechanical dyssynchrony within the RV. Thus, probably this pacing mode should be avoided in pacemaker-dependent patients with heart failure.     

Left ventricular dyssynchrony resulting from right ventricular apical pacing: relevance of baseline assessment

Objectives: Evaluation of left ventricular (LV) dyssynchrony in patients undergoing short‐term right ventricular apical (RVA) pacing and correlation with baseline echocardiographic and clinical characteristics. Background: RVA pacing causes abnormal ventricular depolarization that may lead to mechanical LV dyssynchrony. The relationships between pacing‐induced LV dyssynchrony and baseline echocardiographic and clinical variables have not been fully clarified. Methods: Tissue Doppler echocardiography was performed in 153 patients before and after RVA pacing. LV dyssynchrony was measured by the time between the shortest and longest electromechanical delays in the five basal LV segments (intra‐LV). The prevalence and degree of LV dyssynchrony after RVA pacing was evaluated in three groups: baseline LV ejection fraction (LVEF) <35%, 35–55%, and ≥55%. The intrapatient effect of RVA pacing was determined as the percent increase in intra‐LV value (Δintra‐LV%). The pacing‐induced intra‐LV was correlated with baseline variables. Results: The prevalence and degree of LV dyssynchrony after RVA pacing was significantly higher in patients with lower LVEF (P < 0.001). ΔIntra‐LV% was inversely correlated with baseline intra‐LV and LVEF (B =?2.6, B =?4.2, P < 0.001). Baseline intra‐LV and LV end‐systolic volume correlated positively with intra‐LV after RVA pacing (B = 0.49, B = 0.6, P < 0.001), whereas LVEF showed an inverse correlation. Conclusions: The degree of LV dyssynchrony induced by RVA is variable. Patients with higher baseline LV dyssynchrony, more dilated LV, and more depressed LVEF showed a higher degree of LV dyssynchrony during pacing. These findings may assume importance in predicting the risk of heart failure in pacemaker patients.     

Morphology of the RV electrogram during LV pacing is related to the hemodynamic effect in cardiac resynchronization therapy

Background: Biventricular (BiV) pacing and left ventricular (LV) pacing both improve LV function in patients with heart failure and LV dyssynchrony. We studied the hemodynamic effect of the atrioventricular (AV) interval and the associated changes in the right ventricular (RV) electrogram (EGM) during LV pacing and compared this with the hemodynamic effect of optimized sequential BiV pacing.
Methods: In 16 patients with New York Heart Association (NYHA) class II to IV, sinus rhythm with normal AV conduction, left bundle branch block (LBBB), QRS > 130 ms, and optimal medical therapy, the changes in RV EGM during LV pacing with varying AV intervals were studied. The hemodynamic effect associated with these changes was evaluated by invasive measurement of LVdP/dt_max and compared with the result of optimized sequential BiV pacing in the same patient.
Results: All patients showed electrocardiographic fusion during LV pacing. The morphology of the RV EGM showed changes in the RV activation that indicated a shift in the extent of fusion from LV pacing. These changes were associated with significant changes in LVdP/dt_max. Baseline LV dP/dt_max was 734 ± 177 mmHg/s, which increased to 927 ± 202 mmHg/s (P<0.0001) with optimized LV pacing and to 920 ± 209 mmHg/s (P<0.0001) with optimized sequential BiV pacing.
Conclusion: The RV EGM is a proper indicator for intrinsic activation over the right bundle during LV pacing and reveals the transition to fusion in the RV EGM that is associated with a decrease in LVdP/dt_max. The hemodynamic effect of optimized LV pacing is equal to optimized sequential BiV pacing.     

Use of a retained guidewire to improve the left ventricular pacing threshold

Although transvenous access to the coronary veins has considerably simplified left ventricular (LV) pacing, it can remain a time consuming and arduous task achieving satisfactory pacing positions for the LV electrode. Common problems include negotiating small veins with adequate guide catheter stability, pacing electrode stability once positioned, and phrenic nerve stimulation. We report a case where use of the pacing lead guidewire resulted in a dramatic reduction in the pacing threshold of the LV lead, and saved the patient the need to undergo thoracotomy placement.     

Atrioventricular cross-talk in biventricular pacing: a potential cause of ventricular standstill

The aim of the study was to evaluate, in recipients of biventricular pacing systems, the risk of asystole due to ventricular pacing inhibition by sensing the left atrial signals by the LV lead at conventional sensitivity. Long-term ventricular sensitivity was programmed at > or = 4 m V in 17 consecutive recipients of ventricular resynchronization systems implanted for chronic management of congestive heart failure. Ventricular pacing inhibition due to AV cross-talk on spontaneous left atrial electrogram (AVCSA) was tested at a 2 mV ventricular sensitivity immediately after implantation of the stimulation system and 1 month later. Pacemaker dependence was also tested during temporary VVI pacing at a rate of 30 beats/min. AVCSA was observed in three patients. It was present on the day of implantation in one patient, and developed within the first month in two others. Asystole was observed in two of the three cases of AVCSA. Three pacemaker nondependent patients at the time of system implantation had become pacemaker dependent at 1 month. AVCSA was observed only with LV leads positioned in the great cardiac vein. In conclusion, asystole due to AVCSA was observed in 11% of recipients of ventricular resynchronization stimulation systems. Care should be taken in these patients to minimize the risk of atrial sensing by the LV lead, preferably avoiding its placement in the great cardiac vein. This phenomenon could be eliminated by the programmability of a right ventricular only sensing configuration.     

Electrocardiographic patterns during: pacing the great cardiac and middle cardiac veins

BACKGROUND: The electrocardiogram (ECG) patterns during pacing from the great cardiac vein (GCV) and the middle cardiac vein (MCV) are not well known. METHODS: We recorded 12-lead ECGs during GCV and MCV pacing in 26 patients undergoing implantation of a cardiac resynchronization device. The left ventricular (LV) lead was passed down the GCV (n = 19) or MCV (n = 7) prior to moving it to a lateral or posterolateral vein for permanent implantation. RESULTS AND CONCLUSIONS: Pacing within the GCV resulted in a left bundle branch block (LBBB) morphology with no or minimal R-wave in V(1) in 14 patients and a right bundle branch block (RBBB) pattern (R > S in lead V(1)) in four patients. In one patient, lead V1 during GCV pacing was isoelectric (R = S). A more distal pacing site in the GCV yielded a LBBB pattern in all the patients. All leads placed in the MCV resulted in a LBBB configuration. An ECG pattern with a RBBB pattern was invariably recorded during LV pacing in 125 consecutive outpatients with biventricular pacemakers and LV leads in the posterolatral and lateral coronary veins. Knowledge of the ECG patterns from various pacing sites in the coronary venous system may be helpful for troubleshooting all types of pacing systems, especially those where the coronary venous pacing site is unintentional.     

Biventricular pacing attenuates T-wave alternans and T-wave amplitude compared to other pacing modes

Background: The impact of altered ventricular activation, including biventricular (BV) pacing, on T-wave alternans (TWA) and arrhythmic substrates is unclear. We studied how differing ventricular activation sequence alters TWA; the interval from peak-to-end of the T-wave (TpTe) and T-wave amplitude during right (RV), left (LV), and biventricular (BV) pacing; and right atrial (RA) pacing in patients with preexisting conduction delay.
Methods and Results: We measured TWA during RA, RV, LV, and BV pacing in 33 patients receiving cardiac-resynchronization-therapy-defibrillators. TWA magnitude (V_alt) was lower during BV than RV (P < 0.01), RA (P < 0.01), or LV pacing. As a result, BV-TWA was more often negative than RV-TWA (P < 0.01), LV-TWA, and RA-TWA, particularly when discordant between pacing modes (P < 0.01). Overall, 83% of TWA recordings were abnormal (25% indeterminate), and 17% negative. BV pacing reduced T-wave amplitude (P < 0.05) and TpTe (P < 0.005) compared to RV pacing and LV pacing (P < 0.05; P < 0.005 respectively). Notably, TWA magnitude varied linearly with T-wave amplitude for all pacing modes (P < 0.001). Over 410 ± 252 days' follow-up, RV-TWA predicted the combined endpoint of death and ICD therapy with 86% negative predictive value (P < 0.05). BV-TWA, RA-TWA, and other repolarization indices were not predictive.
Conclusions: BV pacing attenuates TWA in tandem with reduced T-wave magnitude. In these patients with baseline QRS prolongation, RV-TWA predicted events more effectively than BV-TWA and RA-TWA. Further studies are required to understand how altered ventricular activation influences repolarization dynamics and arrhythmic tendency.     

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.     

速度向量成像评价DDD起搏前后心室收缩功能

目的 应用速度向量成像(velocity vector imaging,VVI)技术分析DDD起搏前后心室心肌运动速度、应变、应变率变化规律,初步探讨VVI技术的应用价值.方法 对17例DDD起搏患者于术前术后采用VVI技术检测心室各节段心肌收缩期纵向运动速度、应变、应变率和径向运动速度、环向应变及应变率,并比较术前术后差异.结果 术前术后左、右心室各室壁基底段、中间段、心尖段收缩期纵向峰值运动速度依次递减,基底段的速度最大,心尖段的速度最小;收缩期纵向应变、应变率在基底段、中间段及心尖段差异无统计学意义.左心室各室壁收缩期径向峰值运动速度、环向应变及应变率差异无统计学意义.右室后间隔与游离壁术前、术后平均峰值运动速度与应变率和术后平均应变均高于左室后间隔与侧壁,术后右室平均应变及应变率均高于左室.与术前相比,术后左室平均应变显著降低.结论 VVI技术能准确地定量评价DDD术前后节段性室壁功能及其变化.     

速度向量成像评价DDD起搏前后心室收缩功能

目的 应用速度向量成像(velocity vector imaging,VVI)技术分析DDD起搏前后心室心肌运动速度、应变、应变率变化规律,初步探讨VVI技术的应用价值.方法 对17例DDD起搏患者于术前术后采用VVI技术检测心室各节段心肌收缩期纵向运动速度、应变、应变率和径向运动速度、环向应变及应变率,并比较术前术后差异.结果 术前术后左、右心室各室壁基底段、中间段、心尖段收缩期纵向峰值运动速度依次递减,基底段的速度最大,心尖段的速度最小;收缩期纵向应变、应变率在基底段、中间段及心尖段差异无统计学意义.左心室各室壁收缩期径向峰值运动速度、环向应变及应变率差异无统计学意义.右室后间隔与游离壁术前、术后平均峰值运动速度与应变率和术后平均应变均高于左室后间隔与侧壁,术后右室平均应变及应变率均高于左室.与术前相比,术后左室平均应变显著降低.结论 VVI技术能准确地定量评价DDD术前后节段性室壁功能及其变化.     

速度向量成像评价DDD起搏前后心室收缩功能

目的 应用速度向量成像(velocity vector imaging,VVI)技术分析DDD起搏前后心室心肌运动速度、应变、应变率变化规律,初步探讨VVI技术的应用价值.方法 对17例DDD起搏患者于术前术后采用VVI技术检测心室各节段心肌收缩期纵向运动速度、应变、应变率和径向运动速度、环向应变及应变率,并比较术前术后差异.结果 术前术后左、右心室各室壁基底段、中间段、心尖段收缩期纵向峰值运动速度依次递减,基底段的速度最大,心尖段的速度最小;收缩期纵向应变、应变率在基底段、中间段及心尖段差异无统计学意义.左心室各室壁收缩期径向峰值运动速度、环向应变及应变率差异无统计学意义.右室后间隔与游离壁术前、术后平均峰值运动速度与应变率和术后平均应变均高于左室后间隔与侧壁,术后右室平均应变及应变率均高于左室.与术前相比,术后左室平均应变显著降低.结论 VVI技术能准确地定量评价DDD术前后节段性室壁功能及其变化.     

速度向量成像评价DDD起搏前后心室收缩功能

目的 应用速度向量成像(velocity vector imaging,VVI)技术分析DDD起搏前后心室心肌运动速度、应变、应变率变化规律,初步探讨VVI技术的应用价值.方法 对17例DDD起搏患者于术前术后采用VVI技术检测心室各节段心肌收缩期纵向运动速度、应变、应变率和径向运动速度、环向应变及应变率,并比较术前术后差异.结果 术前术后左、右心室各室壁基底段、中间段、心尖段收缩期纵向峰值运动速度依次递减,基底段的速度最大,心尖段的速度最小;收缩期纵向应变、应变率在基底段、中间段及心尖段差异无统计学意义.左心室各室壁收缩期径向峰值运动速度、环向应变及应变率差异无统计学意义.右室后间隔与游离壁术前、术后平均峰值运动速度与应变率和术后平均应变均高于左室后间隔与侧壁,术后右室平均应变及应变率均高于左室.与术前相比,术后左室平均应变显著降低.结论 VVI技术能准确地定量评价DDD术前后节段性室壁功能及其变化.     

速度向量成像评价DDD起搏前后心室收缩功能

目的 应用速度向量成像(velocity vector imaging,VVI)技术分析DDD起搏前后心室心肌运动速度、应变、应变率变化规律,初步探讨VVI技术的应用价值.方法 对17例DDD起搏患者于术前术后采用VVI技术检测心室各节段心肌收缩期纵向运动速度、应变、应变率和径向运动速度、环向应变及应变率,并比较术前术后差异.结果 术前术后左、右心室各室壁基底段、中间段、心尖段收缩期纵向峰值运动速度依次递减,基底段的速度最大,心尖段的速度最小;收缩期纵向应变、应变率在基底段、中间段及心尖段差异无统计学意义.左心室各室壁收缩期径向峰值运动速度、环向应变及应变率差异无统计学意义.右室后间隔与游离壁术前、术后平均峰值运动速度与应变率和术后平均应变均高于左室后间隔与侧壁,术后右室平均应变及应变率均高于左室.与术前相比,术后左室平均应变显著降低.结论 VVI技术能准确地定量评价DDD术前后节段性室壁功能及其变化.     

速度向量成像评价DDD起搏前后心室收缩功能

目的 应用速度向量成像(velocity vector imaging,VVI)技术分析DDD起搏前后心室心肌运动速度、应变、应变率变化规律,初步探讨VVI技术的应用价值.方法 对17例DDD起搏患者于术前术后采用VVI技术检测心室各节段心肌收缩期纵向运动速度、应变、应变率和径向运动速度、环向应变及应变率,并比较术前术后差异.结果 术前术后左、右心室各室壁基底段、中间段、心尖段收缩期纵向峰值运动速度依次递减,基底段的速度最大,心尖段的速度最小;收缩期纵向应变、应变率在基底段、中间段及心尖段差异无统计学意义.左心室各室壁收缩期径向峰值运动速度、环向应变及应变率差异无统计学意义.右室后间隔与游离壁术前、术后平均峰值运动速度与应变率和术后平均应变均高于左室后间隔与侧壁,术后右室平均应变及应变率均高于左室.与术前相比,术后左室平均应变显著降低.结论 VVI技术能准确地定量评价DDD术前后节段性室壁功能及其变化.     

速度向量成像评价DDD起搏前后心室收缩功能

目的 应用速度向量成像(velocity vector imaging,VVI)技术分析DDD起搏前后心室心肌运动速度、应变、应变率变化规律,初步探讨VVI技术的应用价值.方法 对17例DDD起搏患者于术前术后采用VVI技术检测心室各节段心肌收缩期纵向运动速度、应变、应变率和径向运动速度、环向应变及应变率,并比较术前术后差异.结果 术前术后左、右心室各室壁基底段、中间段、心尖段收缩期纵向峰值运动速度依次递减,基底段的速度最大,心尖段的速度最小;收缩期纵向应变、应变率在基底段、中间段及心尖段差异无统计学意义.左心室各室壁收缩期径向峰值运动速度、环向应变及应变率差异无统计学意义.右室后间隔与游离壁术前、术后平均峰值运动速度与应变率和术后平均应变均高于左室后间隔与侧壁,术后右室平均应变及应变率均高于左室.与术前相比,术后左室平均应变显著降低.结论 VVI技术能准确地定量评价DDD术前后节段性室壁功能及其变化.     

速度向量成像评价DDD起搏前后心室收缩功能

目的 应用速度向量成像(velocity vector imaging,VVI)技术分析DDD起搏前后心室心肌运动速度、应变、应变率变化规律,初步探讨VVI技术的应用价值.方法 对17例DDD起搏患者于术前术后采用VVI技术检测心室各节段心肌收缩期纵向运动速度、应变、应变率和径向运动速度、环向应变及应变率,并比较术前术后差异.结果 术前术后左、右心室各室壁基底段、中间段、心尖段收缩期纵向峰值运动速度依次递减,基底段的速度最大,心尖段的速度最小;收缩期纵向应变、应变率在基底段、中间段及心尖段差异无统计学意义.左心室各室壁收缩期径向峰值运动速度、环向应变及应变率差异无统计学意义.右室后间隔与游离壁术前、术后平均峰值运动速度与应变率和术后平均应变均高于左室后间隔与侧壁,术后右室平均应变及应变率均高于左室.与术前相比,术后左室平均应变显著降低.结论 VVI技术能准确地定量评价DDD术前后节段性室壁功能及其变化.     

速度向量成像评价DDD起搏前后心室收缩功能

目的 应用速度向量成像(velocity vector imaging,VVI)技术分析DDD起搏前后心室心肌运动速度、应变、应变率变化规律,初步探讨VVI技术的应用价值.方法 对17例DDD起搏患者于术前术后采用VVI技术检测心室各节段心肌收缩期纵向运动速度、应变、应变率和径向运动速度、环向应变及应变率,并比较术前术后差异.结果 术前术后左、右心室各室壁基底段、中间段、心尖段收缩期纵向峰值运动速度依次递减,基底段的速度最大,心尖段的速度最小;收缩期纵向应变、应变率在基底段、中间段及心尖段差异无统计学意义.左心室各室壁收缩期径向峰值运动速度、环向应变及应变率差异无统计学意义.右室后间隔与游离壁术前、术后平均峰值运动速度与应变率和术后平均应变均高于左室后间隔与侧壁,术后右室平均应变及应变率均高于左室.与术前相比,术后左室平均应变显著降低.结论 VVI技术能准确地定量评价DDD术前后节段性室壁功能及其变化.     

速度向量成像评价DDD起搏前后心室收缩功能

目的 应用速度向量成像(velocity vector imaging,VVI)技术分析DDD起搏前后心室心肌运动速度、应变、应变率变化规律,初步探讨VVI技术的应用价值.方法 对17例DDD起搏患者于术前术后采用VVI技术检测心室各节段心肌收缩期纵向运动速度、应变、应变率和径向运动速度、环向应变及应变率,并比较术前术后差异.结果 术前术后左、右心室各室壁基底段、中间段、心尖段收缩期纵向峰值运动速度依次递减,基底段的速度最大,心尖段的速度最小;收缩期纵向应变、应变率在基底段、中间段及心尖段差异无统计学意义.左心室各室壁收缩期径向峰值运动速度、环向应变及应变率差异无统计学意义.右室后间隔与游离壁术前、术后平均峰值运动速度与应变率和术后平均应变均高于左室后间隔与侧壁,术后右室平均应变及应变率均高于左室.与术前相比,术后左室平均应变显著降低.结论 VVI技术能准确地定量评价DDD术前后节段性室壁功能及其变化.     

Adverse effects of long-term right ventricular apical pacing and identification of patients at risk of atrial fibrillation and heart failure

In patients needing a pacemaker (PM) for bradycardia indications, the amount of right ventricular (RV) apical pacing has been correlated with atrial fibrillation (AFib) and heart failure (HF) in both DDD and VVI mode. RV pacing was linked with left ventricular (LV) dyssynchrony in almost 50% of patients with PM implantation and atrioventricular (AV) node ablation for AFib. In patients with normal systolic function needing a PM, apical RV pacing resulted in LV ejection fraction (LVEF) reduction. These negative effects were prevented by cardiac resynchronization therapy (CRT). Algorithms favoring physiological AV conduction are possible useful tools able to maintain both atrial and ventricular support and limit RV pacing. However, when chronic RV pacing cannot be avoided, it appears necessary to reconsider the cut-off value of basic LVEF for CRT. In HF patients, RV pacing can induce greater LV dyssynchrony, enhanced by underlying conduction diseases. In this context, a more deleterious effect of RV pacing in implantable cardioverter-defibrillator (ICD) patients with low LVEF can be expected. In some major ICD trials, DDD mode was correlated with increased mortality/HF. This negative impact was attributed to unnecessary RV pacing >40-50%, virtually absent in VVI-40 mode. However, some data suggest that avoiding RV pacing may also not be the best option for patients requiring an ICD. In patients with impaired LV function, AV synchrony should therefore be ensured. The best pacing mode in ICD patients with HF should be defined on an individual basis.