Effect of pacing-induced ventricular dyssynchrony on right ventricular function

Background: Asynchronous electrical activation induced by right ventricular (RV) pacing can cause several abnormalities in left ventricular (LV) function. However, the effect of ventricular pacing on RV function has not been well established. We evaluated RV function in patients undergoing long‐term RV pacing. Methods: Eighty‐five patients and 24 healthy controls were included. After pacemaker implantation, conventional echocardiography and strain imaging were used to analyze RV function. Strain imaging measurements included peak systolic strain and strain rate. LV function and ventricular dyssynchrony by tissue Doppler imaging (TDI) were assessed. Intra‐ and interobserver variabilities of TDI parameters were tested on 15 randomly selected cases. Results: All patients were in New York Heart Association functional class I or II and percentage of ventricular pacing was 96 ± 4%. RV apical induced interventricular dyssynchrony in 49 patients (60%). LV dyssynchrony was found in 51 patients (60%), when the parameter examined was the standard deviation of the time to peak myocardial systolic velocity of all 12 segments greater than 34 ms. Likewise, septal‐to‐lateral delay ≥65 ms was found in 31 patients (36%). All echocardiographic indexes of RV function were similar between patients and controls (strain: ?22.8 ± 5.8% vs ?22.1 ± 5.6%, P = 0.630; strain rate: ?1.47 ± 0.91 s^?1 vs ?1.42 ± 0.39 s^?1, P = 0.702). Intra‐ and interobserver variability for RV strain was 3.1% and 5.3%, and strain rate was 1.3% and 2.1%, respectively. Conclusions: In patients with standard pacing indications, RV apical pacing did not seem to affect RV systolic function, despite induction of electromechanical dyssynchrony. (PACE 2011; 34:155–162)     

Impact of Temporary Interruption of Right Ventricular Pacing for Heart Block on Left Ventricular Function and Dyssynchrony

Background: The increasing data suggest an association between chronic right ventricular (RV) and left ventricular (LV) dysfunction. We sought to determine the effect of temporary interruption of long-term RV pacing on LV function and mechanical dyssynchrony in children and young adults with complete heart block.
Methods: Twelve patients aged 20.0 ± 7.4 years with congenital heart block (group I) and six patients aged 22.7 ± 11.0 years with surgically acquired heart block (group II) with RV pacing were studied. The pacing rate was reduced to less than patient's intrinsic heart rate and maintained for 5 minutes. The LV ejection fraction (EF), three-dimensional systolic dyssynchrony index (SDI), two-dimensional global longitudinal strain and strain rate, and Doppler-derived isovolumic acceleration before and after interruption of RV pacing were compared.
Results: The LVEF and GLS increased while QRS duration decreased after the pacing interruption in both the groups (all P < 0.05). While SDI decreased in both groups I (6.8 ± 2.3%– 3.8 ± 0.8%, P = 0.001) and II (9.2 ± 4.1 %– 5.0 ± 1.6%, P = 0.032), it remained higher in group II than in group I (P = 0.046) after the pacing interruption. The prevalence of LV dyssynchrony (SDI > 4.7%) decreased in group I (83 %– 25%, P = 0.006) but not in group II (67 %– 50%, P = 0.50). The %increase in LVEF correlated positively with %reduction of LV SDI (r = 0.80, P = 0.001).
Conclusions: Temporary interruption of chronic RV pacing acutely improves LV dyssynchrony and systolic function in children and young adults, the magnitude of which is greater in patients with congenital than those with surgically acquired heart block. (PACE 2010; 41–48)     

Right Ventricular Septal Pacing: A Comparative Study of Outflow Tract and Mid Ventricular Sites

Background: Prolonged right ventricle (RV) apical pacing is associated with left ventricle (LV) dysfunction due to dysynchronous ventricular activation and contraction. Alternative RV pacing sites with a narrower QRS compared to RV pacing might reflect a more physiological and synchronous LV activation. The purpose of this study was to compare the QRS morphology, duration, and suitability of RV outflow tract (RVOT) septal and mid‐RV septal pacing. Methods: Seventeen consecutive patients with indication for dual‐chamber pacing were enrolled in the study. Two standard 58‐cm active fixation leads were passed to the RV and positioned in the RVOT septum and mid‐RV septum using a commercially available septal stylet (model 4140, St. Jude Medical, St. Paul, MN, USA). QRS duration, morphology, and pacing parameters were compared at the two sites. The RV lead with less‐satisfactory electrical parameters was withdrawn and deployed in the right atrium. Results: Successful positioning of the pacing leads at the RVOT septum and mid‐RV septum was achieved in 15 patients (88.2%). There were no significant differences in the mean stimulation threshold, R‐wave sensing, and lead impedance between the two sites. The QRS duration in the RVOT septum was 151 ± 14 ms and in the mid‐RV septum 145 ± 13 ms (P = 0.150). Conclusions: This prospective observational study shows that septal pacing can be reliably achieved both in the RVOT and mid‐RV with active fixation leads using a specifically shaped stylet. There are no preferences in regard to acute lead performance or paced QRS duration with either position. (PACE 2010; 33:1169–1173)     

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.     

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.     

The Road to Right Ventricular Septal Pacing: Techniques and Tools

Prolonged right ventricular (RV) apical pacing is associated with progressive left ventricular dysfunction due to dysynchronous ventricular activation and contraction. RV septal pacing allows a narrower QRS compared to RV apical pacing, which might reflect a more physiological and synchronous ventricular activation. Previous clinical studies, which did not consistently achieve RV septal pacing, were not confirmatory and need to be repeated. This review summarizes the anatomy of the RV septum, the radiographic appearances of pacing leads in the RV, the electrocardiograph correlates of RV septal lead positioning, and the techniques and tools required for implantation of an active‐fixation lead onto the RV septum. Using the described techniques and tools, conventional active‐fixation leads can now be reliably secured to either the RV outflow tract septum or mid‐RV septum with very low complication rates and good long‐term performance. Even though physiologic and hemodynamic studies on true RV septal pacing have not been completed, the detrimental effects of long‐term RV apical pacing are significant enough to suggest that it is now time to leave the RV apex and secure all RV leads onto the septum. (PACE 2010; 888–898)     

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.     

Search for the Optimal Right Ventricular Pacing Site: Design and Implementation of Three Randomized Multicenter Clinical Trials

Background: The optimal site to permanently pace the right ventricle (RV) has yet to be determined. To address this issue, three randomized prospective multicenter clinical trials are in progress comparing the long-term effects of RV apical versus septal pacing on left ventricular (LV) function. The three trials are Optimize RV Selective Site Pacing Clinical Trial (Optimize RV), Right Ventricular Apical and High Septal Pacing to Preserve Left Ventricular Function (Protect Pace), and Right Ventricular Apical versus Septal Pacing (RASP).
Methods: Patients that require frequent or continuous ventricular pacing are randomized to RV apical or septal pacing. Optimize RV excludes patients with LV ejection fraction <40% prior to implantation, whereas the other trials include patients regardless of baseline LV systolic function. The RV septal lead is positioned in the mid-septum in Optimize RV, the high septum in Protect Pace, and the mid-septal inflow tract in RASP. Lead position is confirmed by fluoroscopy in two planes and adjudicated by a blinded panel. The combined trials will follow approximately 800 patients for up to 3 years.
Results: The primary outcome in each trial is LV ejection fraction evaluated by radionuclide ventriculography or echocardiography. Secondary outcomes include echo-based measurements of ventricular/atrial remodeling, 6-minute hall walk distance, brain natriuretic peptide levels, and clinical events (atrial tachyarrhythmias, heart failure, stroke, or death).
Conclusion: These selective site ventricular pacing trials should provide evidence of the importance of RV pacing site in the long-term preservation of LV function in patients that require ventricular pacing and help to clarify the optimal RV pacing site.     

Altered left ventricular contraction pattern during right ventricular pacing: assessment using real-time three-dimensional echocardiography

Background: Chronic right ventricular apical (RVA) pacing has been associated with increased risk of heart failure and adverse outcome. The acute effects of RVA pacing on three‐dimensional (3D) ventricular function and mechanical dyssynchrony are not well known. We performed a real‐time 3D echocardiographic (RT3DE) study to assess global and regional left ventricular function during RVA pacing. Methods: Twenty‐six patients with implanted cardiac devices and normal intrinsic atrioventricular conduction were included in the study. RT3DE was performed during intrinsic sinus rhythm and during RVA pacing. Quantification of global and regional left ventricular function was performed offline by time‐volume analysis of 16 myocardial segments. Time to reach minimum regional volume was calculated for each segment as a percentage of the cardiac cycle. The systolic dyssynchrony index (SDI) was defined as the standard deviation of these time periods. Longitudinal function was assessed by time‐volume analysis of apical, midventricular, and basal segments. Results: During RVA pacing, a reversed apical‐to‐basal longitudinal contraction sequence was observed in 58% of all patients. RVA pacing was associated with increased left ventricular (LV) dyssynchrony (SDI increase from 4.4 ± 2.2% to 6.3 ± 2.4%, P = 0.001) and reduced LV ejection fraction (decrease from 53 ± 13% to 47 ± 14%, P = 0.05). Conclusion: RT3DE assessment of LV function provides evidence that pacing from the RVA results in acute alterations in LV contraction sequence and increased LV dyssynchrony. Further studies are warranted to assess the potential of RT3DE to identify patients who might be at increased risk of pacing‐induced heart failure or who might benefit from alternate‐site or multisite pacing. (PACE 2011; 76–81)     

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.     

Pacing within the Ischemic Area Significantly Decreases the Left Ventricular Ejection Fraction during Experimental Acute Myocardial Infarction

Background: The aim of this study was to examine the effects on left ventricular (LV) function of LV apical or/and lateral wall pacing during an experimental acute myocardial infarction. Methods: In 12 anesthetized pigs, epicardial LV pacing at the apex or lateral wall, or at both sites simultaneously, was performed before and after left anterior descending (LAD) ligation. Data concerning LV function were obtained by two‐dimensional echo during spontaneous sinus rhythm (SR) and during pacing before and 15, 45, 60, and 90 minutes after LAD ligation. Results: Before ligation of the LAD, pacing at the lateral wall (48.04 ± 6.25%) or both sites (45.71 ± 6.31%) reduced the LV ejection fraction (EF) significantly (P < 0.01) in comparison to SR (55.44 ± 4.10%). However, during pacing at the apex (50.19 ± 6.50%), the reduction was not significant. After LAD ligation, the EF during lateral pacing (43.02 ± 7.71%) was significantly higher than during apical pacing (38.78 ± 8.26%, P < 0.04) but was not significantly different from that during dual‐site pacing (41.65 ± 8.69%). Conclusions: Pacing within the ischemic LV apical zone after LAD ligation impairs left ventricular ejection fraction, as compared with pacing the nonischemic LV lateral wall, and should therefore be avoided in clinical settings where the LV pacing site may be chosen. (PACE 2011; 63–71)     

Variability of Left Ventricular Electromechanical Activation during Right Ventricular Pacing: Implications for the Selection of the Optimal Pacing Site

Background: The right ventricular septum (RVS) and Hisian area (HA) are considered more “physiological” pacing sites than right ventricular apex (RVA). Studies comparing RVS to RVA sites have produced controversial results. There are no data about variability of electromechanical activation obtained by an approach using fluoroscopy and electrophysiological markers. This study compared the variability of left ventricular (LV) electromechanical activation in patients undergoing short‐term RVA and RVS with that measured during HA pacing based on fluoroscopy and electrophysiological markers. Methods: Tissue Doppler echocardiography was performed in 142 patients before and after RVA (54), RVS (44), and HA (44) pacing. Electromechanical activation was assessed by: (1) electromechanical latency (EML)‐interval between QRS onset and mechanical activation of basal LV; (2) intra‐LV dyssynchrony (intra‐LV)‐interval between earliest to the latest LV basal motion. The intra‐ and interpatients variability among pacing groups were assessed. Results: Pacing from RVA showed longer EML and higher degree of intra‐LV than RVS and HA pacing. RVA and RVS showed a higher variability than HA pacing with regard to intrapatient changes of EML (RVA vs RVS, P = 0.4; RVS vs HA, P = 0.01, RVA vs HA, P = 0.0002) and intra‐LV (RVA vs RVS, P = 0.2; RVS vs HA, P = 0.04; RVA vs HA, P = 0.005). Similar results were found in interpatients variability from paced‐values. Conclusions: RVA and RVS pacing produce a variable effect on LV electromechanical activation that is significantly more pronounced than HA pacing. A pacing site such as HA selected by fluoroscopic and electrophysiological markers maintains baseline and homogeneous LV activation pattern. (PACE 2010; 566–574)     

Site‐Specific Differences in Latency Intervals during Biventricular Pacing: Impact on Paced QRS Morphology and Echo‐Optimized V‐V Interval

Objective: To investigate differences in latency intervals during right ventricular (RV) pacing and left ventricular (LV) pacing from the (postero‐)lateral cardiac vein in cardiac resynchronization therapy (CRT) patients and their relationship to echo‐optimized interventricular (V‐V) intervals and paced QRS morphology. Methods: We recorded digital 12‐lead electrocardiograms in 40 CRT patients during RV, LV, and biventricular pacing at three output settings. Stimulus‐to‐earliest QRS deflection (latency) intervals were measured in all leads. Echocardiographic atrioventricular (AV) and V‐V optimization was performed using aortic velocity time integrals. Results: Latency intervals were longer during LV (34 ± 17, 29 ± 15, 28 ± 15 ms) versus RV apical pacing (17 ± 8, 15 ± 8, 13 ± 7 ms) for threshold, threshold ×3, and maximal output, respectively (P < 0.001), and shortened with increased stimulus strength (P < 0.05). The echo‐optimized V‐V interval was 58 ± 31 ms in five of 40 (12%) patients with LV latency ≥ 40 ms compared to 29 ± 20 ms in 35 patients with LV latency < 40 ms (P < 0.01). During simultaneous biventricular pacing, four of five (80%) patients with LV latency ≥ 40 ms exhibited a left bundle branch block (LBBB) pattern in lead V₁ compared to three of 35 (9%) patients with LV latency < 40 ms (P < 0.01). After optimization, all five patients with LV latency ≥ 40 ms registered a dominant R wave in lead V₁. Conclusions: LV pacing from the lateral cardiac vein is associated with longer latency intervals than endocardial RV pacing. LV latency causes delayed LV activation and requires V‐V interval adjustment to improve hemodynamic response to CRT. Patients with LV latency ≥ 40 ms most often display an LBBB pattern in lead V₁ during simultaneous biventricular pacing, but a right bundle branch block after V‐V interval optimization. (PACE 2010; 1382–1391)     

Atrial Bigeminy Results in Decreased Left Ventricular Function: An Insight into the Mechanism of PVC‐Induced Cardiomyopathy

Background: Premature ventricular complexes have been recently recognized as a reversible cause of cardiomyopathy. The purpose of this study was to determine if premature complexes independent of “dyssynchrony” resulted in increased left ventricular (LV) dimensions and decreased LV function. Methods: Ten mongrel dogs underwent the implantation of a pacemaker and were randomized to a control group (n = 5) or a paced group (n = 5). In the paced group, the pacemaker was connected to two endocardial atrial leads, one inserted into the atrial port and the other one into the ventricular port with an atrioventricular delay adjusted to ensure the presence of coupled pacing simulating atrial bigeminy with conducted beats in the absence of aberrancy. Echocardiographic parameters of LV size (LV end‐diastolic diameter [LV‐EDD], LV end‐systolic diameter [LV‐ESD]), and LV ejection fraction (LVEF) were measured at baseline and after 4 weeks of monitoring (control group) or pacing (paced group). Results: In the control group, LV size decreased with no significant changes in LVEF: 55% at baseline versus 70% at 4 weeks (P = 0.23). In the paced group, LV‐EDD decreased with no significant change in LV‐ESD. Unlike the control group, LVEF decreased significantly from 69 ± 9% at baseline to 32 ± 22% after 4 weeks of pacing (P = 0.05). Conclusion: We have shown that 4 weeks of coupled pacing simulating atrial bigeminy significantly reduced LV function. Our findings suggest that premature complexes independent of ventricular dyssynchrony might lead to the development of cardiomyopathy. (PACE 2012; 35:1232–1235)     

Linking as the Cause of Unnecessary Right Ventricular Pacing

Background: The current report describes a manifestation of linking phenomenon in DDD pacemaker recipients: impairment of atrioventricular (AV) conduction and ensuing unnecessary right ventricular (RV) pacing. Methods: Three patients with second‐degree AV block and sudden impairment of native AV conduction following pacemaker implantation are presented. Loss of native AV conduction was considered functional and related to repetitive retrograde invasion of ventricular depolarization to the AV junction that was “linked” to ventricular pacing triggered by nonconducted P‐waves. Conclusion: This case series demonstrates that linking phenomenon should be considered in analysis of pacemaker behavior, and that retrograde concealment can be responsible for unnecessary RV pacing. (PACE 2010; 1359–1363)     

Effect of Right Ventricular Apical Pacing in Survivors of Myocardial Infarction

Background: Much information is available regarding the possible negative effects of long-term right ventricular (RV) apical pacing, which may cause worsening of heart failure. However, very limited data are available regarding the effects of RV pacing in patients with a previous myocardial infarction (MI).
Methods and Results: We screened 115 consecutive post-MI patients and matched a group of 29 pacemaker (PM) recipients with a group of 49 unpaced patients, for age, left ventricular (LV) ejection fraction, and site of MI. During a median follow-up of 54 months, echocardiograms showed a decrease in LV ejection fraction in the paced group, from 51 ± 10 to 39 ± 11 (P < 0.01), and a minimal change in the unpaced group, from 57 ± 8 to 56 ± 7 (P = 0.98). Similar change was observed in systolic and diastolic diameters and volumes.
Conclusions: The study showed that, in post-MI patients, RV apical pacing was associated with a worsening of LV function, suggesting that, among MI survivors, the need for a PM is a marker of worse outcome .     

Pacemaker optimization in nonresponders to cardiac resynchronization therapy: left ventricular pacing as an available option

Background: Echocardiographic (ECHO)‐guided pacemaker optimization (PMO) in cardiac resynchronization therapy (CRT) nonresponders acutely improves left ventricular (LV) function. However, the chronic results of LV pacing in this group are less understood. Methods: We retrospectively studied 28 CRT nonresponders optimized based on ECHO to LV pacing and compared them to 28 age‐ and gender‐matched patients optimized to biventricular (BiV) pacing. ECHOs with tissue Doppler imaging assessed LV hemodynamics before, immediately after, and 29 ± 16 months after PMO. Also, 56 age‐ and gender‐matched CRT responders were included for comparison of clinical outcomes. Results: PMO resulted in acute improvements in longitudinal LV systolic function and several measures of dyssynchrony, with greater improvements in the LV paced group. Chronic improvements in ejection fraction (EF) (3.2 ± 7.7%), and left ventricle end‐systolic volume (LVESV) (?11 ± 36 mL) and one dyssynchrony measure were seen in the combined group. Chronically, both LV and BiV paced patients improved some measures of systolic function and dyssynchrony although response varied between the groups. Survival at 3.5 years was similar (P = 0.973) between the PMO (58%) and nonoptimized groups (58%) but survival free of cardiovascular hospitalization was significantly (P = 0.037) better in the nonoptimized group. Conclusions : CRT nonresponders undergoing PMO to either LV or BiV pacing have acute improvements in longitudinal systolic function and some measures of dyssynchrony. Some benefits are sustained chronically, with improvements in EF, LVESV, and dyssynchrony. A strategy of ECHO‐guided PMO results in survival for CRT nonresponders similar to that of CRT patients not referred for PMO. (PACE 2012; 35:685–694))     

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.     

The Effect of Ventricular Activation Sequence on Cardiac Performance During Pacing

The aim of this study was to evaluate the importance of a normal ventricular activation pattern for cardiac performance. In nine mongrel clogs, atrial pacing was compared to AV synchronous pacing at three different A V delays (150, 100, and 60 nis). In six dogs, proximal septal AV synchronous pacing was compared to apical A V synchronous pacing at three different A V delays. AV synchronous pacing was performed after RF induced complete heart block. Hemodynarnics were evaluated by assessment of positive and negative dP/dt, cardiac output, and left ventricular and pulmonary pressures. Atrial pacing was superior to AV synchronous pacing with respect to positive and negative dP/dt and cardiac output. This difference was present at all AV delays. Proximal septal pacing was associated with a higher positive and negative dP/dl compared to apical pacing at all AV delays. Left ventricular activation time was significantly shorter during proximal septal pacing than during apical pacing (88 ± 4 vs 115 ± 4 ms, P < 0.001). We conclude that atrial and proximal septal pacing improves cardiac function and shortens the ventricular activation time compared to apical AV synchronous pacing independent of the AV interval.     

Single Site Left Ventricular Pacing induced Dyssynchrony and Cardiomyopathy

Single site left ventricular (LV) pacing in the absence of intrinsic ventricular activity can be as detrimental to LV function as right ventricular apical pacing. This report describes a patient with complete heart block who developed significant dyssynchrony and cardiomyopathy secondary to single site lateral LV pacing. The process was reversed by placement of a second anterior LV lead. (PACE 2013; 36:e35–e37)