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Background Right ventricular (RV) pacing causes delayed activation of remote ventricular segments. We used the ultrahigh-frequency ECG (UHF-ECG) to describe ventricular depolarization when pacing different RV locations.Methods In 51 patients, temporary pacing was performed at the RV septum (mSp); further subclassified as right ventricular inflow tract (RVIT) and right ventricular outflow tract (RVOT) for septal inflow and outflow positions (below or above the plane of His bundle in right anterior oblique), apex, anterior lateral wall, and at the basal RV septum with nonselective His bundle or RBB capture (nsHBorRBBp). The timings of UHF-ECG electrical activations were quantified as left ventricular lateral wall delay (LVLWd; V8 activation delay) and RV lateral wall delay (RVLWd; V1 activation delay).Results The LVLWd was shortest for nsHBorRBBp (11 ms [95% confidence interval = 5-17]), followed by the RVIT (19 ms [11-26]) and the RVOT (33 ms [27-40]; p < .01 between all of them), although the QRSd for the latter two were the same (153 ms (148-158) vs. 153 ms (148-158); p = .99). RV apical capture not only had a longer LVLWd (34 ms (26-43) compared to mSp (27 ms (20-34), p < .05), but its RVLWd (17 ms (9-25) was also the longest compared to other RV pacing sites (mean values for nsHBorRBBp, mSp, anterior and lateral wall captures being below 6 ms), p < .001 compared to each of them.Conclusion RVIT pacing produces better ventricular synchrony compared to other RV pacing locations with myocardial capture. However, UHF-ECG ventricular dysynchrony seen during RVIT pacing is increased compared to concomitant capture of basal septal myocytes and His bundle or proximal right bundle branch.

Introduction: We investigated whether pacing-induced electrical dyssynchrony at the time of cardiac resynchronization therapy (CRT) device implantation was associated with chronic CRT response. Methods and Results: We included a total of 69 consecutive heart failure patients who received a CRT device. Left (LVp-RVs) and right (RVp-LVs) pacing-induced interlead delays were measured intraoperatively and used to determine if there was paced left ventricular (LV) dyssynchrony, defined as present when LVp-RVs is larger than RVp-LVs. CRT response was defined as a reduction in LV end-systolic volume ≥15%, 6 months after implantation. Paced left ventricular dyssynchrony (PLVD) was associated with ischemic cardiomyopathy (ICM) (χ 2: 8; P =.005) but not with QRS morphology nor with pacing lead positions. In a univariate analysis, PLVD (odds ratio [OR], 6.53; 95% confidence interval [CI], 2.2-18.9; P =.001), atypical left bundle branch block (LBBB) (OR, 3.3; 95% CI, 1.2-9.4; P =.022), and ICM (OR, 5.2; 95% CI, 1.6-17; P =.006) were associated with nonresponse. In a multivariate analysis, both PLVD (OR, 9.74; 95% CI, 2.8-33.9; P 2 to enter: 8; P

Pacing is a well established therapy for bradycardia support and certain types of heart failure. Despite technological advances the optimal pacing lead position remains controversial. Right ventricular pacing, particularly apical has been the site of choice but the induction of abnormal cardiac depolarization and the recognition of an increased risk of impairment of left ventricular systolic function, heart failure and mortality has driven a desire for a true physiological pacing system. A number of different lead positions have been determined and of these His bundle pacing appears to most closely mimic normal ventricular conduction. This article reviews the background to the development of physiological pacing, evaluates historical data for right ventricular pacing and the basis for change and new lead positions.

Pacing is an established and ubiquitous treatment of bradycardias and some types of heart failure. The optimal pacing lead position which maximizes cardiac function and minimizes deterioration of ventricular function remains controversial. The desire to achieve a physiological pacing system that mimics cardiac function has led to the investigation of several potential pacing sites. This editorial provides an overview of past and current pacing lead position and summaries the current and future direction of physiological pacing.

Introduction Fifteen to thirty percent of patients with impaired cardiac function have ventricular dyssynchrony and warrant cardiac resynchronization therapy (CRT). While leadless pacemakers eliminate lead-related complications, their current form factor is limited to single-chamber pacing. In this study, we demonstrate the feasibility of multisite, simultaneous pacing using miniaturized pacing nodes powered through wireless power transfer (WPT). Methods A wireless energy transfer system was developed based on resonant coupling at approximately 200 MHz to power multiple pacing nodes. The pacing node comprises circuitry to efficiently convert the harvested energy to output stimuli. To validate the use of these pacing nodes, ex vivo studies were carried out on Langendorff rodent heart models (n = 4). To mimic biventricular pacing, two beating Langendorff rodent heart models, kept 10 cm apart, were paced using two distinct pacing nodes, each attached on the ventricular epicardial surface of a given heart. Results All ex vivo Langendorff heart models were successfully paced with a simple coil antenna at 2 to 3 cm from the pacing node. The coil was operated at 198 MHz and 0.3 W. Subsequently, simultaneous pacing of two Langendorff heart models 30 cm apart using an output power of 5 W was reliably demonstrated. Conclusion WPT provides a feasible option for multisite, wireless cardiac pacing. While the current system remains limited in design, it offers support and a conceptual framework for future iterations and eventual clinical utility.

Electrocardiographic VV Optimization. Introduction: Echocardiographic optimization of the VV interval may improve CRT response, but it is time-consuming and not routinely performed. The aim of this study was to compare the response to cardiac resynchronization therapy (CRT) when the interventricular pacing (VV) interval was optimized by Tissue Doppler Imaging (TDI) to CRT response when it was optimized following QRS width criteria. Methods and Results: The study included 156 consecutive CRT patients with severe heart failure and left bundle-branch block configuration. Atrioventricular interval was selected according to a pulsed Doppler assessment, and VV optimization was randomly assigned to echocardiography (ECHO group, n = 78) or electrocardiography (ECG group, n = 78). Optimal VV was defined for the ECHO group as producing the best LV intraventricular synchrony according to TDI displacement curves and for the ECG group as resulting in the narrowest QRS measured from the earliest deflection. At 6-month follow-up, percentage of echocardiographic responders (defined as neither death nor heart transplantation and a LV end-systolic volume reduction >10%) was higher in the ECG optimized group (50.0% vs 67.9%; P = 0.023), whereas clinical response (defined as neither death nor heart transplantation and >10% improvement in the 6-minute walking test) was similar in both groups (71.8% vs 73.1%; P = 0.858). Conclusions: VV optimization based on QRS width obtained a higher percentage of responders in terms of LV reverse remodeling compared to the TDI method. (J Cardiovasc Electrophysiol, Vol. 22, pp. 1129-1134, October 2011)

Background: Right ventricular (RV) pacing may be detrimental to ventricular function. However, the acute effects of electromechanical dyssynchrony on RV function are not well characterized in children. We studied acute effects of electromechanical dyssynchrony, induced by RV apical and RV outflow pacing, in children with normal hearts, evaluating electromechanical synchrony, hemodynamic response, and RV function. Methods: Seventeen children (mean ± SD, 12 ± 4 years) with normal cardiac structure/function were paced after accessory pathway ablation, at baseline (AOO), and with AV pacing (DOO) from the RV apex and RV outflow. QRS duration was determined from surface ECG. Intra- and interventricular mechanical dyssynchrony and regional ventricular function were determined using tissue Doppler imaging. Global RV systolic and diastolic functions were assessed by RV dP/dTmax and RV dP/dTneg using pressure-tipped transducers. Regional RV function was assessed by tissue Doppler imaging. Cardiac index (CI) and blood pressures were measured. Results: RV apical and outflow pacing induced significant electromechanical dyssynchrony manifested by lengthening of the QRS duration, increased LV intraventricular delay (49 ± 34 ms, 53 ± 43 ms, respectively, P < 0.001), and increased interventricular delay (60 ± 29 ms, 55 ± 37 ms, P < 0.0001) versus AOO pacing. However, there was no change in blood pressure, CI, RV dp/dTmax, RV dP/dTneg, or regional tissue Doppler velocities, indicating preserved hemodynamics and preserved global and regional RV systolic and diastolic function. Conclusions: In children with normal cardiac function and structure, pacing-induced electromechanical dyssynchrony did not acutely affect RV systolic and diastolic function and did not acutely alter global hemodynamics. Therefore, electromechanical dyssynchrony may only be an important therapeutic target in the setting of decreased RV function.

Introduction: Patients with heart block have conventionally received a pacemaker that stimulates the right ventricular apex (RVA) to restore heart rate control. While RVA pacing has been shown to create systolic dyssynchrony acutely, dyssynchrony can also occur in diastole. The effects of acute RVA pacing on diastolic synchrony have not been investigated. RVA pacing acutely impairs diastolic function by increasing the time constant of relaxation, decreasing the peak lengthening rate and decreasing peak negative dP/dt. We therefore hypothesized that acute RVA pacing would cause diastolic dyssynchrony in addition to creating systolic dyssynchrony. Methods and Results: Fourteen patients (13 ± 4 years old) with non-preexcited supraventricular tachycardia underwent ablation therapy with subsequent testing to confirm elimination of the tachycardia substrate. Normal cardiac structure and function were then documented on two-dimensional echocardiography and 12-lead electrocardiography prior to enrollment. Tissue Doppler images were collected during normal sinus rhythm (NSR), right atrial appendage pacing (AAI), and VVI-RVA pacing during the postablation waiting interval. Systolic and diastolic dyssynchrony were quantified using cross-correlation analysis of tissue Doppler velocity curves. Systolic dyssynchrony increased 81% during RVA pacing relative to AAI and NSR (P < 0.01). Diastolic synchrony was not affected by the different pacing modes (P = 0.375). Conclusion: Acute dyssynchronous activation of the LV created by RVA pacing resulted in systolic dyssynchrony with preserved diastolic synchrony in pediatric patients following catheter ablation for treatment of supraventricular tachycardia. Our results suggest that systolic and diastolic dyssynchrony are not tightly coupled and may develop through separate mechanisms.

Biventricular and LV Pacing Comparison. Introduction: We conducted an acute echocardiographic study comparing hemodynamic and ventricular dyssynchrony parameters during left ventricular pacing (LVP) and biventricular pacing (BVP). We sought to clarify the mechanisms responsible for similar hemodynamic improvement despite differences in electrical activation. Methods and Results: Thirty-three patients underwent echocardiography prior to implantation with a multisite pacing device (spontaneous rhythm [SR]) and 2 days after implantation (BVP and LVP). Interventricular dyssynchrony (pulsed-wave Doppler), extent of myocardium displaying delayed longitudinal contraction (%DLC; tissue tracking), and index of LV dyssynchrony (pulsed-wave tissue Doppler imaging) were assessed. Compared to SR, BVP and LVP caused similar significant improvement of cardiac output (LVP: 3.2 ′ 0.5, BVP: 3.1 ′ 0.7, SR: 2.3 ′ 0.6 L/min; P < 0.01) and mitral regurgitation (LVP: 25.1 ′ 10, BVP: 24.7 ′ 11, baseline: 37.9 ′ 14% jet area/left atria area; P < 0.01). LVP resulted in a smaller index of LV dyssynchrony than BVP (29 ′ 10 vs 34 ′ 14; P < 0.05). However, LVP exhibited a longer aortic preejection delay (220 ′ 34 vs 186 ′ 28 msec; P < 0.01), longer LV electromechanical delays (244.5 ′ 39 vs 209.5 ′ 47 msec; P < 0.05), greater interventricular dyssynchrony (56.6 ′ 18 vs 31.4 ′ 18; P < 0.01), and higher%DLC (40.1 ′ 08 vs 30.3 ′ 09; P < 0.05), leading to shorter LV filling time (387 ′ 54 vs 348 ′ 44 msec; P < 0.05) compared to BVP. Conclusion: Although LVP and BVP provide similar hemodynamic improvement, LVP results in more homogeneous but substantially delayed LV contraction, leading to shortened filling time and less reduction in postsystolic contraction. These data may influence the choice of individual optimal pacing configuration.

Acceleration-Dependent Left Bundle Branch Block and CRT. Cardiac resynchronization therapy (CRT) has been proposed to improve hemodynamics in patients with heart failure and left bundle branch block (LBBB) by resynchronization of left ventricular (LV) dyssynchrony. The current report concerns a patient with narrow QRS complex without LV dyssynchrony who experienced an acute exacerbation of heart failure following exercise. Careful analysis revealed that an increase of heart rate induced acceleration-dependent LBBB with severe LV dyssynchrony and mitral regurgitation followed by acute heart failure and hemodynamic collapse. CRT prevented these adverse reactions. Accordingly, optimal evaluation for CRT may include testing for LV dyssynchrony during exercise.

Introduction: Right ventricular apical (RVA) pacing creates ventricular dyssynchrony and may compromise left ventricular ejection fraction (LVEF). The impact of RVA pacing in patients who have undergone atrioventricular junction (AVJ) ablation for atrial fibrillation (AF) is unclear. We sought to determine whether RVA pacing after AVJ ablation for patients with AF compromises LVEF in the short- or long-term. Methods/Results: We studied 286 patients with AF who underwent AVJ ablation and RVA pacing at our institution between 1990 and 2002. Patients were stratified into a short-term follow-up group (LVEF reassessed by echocardiography within a year after AVJ ablation, n = 134) and a long-term group (LVEF reassessed after a year, n = 152). Among all 286 patients (mean follow-up 20 months), we observed no change in mean LVEF after AVJ ablation and RVA pacing (48% before vs. 48% after, P = 0.42). Short-term follow-up patients had a statistically significant improvement in mean LVEF (46% before vs. 49% after, P = 0.03), whereas there was no statistically significant change in mean LVEF in long-term follow-up patients (49% before vs. 48% after, P = 0.37). Only 9% of short-term patients, 15% of long-term patients, and 1% of patients with baseline LVEF ≤ 40% experienced ≥10% absolute decrease in LVEF. Baseline LVEF > 40% was a multivariate predictor of LVEF decline. Conclusions: RVA pacing after AVJ ablation does not compromise LVEF in the short- or long-term for the vast majority of patients. Better predictors are needed to help us select patients for biventricular pacing after AVJ ablation.

largest study to date was reported by Dubin and colleagues. 2 They retrospectively reviewed the records of 103 patients at multiple institutions, who had undergone placement of resynchronization devices. Unfortunately, the centers used multiple and diverse criteria for deciding when resynchronization therapy was to be employed and multiple means of assessing outcomes. Both articles provide an excellent beginning from which to develop this type of therapy in children, but should not be looked upon as providing definitive criteria for such use. The current major issues with the use of CRT in this patient population are similar to those posed in the adult population and relate to indications for resynchronization therapy, specific measures of ventricular dyssynchrony, and implant methodology as it relates to this unique group of patients. However, the answers may be very different. To date, indications for consideration of ventricular resynchronization have included advanced heart failure unresponsive to medication together with some indication for left ventricular dyssynchrony with or without a wide QRS complex. Patient symptomatology has been variable, ranging from being listed for transplantation to NYHA class I. 2 Use of ejection fraction alone may not be a good indicator for CRT need. The degree of symptoms and the likelihood of patient improvement must be balanced by the risk of CRT placement, 2 and quantitative indicators of a declining clinical state should be used. In all series reported to date, there has been a significant number of nonresponders. The question then arises as to the difference between responders and nonresponders. Dubin et al. 2 have suggested that perhaps the nonresponders were children who had less advanced dysfunction and higher initial ejection fractions, and therefore failed to show much improvement. Better patient selection criteria hopefully will improve this.