Intrinsic Left Bundle Branch Block Research Articles

Left bundle branch vs biventricular pacing for cardiac resynchronization therapy

Abstract Background/Introduction Left bundle branch pacing (LBBP) has emerged as a predominant conduction system pacing technique for reducing QRS duration in patients with intrinsic left bundle branch block (LBBB). It represents a potentially optimal alternative to cardiac resynchronization therapy (CRT) through biventricular pacing (BiVP). Purpose This study aims to compare the efficacy of LBBP-CRT with BiVP-CRT in patients experiencing heart failure with reduced left ventricular ejection fraction. Methods This single-center prospective study involved patients with heart failure and reduced ventricular ejection fraction, encompassing both ischemic and nonischemic cardiomyopathy. LBBP-CRT was employed when BiVP was unsuccessful for any reason, with LBBP-CRT implanted during the same procedure. After 3 and 6 months of preplanned follow-up, comparisons were made between the New York Heart Association (NYHA) functional class and QRS duration in the BiVP-CRT and LBBP-CRT groups. Results Sixty consecutive patients were included in the study (39 males, mean age 64.1 ± 10.6 years, LVEF 29.6% ± 5.6%). All patients completed follow-up, with 32 receiving LBBP-CRT and 28 receiving BiVP-CRT. All 32 LBBP-CRT patients achieved LBB capture, with 14 undergoing selective LBBP and 18 undergoing nonselective LBBP. The LBBP-CRT group exhibited shorter procedure and x-ray exposure times ((11.95 ± 5.77 vs 18.66 ± 10.12). The LBBP lead demonstrated a lower LBB capture threshold at implantation (0.7 ± 0.26 V vs. 1.1 ± 0.40 V; p= 0.039) compared to the CS LV lead in the BiVP-CRT group. Pacing parameters remained stable at the 6-month follow-up (0.72 ± 0.20 V vs. 1.1 ± 0.57 V; p=0.07). During the 3 and 6-month follow-up, pacing parameters remained stable in both groups. Only one patient in the LBBP-CRT group experienced dislodgment of the CS LV lead two days after the procedure, while no patients in the LBBP-CRT group had lead dislodgment. QRS duration significantly shortened in LBBP (171.6 ± 14.3 ms to 131.5 ± 12.5 ms; p=0.047) and remained not significantly shortened in BiVP (174.7 ± 14.1 ms to 150.6 ± 12.9 ms; p=0.06). Both LBBP and BiVP demonstrated improvement in NYHA functional class at the 3 and 6-month follow-up, with statistically significant differences observed between the two groups (change in NYHA functional class from baseline to 6 months -1.2 ± 0.1 vs -0.94 ± 0.11 p=0.047). Throughout the 6-month follow-up, neither the LBBP-CRT nor BiVP-CRT groups experienced rehospitalizations for heart failure, ventricular arrhythmia events, or all-cause death. Conclusions In this series, LBBP-CRT exhibited improvements in NYHA functional class and significantly shortened QRS duration when compared to BiVP-CRT in patients with reduced left ventricular ejection fraction and LBBB.

PO-03-109 RIGHT VENTRICULAR PACING EXACERBATE ELECTRICAL DYSSYNCHRONY BEYOND INTRINSIC LEFT BUNDLE BRANCH BLOCK

Right ventricular (RV) pacing produces an iatrogenic form of left bundle branch block (LBBB). Intrinsic LBBB (I-LBBB) can cause adverse hemodynamic effects due to ventricular dyssynchrony, mainly in patients with heart failure and reduced ejection fraction (HFrEF). Although RV pacing is thought to create a similar activation pattern as LBBB, some studies suggest RV apical pacing can be harmful even in patients with I-LBBB. Currently, the mechanism responsible for this harm is not fully understood. We aimed to quantify and compare the degree of ventricular electrical dyssynchrony, as measured on the surface ECG, during I-LBBB, and RV pacing in patients with HFrEF (left ventricular EF ≤40%) and I-LBBB. Patients with HFrEF and prophylactic defibrillator therapy were prospectively recruited. For each patient, 3-minute, high-resolution (1024 Hz), digital 12-lead ECGs were recorded during I-LBBB rhythm and then RV pacing at 60 bpm or intrinsic heart rate (whichever was higher). High-resolution ECGs were analyzed to quantify abnormal intra-QRS peaks (QRSp) as a measure of ventricular electrical dyssynchrony. QRSp was defined as the mean number of peaks detected in the QRS complex that deviated from a smoothing-filtered version of the QRS. QRSp was automatically quantified for each precordial lead using validated custom software. Mean QRSp was defined as the average of QRSp in precordial leads. Thirty patients with HFrEF (66±9 yrs, 50% male, LVEF 30±8%) and I-LBBB (QRS duration [QRSd]: 172±22 ms) were included. Changes in mean QRSp between I-LBBB and RV apical pacing are shown in (Figure1A). RV pacing increased the mean QRSp in 27 patients (90%) as compared to I-LBBB, suggesting overall more electrical dyssynchrony during RV pacing. Changes in QRSd between I-LBBB and RV pacing are shown in (Figure 1B). RV pacing resulted in QRSd widening beyond I-LBBB QRSd in 18 patients (60%), while QRSd did not change in the remaining patients. During RV pacing (versus I-LBBB), Mean QRSp changed in more patients as compared to QRSd (27 patients versus 18 patients; p = 0.007). Although RV pacing produces an iatrogenic form of LBBB, ventricular electrical activation is more dyssynchronous during RV pacing as measured by changes in mean QRSp and QRSd. Compared to QRSd, mean QRSp is a more sensitive marker of change in ventricular electrical dyssynchrony between RV pacing and I-LBBB. Our results suggest RV pacing can exacerbate ventricular electrical dyssynchrony in those with I-LBBB.

Randomized Trial of Left Bundle Branch vs Biventricular Pacing for Cardiac Resynchronization Therapy

BackgroundLeft bundle branch pacing (LBBP) is the most rapidly growing conduction system pacing technique that is capable of correcting intrinsic left bundle branch block (LBBB). As such, it is potentially an optimal alternative to cardiac resynchronization therapy (CRT) with biventricular pacing (BiVP). ObjectivesThe authors sought to compare the efficacy of LBBP-CRT with BiVP-CRT in patients with heart failure and reduced left ventricular ejection fraction (LVEF). MethodsThis is a prospective, randomized trial of patients with nonischemic cardiomyopathy and LBBB with 6-month preplanned follow-up. Crossovers were allowed if LBBP or BiVP were unsuccessful. The primary endpoint was the difference in LVEF improvement between 2 groups. The secondary endpoints included changes in echocardiographic measurements, N-terminal pro–B-type natriuretic peptide (NT-proBNP), New York Heart Association functional class, 6-minute walk distance, QRS duration, and CRT response. ResultsThe study included 40 consecutive patients (20 males, mean age 63.7 years, LVEF 29.7% ± 5.6%). Crossovers occurred in 10% of LBBP-CRT and 20% of BiVP-CRT. All patients completed follow-up. Intention-to-treat analysis showed significantly higher LVEF improvement at 6 months after LBBP-CRT than BiVP-CRT (mean difference: 5.6%; 95% CI: 0.3-10.9; P = 0.039). LBBP-CRT also appeared to have greater reductions in left ventricular end-systolic volume (−24.97 mL; 95% CI: −49.58 to −0.36 mL) and NT-proBNP (−1,071.80 pg/mL; 95% CI: −2,099.40 to −44.20 pg/mL), and comparable changes in New York Heart Association functional class, 6-minute walk distance, QRS duration, and rates of CRT response compared with BiVP-CRT. ConclusionsLBBP-CRT demonstrated greater LVEF improvement than BiVP-CRT in heart failure patients with nonischemic cardiomyopathy and LBBB. (Left Bundle Branch Pacing Versus Biventricular Pacing for Cardiac Resynchronization Therapy [LBBP-RESYNC]; NCT04110431)

Better CRT Response in Patients Who Underwent Atrioventricular Node Ablation or Upgrade From Pacemaker: A Nomogram to Predict CRT Response.

Background: Response rates for cardiac resynchronization therapy (CRT) in patients without intrinsic left bundle-branch block (LBBB) morphology are poor.Objective: We sought to develop a nomogram model to predict response to CRT in patients without intrinsic LBBB.Methods: We searched electronic health records for patients without intrinsic LBBB who underwent CRT at Mayo Clinic. Logistic regression and Cox proportional hazards regression analysis were performed for the odds of response to CRT and risk of death, respectively. Results were used to develop the nomogram model.Results: 761 patients without intrinsic LBBB were identified. Six months after CRT, 47.8% of patients demonstrated improvement of left ventricular ejection fraction by more than 5%. The 1-, 3-, and 5-year survival rates were 95.9, 82.4, and 66.70%, respectively. Patients with CRT upgrade from pacemaker [odds ratio (OR), 1.67 (95% CI, 1.05–2.66)] or atrioventricular node (AVN) ablation [OR, 1.69 (95% CI, 1.09–2.64)] had a greater odds of CRT response than those patients who had new implant, or who did not undergo AVN ablation. Patients with right bundle-branch block had a low response rate (39.2%). Patients undergoing AVN ablation had a lower mortality rate than those without ablation [hazard ratio, 0.65 (95% CI, 0.46–0.91)]. Eight clinical variables were automatically selected to build a nomogram model and predict CRT response. The model had an area under the receiver operating characteristic curve of 0.71 (95% CI, 0.63–0.78).Conclusions: Among patients without intrinsic LBBB undergoing CRT, upgrade from pacemaker and AVN ablation were favorable factors in achieving CRT response and better long-term outcomes.

B-PO05-181 HIS BUNDLE PACING PRODUCES MORE PHYSIOLOGICAL VENTRICULAR REPOLARISATION THAN BIVENTRICULAR PACING IN HEART FAILURE WITH LEFT BUNDLE BRANCH BLOCK

Biventricular pacing (BVP) shortens left ventricular activation time (LVAT) in patients with heart failure and left bundle branch block (LBBB). His bundle pacing can correct LBBB (HBP-CRT). The effects of BVP and HBP-CRT on ventricular repolarisation are not known. To measure the effects of HBP-CRT and BVP on LV repolarisation using non-invasive epicardial mapping (ECGI). Participants were recruited in 2 groups. 1) Patients scheduled for BVP for heart failure with LBBB, 2) Individuals with normal QRS and LV function. We defined HBP-CRT as LVAT shortening >10ms. We compared the effects of HBP-CRT and BVP on ECGI-derived dispersion of repolarisation and activation-recovery intervals. 21 HBP-CRT and 21 narrow intrinsic QRS were recruited. LV repolarisation dispersion was reduced by HBP-CRT (-42.0ms, 95%CI: -52.3 to -31.7, p <0.001) but not BVP (11.9ms, -6.2 to 30.1, p=0.182, 18.5ms). Change in LV repolarisation dispersion from BVP to HBP-CRT was -56.5ms (-70.5 to 42.5, p<0.001). LV repolarisation dispersion with HBP-CRT was not different from narrow intrinsic QRS (2.8ms, -16.2 to 21.7, p=0.981). Reduction in LV repolarisation dispersion with HBP-CRT from intrinsic LBBB was similar to LVAT shortening (-45.9ms, 95%CI: -59.3 to -32.4). However, LV activation-recovery interval dispersion was also reduced by HBP-CRT (-56.5 ms, -70.5 to -42.5ms, p<0.001). HBP-CRT can normalise repolarisation dispersion, producing more physiological repolarisation than BVP. This occurs through effects on both activation and action-potential duration. HBP-CRT may prevent ventricular arrhythmias in heart failure with LBBB to a greater extent than BVP.

His resynchronization therapy produces more physiological ventricular repolarisation compared with biventricular pacing

Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): British Heart Foundation BACKGROUND Biventricular pacing (BVP) is known to shorten activation time in patients with heart failure and left bundle branch block (LBBB) but its effects on repolarisation are not well studied. His bundle pacing (HBP) can correct LBBB to deliver cardiac resynchronization therapy (HBP-CRT), producing more physiological ventricular activation time and pattern than BVP. It is not known whether this translates to more physiological repolarisation, and if so whether the effect is mediated through its effects on activation. PURPOSE We measured the effects of HBP-CRT and BVP on left ventricular repolarisation using non-invasive epicardial mapping (ECGI). METHODS Patients were recruited in two groups. 1) Patients scheduled for clinically indicated BVP procedures for heart failure with LBBB, 2) Individuals with narrow QRS, normal ventricular function and intact conduction systems. Using non-invasive electrocardiographic imaging, we identified patients with LBBB in whom HBP shortened ECGI-derived left ventricular (LV) activation time by &amp;gt;10ms. We compared the effects of HBP and BVP on ECGI-derived dispersion of LV repolarisation times and activation-recovery intervals (a surrogate for action potential duration). RESULTS 21 patients in whom HBP shortened LV activation time by &amp;gt;10ms and an equal number of individuals with narrow intrinsic QRS were recruited. LV repolarisation dispersion was reduced by HBP-CRT (-42.0 ms, 95% confidence interval (CI): -52.3 to -31.7 ms, p &amp;lt;0.001) but not by BVP (11.9 ms, 95% CI: -6.24 to 30.1 ms, p = 0.182). The mean within-patient change in LV repolarisation dispersion from BVP to HBP-CRT was -56.5 ms (95% CI: -70.5 to -42.5 ms, p &amp;lt; 0.001). LV repolarisation dispersion with HBP-CRT was not different from individuals with narrow intrinsic QRS (2.75 ms, 95% CI: -16.2 to 21.7 ms, p = 0.981). The magnitude of reduction in LV repolarisation dispersion with HBP-CRT from intrinsic LBBB appeared similar to the magnitude of LV activation time shortening (-54.9 ms, 95% CI: -68.2 to -41.6 ms, p &amp;lt; 0.001). However, LV activation-recovery interval dispersion was also reduced by HBP-CRT (-44.3 ms, 95% CI: -69.2 to -19.3 ms, p &amp;lt; 0.001). Repolarisation mapping demonstrated normalisation of repolarisation pattern by HBP-CRT. CONCLUSIONS HBP-CRT can normalise repolarisation dispersion, producing more physiological repolarisation compared with BVP, which does not resolve the repolarisation abnormality of LBBB. HBP-CRT improves repolarisation through both activation resynchronization and modulation of action-potential duration. If these acute results translate to longer term outcomes, HBP-CRT may reduce the risk of ventricular arrhythmias in heart failure with LBBB to a greater extent than BVP. Abstract Figure. Epicardial Repolarisation Maps

Cardiac resynchronization therapy by left bundle branch area pacing in patients with heart failure and left bundle branch block

Cardiac resynchronization therapy (CRT) via biventricular pacing has demonstrated clinical benefits in patients with heart failure (HF) and ventricular dyssynchrony. Other approaches of CRT is little known. The purpose of this study was to assess the feasibility, safety, and efficacy of left bundle branch area pacing (LBBAP) in patients with HF and left bundle branch block (LBBB). Eleven consecutive patients with HF, reduced left ventricular ejection fraction and LBBB and indicated for CRT were recruited. LBBAP was achieved via transventricular septal approach and characterized by narrower QRS duration, shortened peak left ventricular activation time, and right bundle branch conduction delay on the electrocardiogram. Electrocardiogram, echocardiogram, and cardiac function were evaluated at baseline and follow-up. Interventricular mechanical delay and 3-dimensional tissue synchronization imaging during LBBAP and intrinsic LBBB status were measured by echocardiography at follow-up. LBBAP significantly shortened QRS duration (from baseline 180.00 ± 15.86 ms to 129.09 ± 15.94 ms; P < .01) and left ventricular activation time (from baseline 108.18 ± 15.54 ms to 80.91 ± 9.95 ms; P < .01). Interventricular mechanical delay and the standard deviation of tissue synchronization imaging of 12 left ventricular (LV) segments were significantly shorter during LBBAP than in intrinsic LBBB status (both with P < .01). At a mean follow-up period of 6.7 months, New York Heart Association functional class, plasma level of B-type natriuretic peptide, LV end-systolic diameter, and left ventricular ejection fraction were significantly improved (all with P < .05 vs baseline). The study demonstrates that LBBAP is clinically feasible in patients with systolic HF and LBBB. LBBAP can be a new CRT technique to correct LBBB, provide ventricular synchrony, and improve clinical symptoms with LV reverse remodeling.

Long-Term Outcome After CRT in the Presence of Mechanical Dyssynchrony Seen With Chronic RV Pacing or Intrinsic LBBB

ObjectivesThe aim of this study was to compare the volumetric response and the long-term survival after cardiac resynchronization therapy (CRT) in patients with intrinsic left bundle branch block (LBBB) versus chronic right ventricular pacing (RVP) with respect to the presence of mechanical dyssynchrony (MD). BackgroundChronic RVP induces an iatrogenic LBBB and asynchronous left ventricular contraction that is potentially reversible by upgrading to CRT. MethodsA total of 914 patients eligible for CRT (117 with conventional pacemakers and 797 with intrinsic LBBB) were included in the study. MD was visually assessed before CRT and was defined as the presence of either apical rocking and/or septal flash on baseline echocardiograms. Patients with a left ventricular end-systolic volume decrease of ≥15% during the follow-up were considered responders. Patients were followed for all-cause mortality during the median follow-up of 48 months (interquartile range: 29 to 66 months). ResultsMD was observed in 51% of patients with RVP versus 77% in patients with intrinsic LBBB (p < 0.001). Patients with RVP and MD had a similar likelihood of volumetric response as did patients with intrinsic LBBB and MD (adjusted odds ratio: 0.71; 95% confidence interval: 0.33 to 1.53; p = 0.385). There was no significant difference in long-term survival between patients with RVP and intrinsic LBBB (adjusted hazard ratio: 1.101; 95% confidence interval: 0.658 to 1.842; p = 0.714). Patients with visual MD and either intrinsic LBBB or RVP had a more favorable survival than those without MD (p < 0.001). ConclusionsThe likelihood of volumetric response and a favorable long-term survival of patients with RVP was similar to those of patients with intrinsic LBBB and were mainly determined by the presence of MD and not by the nature of LBBB.

Improvement in CRT: new strategies, better choices.

Cardiac resynchronisation therapy (CRT) emerged more than a decade ago as a useful form of device therapy for heart failure associated with abnormal ventricular conduction indicated by a wide QRS complex [1, 2]. According to the Guidelines of the European Society of Cardiology (ESC) entitled Cardiac Pacing and Cardiac Resynchronization Therapy (ESC Clinical Practice Guidelines, 2013), CRT has currently a Class I indication in patients with 1) chronic heart failure (NYHA Class II-IV despite optimal medical treatment), 2) a left bundle branch block (LBBB) on the ECG with a QRS width >120 ms (preferably >150 ms), and 3) a left ventricular ejection fraction < 35 % [3]. The magnitude of CRT benefit increases in females, in patients with non-ischaemic cardiomyopathy, and in patients with a wide QRS complex: the longer the QRS duration the more favourable the response. CRT consists of biventricular pacing with or without an internal cardioverter defibrillator (ICD): in combination with an ICD, CRT is called CRT-D (efibrillator); without an ICD, the treatment is called CRT-P (acing). According to Daubert et al. [4], the prescription of CRT-D is currently restricted to patients in need of secondary prevention of ventricular arrhythmias or, for primary prevention, in younger patients without major concomitant illnesses. The preferential choice of CRT-P for the remainder of the ambulatory patients in NYHA class III or IV is currently acceptable. Because of insufficient data regarding the performance of CRT-P in patients presenting in NYHA functional class I or II, CRT-D is currently the device of choice for this sub-population. In the choice between CRT-D and CRT-P, the 2013 ESC guidelines - endorsed by our national society, the NVVC- clearly state: Owing to the potential incremental survival benefit of CRT-D over CRT-P, the prevailing opinion among the members of this Task Force is in favour of a superiority of CRT-D in terms of total mortality and sudden death. However, no strict recommendations can be made, and the Task Force prefers to merely offer guidance regarding the selection of patients for CRT-D or CRT-P, based on overall clinical condition, device-related complications and cost. Speaking of device-related complications and costs, these are crucial issues to be considered as there are still 20–30 % non-responders to CRT despite following the appropriate guideline indication [5–7]. Therefore, new strategies and more appropriate CRT approaches have to be implemented providing higher rates of success. Recently, Vernooij et al. [8] from Maastricht (the Netherlands) proposed new strategies to improve the outcome of CRT. As the implantation of CRT devices comes with substantial costs, in particular CRT-D, the authors plead for a more strict and rigid application of the guidelines, or even extension of the guidelines. Outcomes from CRT can be improved by appropriate patient selection, careful positioning of right and left ventricular pacing electrodes, and optimal timing of electrode stimulation. LBBB remains the predominant substrate for CRT, and patients with this conduction abnormality yield the most benefit. However, other features, such as QRS morphology, mechanical dyssynchrony, myocardial scarring, and the aetiology of heart failure, might also determine the benefit of CRT. No single left ventricular pacing site suits all patients, but a late-activated site, during either the intrinsic LBBB rhythm or right ventricular pacing, should be selected. Positioning the lead inside a scarred region substantially impairs outcomes. Optimisation of stimulation intervals improves cardiac pump function in the short term, but CRT procedures must become easier and more reliable, perhaps with the use of electrocardiographic measures, to improve long-term outcomes. For instance, Molenaar et al. [9] showed that a 10 % increase in stroke volume can be achieved for optimisation of atrioventricular (AV) delay during exercise. In that study, a considerable number of patients showed benefit with lengthening of the AV delay during exercise. In summary, sharper indications for CRT, and the permanent consideration of choosing CRT-P or CRT-D, would be cost-saving and might provide health benefits. This is in line with the recent findings by Looi et al. [10] who showed that CRT-D did not offer additional survival advantage over CRT-P at longer-term follow-up, as the clinical benefit of a defibrillator attenuated with time. As mentioned before, further work is therefore needed to define which subsets of patients would benefit from CRT in combination with an ICD. Lastly, there remains an urgent need for randomised clinical trials in CRT subgroups such as in patients with right bundle branch block, NYHA Class I, atrial fibrillation, and in patients with specific conditions (pacing in children, congenital heart disease). When these studies have been completed, then we might speak of true CRT optimisation to better serve patients with chronic heart failure.

Strategies to improve cardiac resynchronization therapy.

Cardiac resynchronization therapy (CRT) emerged 2 decades ago as a useful form of device therapy for heart failure associated with abnormal ventricular conduction, indicated by a wide QRS complex. In this Review, we present insights into how to achieve the greatest benefits with this pacemaker therapy. Outcomes from CRT can be improved by appropriate patient selection, careful positioning of right and left ventricular pacing electrodes, and optimal timing of electrode stimulation. Left bundle branch block (LBBB), which can be detected on an electrocardiogram, is the predominant substrate for CRT, and patients with this conduction abnormality yield the most benefit. However, other features, such as QRS morphology, mechanical dyssynchrony, myocardial scarring, and the aetiology of heart failure, might also determine the benefit of CRT. No single left ventricular pacing site suits all patients, but a late-activated site, during either the intrinsic LBBB rhythm or right ventricular pacing, should be selected. Positioning the lead inside a scarred region substantially impairs outcomes. Optimization of stimulation intervals improves cardiac pump function in the short term, but CRT procedures must become easier and more reliable, perhaps with the use of electrocardiographic measures, to improve long-term outcomes.

Deterioration of left ventricular ejection fraction and contraction synchrony during right ventricular pacing in patients with left bundle branch block

Electrocardiographic left bundle branch block (LBBB) may be intrinsic, due to ventricular conduction system disease, or induced by right ventricular pacing. Prior reports clearly delineate the derogatory impact of LBBB on left ventricular (LV) mechanical synchrony and global function, and suggest that the intrinsic and induced varieties are equivalent. This study sought to determine the difference in LV synchrony and global function between intrinsic LBBB and right ventricular apical pacing induced LBBB. Ten patients with heart failure, diminished ejection fraction (EF) (33±11%), intrinsic LBBB and an implanted cardiac pacing device were studied. In each patient, separate gated SPECT acquisitions were performed during intrinsic ventricular activation (atrial pacing) and during induced LBBB (atrial and right ventricular pacing). During each condition, LVEF, contraction synchrony (phase standard deviation, PSD), and spatial pattern of activation were measured. Compared to intrinsic, induced LBBB was associated with decreased EF (30±11% vs 33±11%, P=.007), contraction synchrony (PSD 49.7±23.2° vs 41.6±19.8, P=.02), and a disparate spatial pattern of activation. Induced LBBB is associated with significantly worse global and regional LV mechanical function than intrinsic LBBB.

Further Deterioration of LV Ejection Fraction and Mechanical Synchrony During RV Apical Pacing in Patients with Heart Failure and LBBB

Electrocardiographic left bundle branch block (LBBB) may be due to intrinsic disease of the left bundle branch or induced by right ventricular apical (RVA) pacing. Prior reports clearly delineate the derogatory impact of LBBB on left ventricular (LV) mechanical function but suggest equivalent impact between varieties. We hypothesized that their effects were disparate and performed a within-patient comparison to test this notion. Patients (n = 20) with heart failure, intrinsic LBBB, and an implanted pacing device with right atrial and RVA leads were studied. Each patient underwent transthoracic three-dimensional speckle-tracking echocardiography during atrial pacing (intrinsic LBBB) and short atrioventricular delay atrial-RVA pacing, and these studies were compared. Relative to intrinsic LBBB, RVA pacing-induced LBBB produced greater intra-LV and interventricular dyssynchrony, a deterioration in LV function, and a shift in the site of latest activation. In patients with heart failure and LBBB, acute RVA pacing induces greater mechanical dyssynchrony and further impairs LV function.

Vectorcardiography as a Tool for Easy Optimization of Cardiac Resynchronization Therapy in Canine Left Bundle Branch Block Hearts

Background— In cardiac resynchronization therapy (CRT), optimization of left ventricular (LV) stimulation timing is often time consuming. We hypothesized that the QRS vector in the vectorcardiogram (VCG) reflects electric interventricular dyssynchrony, and that the QRS vector amplitude (VA QRS ), halfway between that during left bundle branch block (LBBB) and LV pacing, reflects optimal resynchronization, and can be used for easy optimization of CRT. Methods and Results— In 24 canine hearts with LBBB (12 acute, 6 with heart failure, and 6 with myocardial infarction), the LV was paced over a wide range of atrioventricular (AV) delays. Surface ECGs were recorded from the limb leads, and VA QRS was calculated in the frontal plane. Mechanical interventricular dyssynchrony (MIVD) was determined as the time delay between upslopes of LV and right ventricular pressure curves, and systolic function was assessed as LV dP/dt max . VA QRS and MIVD were highly correlated ( r =0.94). The VA QRS halfway between that during LV pacing with short AV delay and intrinsic LBBB activation accurately predicted the optimal AV delay for LV pacing (1 ms; 95% CI, –5 to 8ms). Increase in LV dP/dt max at the VCG predicted AV delay was only slightly lower than the highest observed ∆LV dP/dt max (–2.7%; 95% CI, –3.6 to –1.8%). Inability to reach the halfway value of VA QRS during simultaneous biventricular pacing (53% of cases) was associated with suboptimal hemodynamic response, which could be corrected by sequential pacing. Conclusions— The VA QRS reflects electric interventricular dyssynchrony and accurately predicts optimal timing of LV stimulation in canine LBBB hearts. Therefore, VCG may be useful as a reliable and easy tool for individual optimization of CRT.

Patients with left bundle branch block pattern and high cardiac risk myocardial SPECT: does the current management suffice?

Myocardial perfusion SPECT (MPS) is frequently used for cardiovascular risk stratification. The significance of MPS in patients with abnormal electrical ventricular activation is often questionable. This review assesses the value of MPS for risk stratification of patients with intrinsic left bundle branch block or that due to right ventricular apical pacing. We reviewed the literature by a search of the MEDLINE database (January 1980 to September 2010). The terms prognosis or prognostic value were combined with SPECT and LBBB or pacing or pacemakers. MPS was categorised as low and high risk according to the original definitions. We identified 11 studies suitable for review. A low-risk MPS is associated with a low risk of cardiac events whereas high-risk MPS carries a 4.8-fold increased risk, 95% CI [3.2 - 7.2] (p < 0.0001). Despite secondary prevention and an improved medical and interventional care, these figures have hardly changed over time. A low-risk MPS permits a policy of watchful waiting whereas a high-risk MPS requires further analysis and treatment. The persistent high cardiac death and acute myocardial infarction rate after a high-risk MPS suggest that the current management of these patients does not suffice and needs reconsideration.

Assessment of left ventricular dyssynchrony in pacing-induced left bundle branch block compared with intrinsic left bundle branch block

Although electrocardiographic and echocardiographic findings with right ventricular (RV) pacing mimic intrinsic left bundle branch block (LBBB), left ventricular (LV) mechanical activation pattern may differ. We compared mechanical activation pattern of the LV in RV-pacing-induced LBBB with intrinsic LBBB in symptomatic chronic heart failure patients. We studied 37 patients with chronic RV-pacing and 37 patients with intrinsic LBBB who were referred for cardiac resynchronization therapy. Echocardiographic study including 2D speckle tracking longitudinal strain and M-mode were performed at baseline. Patients with intrinsic LBBB were younger, had higher prevalence of ischaemic heart disease, and had more severe depressed LV function. The basal-septal segments were the earliest activated sites in 11% of patients in RV-pacing-induced LBBB compared with 30% in intrinsic LBBB (P= 0.04). The mid- and basal-lateral segments were the latest activated sites in 57% of patients in RV-pacing-induced LBBB compared with 30% in intrinsic LBBB (P = 0.03). Left ventricular dyssynchrony, using longitudinal strain, time delay ≥ 130 ms between either mid-septal or apico-septal and either basal or mid-lateral segments was present in 71% of patients with RV-pacing-induced LBBB compared with 59% in intrinsic LBBB (P = 0.03). Using M-mode, LV dyssynchrony was present in 11% of patients with RV-pacing-induced LBBB compared with 59% in intrinsic LBBB (P = 0.02). Right ventricular-pacing results in less early basal activation and more often early mid-septal and late lateral wall activation in comparison with intrinsic LBBB. Imaging techniques that only visualize the basal- or mid-part of the LV may result in a serious underestimation of dyssynchrony in patients with pacing-induced LBBB.

Cardiac Resynchronization Therapy in Patients With Intrinsic and Right Ventricular Pacing-Induced Left Bundle Branch Block Pattern

We studied 95 consecutive patients, mean age 70 years, who received cardiac resynchronization therapy (CRT) for class III or IV heart failure with a left ventricular (LV) ejection fraction < or =35% and a QRS duration > or =120 ms. Sixty-seven patients had intrinsic left bundle branch block (LBBB) (group 1), and 28 patients had right ventricular pacing-induced LBBB (group 2). The time difference (TPW-TDI) between onset of QRS to the end of LV ejection by pulsed wave Doppler and onset of QRS to the end of systolic wave in the basal segment with greatest delay by tissue Doppler imaging was measured before CRT and at the last follow-up after CRT. TPW-TDI >50 ms was defined as left ventricular mechanical dyssynchrony. A positive response to CRT was defined as LV volume at end-systole decreasing > or =15% after CRT. The percentage of CRT responders in group 2 was significantly greater than that in group 1 (68% versus 42%, P = 0.04) during follow-up of 16 months. After adjusting for age, gender, and clinical features, this pattern of CRT response persisted (P = 0.008). Similarly, there was a greater reduction in QRS duration in group 2 (178 ms) after CRT versus 154 ms for group 1, P = 0.01. There was no significant difference in TPW-TDI between the 2 groups at baseline or at follow-up. There was no significant difference in mortality (15% versus 14%) and Kaplan-Meier survival plot during follow-up. Patients with heart failure and right ventricular pacing-induced LBBB have a better response rate to CRT than patients with intrinsic LBBB. The change in left ventricular mechanical dyssynchrony after CRT was similar in these 2 groups of patients.

Is the left ventricle the preferred pacing site in all children with atrioventricular block?

This editorial refers to ‘Preserved cardiac synchrony and function with single-site left ventricular epicardial pacing during mid-term follow-up in paediatric patients’ by M. Tomaske et al., on page 1168 Cardiac pacing for the treatment of bradycardia has been applied in children of all age groups for many years. In the paediatric population, the most common indications for cardiac pacing are auto-immune-mediated congenital atrioventricular block (CAVB) and acquired CAVB after congenital heart surgery. Traditionally, the right ventricular (RV) apex has been used for transvenous ventricular pacing leads because it is easily accessible and allows a stable position and low pacing thresholds. In young children, many centres prefer to place epicardial ventricular pacing leads, which are usually attached to either the RV apex or the RV free wall. Although thousands of children have profited from pacing the RV, there is increasing evidence that long-term RV apical pacing (RVP) eventually can result in LV failure. In animal studies, it has been demonstrated that chronic RVP leads to decreased LV function, dilatation, and asymmetric septal hypertrophy. 1 Clinical studies in adults have demonstrated that RVP is associated with increased mortality and morbidity related to heart failure. 2 Reports in children have also shown that long-term RVP causes LV mechanical dyssynchrony, which is associated with decreased LV function. 3,4 The deleterious effect of permanent RV pacing has become an important topic in cardiac pacing in the paediatric population, since this group requires pacemaker therapy over many decades. This young pacemaker population also includes a significant number of children with complex congenital heart disease at high risk for future heart failure. Literature data indicate that in children with normal cardiac anatomy, long-term RVP will lead to LV failure in 7%. 4 A very recent study by Gebauer et al. 5 reported even higher percentage (13%) of LV dilatation in a retrospective cohort of 82 patients after a mean pacing period of 7.4 years. In this study, children with epicardial RV free wall pacing had a higher risk of LV dilatation and LV dysfunction compared with those with RVP. 5 Furthermore, small case series has demonstrated that children with congenital CAVB who developed RV pacing-associated cardiomyopathy showed impressive improvement of LV function after cardiac resynchronization therapy (CRT). These findings indicate that mechanical dyssynchrony induced by RV pacing appeared to be the key factor in the development of heart failure in this group of congenital CAVB. Also, the CRT data in children and patients with congenital heart disease from three large studies have shown that 45‐70% of children undergoing CRT for heart failure had pacing-induced ventricular dyssynchrony. 6 So, if the RV apex appears inappropriate for long-term ventricular pacing, what then should we use as an alternative? In the RV, selective pacing sites at the high RV septum and RV outflow tract region may produce more synchronous contraction patterns and better haemodynamics. Therefore, RV septal pacing could decrease the long-term detrimental effects of RV pacing. Advanced tools and lead technology nowadays allow for pacing these specific RV sites, also in paediatric patients. However, to date, long-term clinical studies have been conflicting, and large randomized trials are now expected to demonstrate the significance of selective site RV pacing in the protection of LV function. 7 LV pacing appears to be less harmful than RVP as shown in acute haemodynamic studies in patients with normal LV function. 8 Animal studies as well as an acute haemodynamic study in children have suggested that the LV apex is the optimal pacing site in the LV. 9 Trials in adult patients have shown that single-site LV free wall pacing (LVP), comparable with biventricular pacing, has beneficial haemodynamic effects in patients with heart failure and left bundle branch block. 10 Also, a small study in children with LV dysfunction and RVP or intrinsic left bundle branch block has demonstrated improvement of LV function 1 month after single-site LVP. 11

Biventricular Pacemaker Upgrade in Previously Paced Heart Failure Patients—Improvements in Ventricular Dyssynchrony

Background Cardiac resynchronization therapy (CRT) reduces symptoms and mortality in patients with left bundle branch block (LBBB) and severe chronic heart failure. There are few data demonstrating the effects of CRT on contemporary dyssynchrony variables in patients with advanced heart failure who have been chronically paced from the right ventricle (RV). Methods and Results We reviewed baseline and follow-up clinical and echocardiographic data on patients receiving CRT in a single centre. Indices of global left ventricular (LV) function and dyssynchrony before and after CRT were measured. Patients were then divided into those receiving their first device (n = 39) and those receiving CRT as an upgrade to existing RV pacemakers (n = 32). Baseline demographic variables, indices of global LV function, symptomatic status, renal function, hemodynamics, and diuretic requirements were not different between previously paced patients and nonpaced patients. Mean length of RV pacing in the previously paced patients was 59 months (range 12–167 months). Patients in the previously paced group had a broader QRS complex than patients with intrinsic LBBB. Aortopulmonary delay of longer than 40 ms was present in 68% of all subjects, 67% had intraventricular septal and posterior wall motion delay longer than 130 ms, and 59% had an intraventricular delay as measured by tissue Doppler imaging of longer than 65 ms. There was no difference between paced and nonpaced patients for any of these measures of dyssynchrony. QRS duration was reduced to a greater extent in the previously paced patients than those with no previous device therapy. CRT led to important reductions in each dyssynchrony variable in both patients with previous RV pacing and those with intrinsic LBBB. The magnitude of these changes in measures of dyssynchrony was not different between the 2 groups. In all patients undergoing CRT, 50% had a reduction in furosemide dose at 3 months, 56% an improvement of at least 1 grade in New York Heart Association status, and 66% an improvement of at least 5% in LVEF. Divided by group, previously paced patients were no more or less likely than newly implanted patients to achieve one or more of these clinical outcomes. Conclusion Our data suggest that patients with RV pacing and heart failure have similar dyssynchrony as patients with intrinsic LBBB. CRT leads to improvements in LV global function, dyssynchrony variables and symptoms in patients chronically paced from the RV that are similar to those observed in patients with LBBB without preexisting devices.

Resynchronization therapy produces greater improvement in left venticular function in patients with pacer induced compared to those with intrinsic left bundle branch block

Resynchronization therapy produces greater improvement in left venticular function in patients with pacer induced compared to those with intrinsic left bundle branch block

Study of the influence of left bundle branch block on the signal-averaged electrocardiogram: A qualitative and quantitative analysis

To study the influence of left bundle branch block (LBBB) on the signal-averaged electrocardiogram (SAECG), quantitative and qualitative analyses of SAECG parameters were undertaken in 48 patients with electrocardiographic evidence of intrinsic LBBB and in 39 patients with a “normal” surface QRS duration (<120 msec) who underwent right ventricular pacing-induced LBBB. We assumed pacing of the right ventricular apex to be a suitable model of this conduction defect. Sustained monomorphic ventricular tachycardia (SMVT) was inducible in 16 of 48 patients with intrinsic LBBB and in 23 of 39 patients with pacing-induced LBBB. Utilizing a filter setting of 25 to 250 Hz, late potentials were defined as a total filtered QRS duration ≥120 msec, a root mean square voltage in the terminal 40 msec (RMS 40) of ≤25 μV, and the duration of signals < 40 μV (LAS 40) of ≥38 msec. Only RMS 40 and LAS 40 criteria were used in patients with LBBB. Prolongation of LAS 40 and fragmentation of signals in the terminal portion of the filtered QRS were characteristic of all patients with LBBB aberration. Of those patients with intrinsic LBBB, the mean total filtered QRS duration, RMS 40, and LAS 40 for inducible and noninducible patients were significantly different (170 ± 28, 16 ± 10, 55 ± 24, and 153 ± 18 msec, 25 ± 10 μV, 33 ± 16.9 msec; p = 0.04, 0.009, and 0.007, respectively). Noninducible patients with a normal QRS duration demonstrated a 60% decrement in the mean RMS 40 value during pacing-induced LBBB. These changes resulted in a 59% false positive incidence of late potentials during pacing-induced LBBB. This correlated with a similarly low mean RMS 40 value in patients with intrinsic LBBB and no inducible SMVT, hence giving rise to a false positive incidence of late potentials of 63%. Since “standard” RMS 40 and LAS 40 criteria resulted in low specificity and positive predictive value, new parameters were selected and analyzed. The combination of RMS 40 ≤ 17 μV plus LAS 40 ≥ 55 msec yielded the best overall statistical result, with a sensitivity, specificity, and total predictive accuracy of 69%, 81%, and 77%, respectively. in conclusion: (1) A reduction of RMS 40, prolongation of LAS 40, and fragmentation of signals in the terminal portion of the filtered QRS are charateristics of LBBB. (2) New RMS 40 and LAS 40 criteria for late potentials possessed higher total predictive accuracy for inducible sustained monomorphic VT than “standard” criteria in patients with LBBB.