Search

Background: Optimization of atrial‐ventricular delay (AVD) during atrial sensing (SAVD) and pacing (PAVD) provides the most effective cardiac resynchronization therapy (CRT). We demonstrate a novel electrocardiographic methodology for quantifying electrical synchrony and optimizing SAVD/PAVD. Methods: We studied 40 CRT patients with LV activation delay. Atrial‐sensed to RV‐sensed (As‐RVs) and atrial‐paced to RV‐sensed (Ap‐RVs) intervals were measured from intracardiac electrograms (IEGM). LV‐only pacing was performed over a range of SAVD/PAVD settings. Electrical dyssynchrony (cardiac resynchronization index; CRI) was measured at each setting using a multilead ECG system placed over the anterior and posterior torso. Biventricular pacing, which included multiple interventricular delays, was also conducted in a subset of 10 patients. Results: When paced LV‐only, peak CRI was similar (93 ± 5% vs. 92 ± 5%) during atrial sensing or pacing but optimal PAVD was 61 ± 31 ms greater than optimal SAVD. The difference between As‐RVs and Ap‐RVs intervals on IEGMs (62 ± 31 ms) was nearly identical. The slope of the correlation line (0.98) and the correlation coefficient r (0.99) comparing the 2 methods of assessing SAVD‐PAVD offset were nearly 1 and the y‐intercept (0.63 ms) was near 0. During simultaneous biventricular (BiV) pacing at short AVD, SAVD and PAVD programming did not affect CRI, but CRI was significantly (p <.05) lower during atrial sensing at long AVD. Conclusions: A novel methodology for measuring electrical dyssynchrony was used to determine electrically optimal SAVD/PAVD during LV‐only pacing. When BiV pacing, shorter AVDs produce better electrical synchrony. [ABSTRACT FROM AUTHOR]

Background: Pulmonary arterial hypertension (PAH) leads to myocardial remodeling, manifesting as mechanical dyssynchrony (M-dys) and electrical dyssynchrony (E-dys), in both right (RV) and left ventricles (LV). However, the impacts of layer-specific intraventricular M-dys on biventricular functions and its association with E-dys in PAH remain unclear. Methods: Seventy-nine newly diagnosed patients with PAH undergoing cardiac magnetic resonance scanning were consecutively recruited between January 2011 and December 2017. The biventricular volumetric and layer-specific intraventricular M-dys were analyzed. The QRS duration z-scores were calculated after adjusting for age and sex. Results: 77.22 % of patients were female (mean age 30.30 ± 9.79 years; median follow-up 5.53 years). Further, 29 (36.71 %) patients succumbed to all-cause mortality by the end of the study. At the baseline, LV layer–specific intraventricular M-dys had apparent transmural gradients compared with RV in the radial and circumferential directions. However, deceased patients lost the transmural gradients. The LV longitudinal strain rate time to late diastolic peak in the myocardial region (LVmyoLSRTTLDPintra) predicted long-term survival. The Kaplan–Meier curve revealed that patients with PAH with LVmyoLSRTTLDPintra

Background: Recent clinical trials have demonstrated that tafamidis (Pfizer Inc., New York, NY, USA) reduced all-cause mortality and the number of cardiovascular hospitalizations compared with placebo in patients with transthyretin cardiac amyloidosis. However, the optimal surrogate markers during tafamidis treatment remain unknown. Methods: Consecutive patients with transthyretin cardiac amyloidosis who received tafamidis in our institute between May 2019 and December 2022 were retrospectively evaluated. The prognostic impact of an increase in troponin I levels during tafamidis therapy was evaluated. Results: A total of 18 patients (median age 77 years, 84% male) were included. For 14-month tafamidis therapy on median, cardiac troponin I levels increased in five patients. The cumulative incidence of all-cause hospitalization was significantly higher in the troponin-increased group than in the others (100% versus 33%, p < 0.0001). Troponin increase was independently associated with the cumulative incidence of all-cause hospitalization with an adjusted hazard ratio of 5.14 (95% confidence interval 1.02–25.9, p = 0.048). Conclusions: The increase in cardiac troponin levels may be a reasonable surrogate marker of response to tafamidis therapy in patients with transthyretin cardiac amyloidosis. [ABSTRACT FROM AUTHOR]

Background: Pacing at sites of longest interventricular delay has been associated with greater reverse remodeling in cardiac resynchronization therapy (CRT). However, the effects of pacing at such sites on clinical outcomes is less well studied.Objective: To assess the association between interventricular delay and clinical outcomes in CRT patients implanted with quadripolar left ventricular (LV) leads.Methods: RALLY-X4 was a registry study of the Acuity X4 quadripolar LV leads. Interventricular delay was measured during unpaced basal rhythm from the right ventricular (RV) lead to the LV lead electrode (E1 to E4) chosen for CRT pacing. Patients were stratified by median RV-LV delay (80 ms) into short and long delay groups, and they were also analysed by multivariable modelling. The primary composite outcome measure was all-cause mortality and heart failure hospitalization (HFH) at 18 months.Results: There were 581 patients with complete RV-LV delay data. The mean LV ejection fraction (EF) was 27% and 73% had a typical left bundle branch block. Predictors of long RV-LV delay included female sex, LBBB and QRS duration >150ms. Survival free of the primary outcome at 18 months follow up was 87% in the long activation delay group compared with 77% in the short delay group (p=0.0042). Multivariate analysis showed that RV-LV delay was a, independent predictor of survival free of HFH (p=0.028).Conclusions: Among CRT patients with quadripolar LV pacing leads, longer baseline interventricular activation delay was significantly associated with the composite endpoint of all-cause mortality and heart failure hospitalization. [ABSTRACT FROM AUTHOR]

Identifying electrical dyssynchrony is crucial for cardiac pacing and cardiac resynchronization therapy (CRT). The ultra-high-frequency electrocardiography (UHF-ECG) technique allows instantaneous dyssynchrony analyses with real-time visualization. This review explores the physiological background of higher frequencies in ventricular conduction and the translational evolution of UHF-ECG in cardiac pacing and CRT. Although high-frequency components were studied half a century ago, their exploration in the dyssynchrony context is rare. UHF-ECG records ECG signals from eight precordial leads over multiple beats in time. After initial conceptual studies, the implementation of an instant visualization of ventricular activation led to clinical implementation with minimal patient burden. UHF-ECG aids patient selection in biventricular CRT and evaluates ventricular activation during various forms of conduction system pacing (CSP). UHF-ECG ventricular electrical dyssynchrony has been associated with clinical outcomes in a large retrospective CRT cohort and has been used to study the electrophysiological differences between CSP methods, including His bundle pacing, left bundle branch (area) pacing, left ventricular septal pacing and conventional biventricular pacing. UHF-ECG can potentially be used to determine a tailored resynchronization approach (CRT through biventricular pacing or CSP) based on the electrical substrate (true LBBB vs. non-specified intraventricular conduction delay with more distal left ventricular conduction disease), for the optimization of CRT and holds promise beyond CRT for the risk stratification of ventricular arrhythmias.

Background: Nonresponse to cardiac resynchronization therapy (CRT) occurs in ∼30%-50% of patients. There are no well-accepted clinical approaches for optimizing CRT in nonresponders.Objective: The purpose of this study was to demonstrate the effect of CRT optimization using electrical dyssynchrony mapping on left ventricular (LV) function, size, and dyssynchrony in selected patients with nonresponse/incomplete response to CRT.Methods: We studied 39 patients with underlying left bundle branch block or interventricular conduction delay who had an LV ejection fraction of ≤40% after receiving CRT and had significant electrical dyssynchrony. Electrical dyssynchrony was measured at multiple atrioventricular delays and interventricular delays. The QRS area between combinations of 9 anterior and 9 posterior electrograms (QRS area under the curve) was calculated, and cardiac resynchronization index (CRI) was defined as the percent change in QRS area under the curve compared to native conduction. Electrical dyssynchrony maps depicted CRI over the wide range of settings tested. Patients were programmed to an optimal device setting, and echocardiograms were recorded 5.9 ± 3.7 months postoptimization.Results: CRI increased from 49.4% ± 24.0% to 90.8% ± 10.5%. CRT optimization significantly improved LV ejection fraction from 31.8% ± 4.7% to 36.3% ± 5.9% (P < .001) and LV end-systolic volume from 108.5 ± 37.6 to 98.0 ± 37.5 mL (P = .009). Speckle-tracking measures of LV strain significantly improved by 2.4% ± 4.5% (transverse; P = .002) and 1.0% ± 2.6% (longitudinal; P = .017). Aortic to pulmonic valve opening time, a measure of interventricular dyssynchrony, significantly (P = .040) decreased by 14.9 ± 39.4 ms.Conclusion: CRT optimization of electrical dyssynchrony using a novel electrical dyssynchrony mapping technology significantly improves LV systolic function, LV end-systolic volume, and mechanical dyssynchrony. This methodology offers a noninvasive, practical clinical approach to treating nonresponders and incomplete responders to CRT. [ABSTRACT FROM AUTHOR]

• Electrical dyssynchrony occurs in 20% of patients with cardiac amyloidosis and is more common in elderly white patients with transthyretin amyloidosis and coronary artery disease. • QRS prolongation is not determined by the degree of left ventricular wall thickness. • Electrical dyssynchrony is associated with a higher New York Heart Association class, higher risk for permanent pacemaker implant and higher risk for all-cause mortality. Conduction-system involvement in cardiac amyloidosis (CA) is common. The prevalence, clinical correlates and impact on outcome related to ventricular electrical dyssynchrony in CA remain insufficiently elucidated. Data from a prospectively maintained registry of patients with CA diagnosed in the Cleveland Clinic's amyloidosis clinic was used to determine the frequency of electrical dyssynchrony (defined as a QRS > 130 msec). The relation with the clinical profile and clinical outcome was assessed. To determine the impact of hypertrophy on QRS prolongation, a QRS-matched cohort without CA was used for comparison of cardiac magnetic resonance imaging. A total of 1140 patients with CA (39% AL, 61% TTR) were evaluated, of whom 230 (20%) had electrical dyssynchrony. The type of conduction block was predominantly a right bundle branch block (BBB, 48%) followed by left BBB (35%) and intraventricular conduction delay (17%). Presence of transthyretin amyloidosis (ATTR-CA), older age, male gender, white race, and coronary artery disease were independently (P < 0.05 for all) associated with electrical dyssynchrony, and patients were more commonly prescribed a mineralocorticoid receptor antagonist. In ATTR-CA, specifically, every increase in ATTR-CA disease stage was associated with a 1.55-fold (1.23--1.95; P < 0.001) increased odds for electrical dyssynchrony. In a subset of patients with CA who underwent cardiac magnetic resonance imaging (n = 41), left ventricular mass index was unrelated to the QRS duration (r = 0.187; P = 0.283) in CA, in contrast to a non-CA QRS-matched cohort (r = 0.397; P < 0.001). Patients with electrical dyssynchrony were more symptomatic at initial presentation, as illustrated by a higher New York Heart Association class (P = 0.041). During a median follow-up of 462 days (IQR:138--996 days), a higher proportion of patients with electrical dyssynchrony died from all-cause death (P = 0.037) or developed a permanent pacing indication (3% vs 10.4%; P < 0.001) during follow-up. Electrical dyssynchrony is common in CA, especially in ATTR-CA, and is associated with worse functional status and clinical outcome. Given the high rate of permanent pacing indications at follow-up, additional studies are necessary to determine the best monitoring and pacing strategies in CA. [Display omitted] [ABSTRACT FROM AUTHOR]

There is no clinical methodology for quantification or display of electrical dyssynchrony over a wide range of atrial-ventricular delays (AVD) and ventricular-ventricular delays (VVD) in patients with cardiac resynchronization therapy (CRT). This study aimed to develop a new methodology, based on wavefront fusion, for mapping electrical synchrony. A cardiac resynchronization index (CRI) was measured at multiple device settings in 90 patients. Electrical dyssynchrony maps (EDM) were constructed for each patient to display CRI at any combination of AVD and VVD. An optimal synchrony line (OSL) depicted the AVD/VVD combinations producing the highest CRIs. Fusion of right ventricular paced (RVp), left ventricular paced (LVp), and native wavefront offsets were calculated. CRI significantly increased (p < 0.0001) from 58.0 ± 28.1% at baseline to 98.3 ± 1.7% at optimized settings. EDMs in patients with high-grade heart block (n = 20) had an OSL parallel to the simultaneous biventricular pacing (BiVP VV-SIM) line with leftward shift across all AVDs (RVp-LVpOFFSET = 50.5 ± 29.8 ms). EDMs in patients with intact AV node conduction (n = 64) had an OSL parallel to the BiVP VV-SIM line with leftward shift at short AVDs (RVp-LVpOFFSET = 33.4 ± 23.3 ms), curvilinear at intermediate AVDs (triple fusion), and vertical at long AVDs (native-LVpOFFSET = 85.2 ± 22.8 ms) in all patients except those with poor LV lead position (n = 6). A new methodology is described for quantifying and graphing electrical dyssynchrony over a physiologic range of AVDs/VVDs. This methodology offers a noninvasive, practical, clinical approach for measuring electrical synchrony that could be applied to optimization of CRT devices. • A non-invasive method of assessing cardiac electrical synchrony is described. • Synchrony over a range of cardiac resynchronization device settings is mapped. • Optimal device settings can be found, potentially improving patient outcomes. • Timing of RV-paced, LV-paced and native electrical wavefronts can be quantified. • Lack of resynchronization over the entire map suggests poor lead position. [ABSTRACT FROM AUTHOR]

Background: Palliation of the single ventricle (SV) circulation is associated with a burden of lifelong complications. Previous studies have identified that the need for a permanent ventricular pacing system (PPMv) may be associated with additional adverse long-term outcomes.Objectives: The goal of this study was to quantify the attributable risk of PPMv in patients with SV, and to identify modifiable risk factors.Methods: This international study was sponsored by the Pediatric and Congenital Electrophysiology Society. Centers contributed baseline and longitudinal data for functionally SV patients with PPMv. Enrollment was at implantation. Controls were matched 1:1 to PPMv subjects by ventricular morphology and sex, identified within center, and enrolled at matched age. Primary outcome was transplantation or death.Results: In total, 236 PPMv subjects and 213 matched controls were identified (22 centers, 9 countries). Median age at enrollment was 5.3 years (quartiles: 1.5-13.2 years), follow-up 6.9 years (3.4-11.6 years). Median percent ventricular pacing (Vp) was 90.8% (25th-75th percentile: 4.3%-100%) in the PPMv cohort. Across 213 matched pairs, multivariable HR for death/transplant associated with PPMv was 3.8 (95% CI 1.9-7.6; P < 0.001). Within the PPMv population, higher Vp (HR: 1.009 per %; P = 0.009), higher QRS z-score (HR: 1.19; P = 0.009) and nonapical lead position (HR: 2.17; P = 0.042) were all associated with death/transplantation.Conclusions: PPMv in patients with SV is associated with increased risk of heart transplantation and death, despite controlling for increased associated morbidity of the PPMv cohort. Increased Vp, higher QRS z-score, and nonapical ventricular lead position are all associated with higher risk of adverse outcome and may be modifiable risk factors. [ABSTRACT FROM AUTHOR]

Current cardiac resynchronization therapy (CRT) implant guidelines emphasize the presence of electrical dyssynchrony (left bundle branch block (LBBB) and QRS > 150 ms) yet have modest predictive value for response and have not reduced the 30% nonresponse rate. Optimized programming to optimize CRT delivery has promised much but to date has largely been ineffective. What is missing is the understanding of LV paced effects (which are unpredictable) and optimal paced AV interval (that can be conserved during physiologic variations) that then can be incorporated into an individualized programming prescription. Automatic device-based algorithms that deliver electrical optimization and maintain this during ambulatory fluctuations in AV interval are discussed. [ABSTRACT FROM AUTHOR]

Aims: Cardiac resynchronization therapy (CRT) response is proportional to QRS duration (QRSd). We hypothesize that this is, in part, due to slower conduction velocity and hence wider range of programmed device settings that produce adequate electrical wavefront fusion and resynchronization in wider QRSd patients.Methods: CRT patients (n = 122) with left ventricular (LV) conduction delay, sinus rhythm and intact atrioventricular node conduction were studied. Patients were categorized by QRSd: narrow (<120 ms; n = 20); moderate (120-150 ms, n = 37); and prolonged (≥150 ms; n = 65). Electrocardiographic data was acquired during native rhythm and LV-only pacing at varying atrioventricular delays (AVDs). Electrical synchrony was quantified as cardiac resynchronization index (CRI) using multi‑lead electrocardiographic systems and a proprietary algorithm that quantified wavefront fusion. A Gaussian distribution equation was fitted to CRI response.Results: Peak CRI was high (87.6 ± 6.3%) and similar (p = 0.716) across QRSd groups. The standard deviation of the Gaussian distribution significantly correlated with QRSd (R = 0.614, p < 0.001), and progressively and significantly (p < 0.001) increased as QRSd increased from narrow (34.8 ± 10.0 ms), to moderate (50.6 ± 8.4 ms), to prolonged (67.6 ± 18.3 ms). At AVDs 20 and 40 ms from optimal, CRI differed significantly (p < 0.001) between groups, with progressively higher CRI values as native QRSd increased.Conclusion: Electrical resynchronization with optimally programmed LV-only pacing was similar between patients with varying QRSd, including patients with narrow QRSd. The resynchronization window that corresponded with optimal electrical resynchronization decreased as native QRSd decreased. This finding provides one potential explanation for the lack of significant benefit of CRT in narrow QRSd patients in previous studies. [ABSTRACT FROM AUTHOR]

Objectives: High percentages of pacing were associated to maximal symptomatic and mortality benefit from cardiac resynchronization therapy (CRT). Loss of CRT pacing is linked to intrinsic ventricular activation preceding biventricular pacing (BiV), as it occurs in patients with atrial fibrillation (AF). Last generation CRT devices incorporate the ventricular sense response (VSR) mechanism to maintain biventricular pacing in patients with atrial arrhythmias. This work aimed to characterize electrical dyssynchrony differences among baseline, BiV and VSR pacing, and determine whether the VSR mode is as beneficial as the BiV mode in terms of electrical dyssynchrony.Methods: Thirty-two patients implanted with CRT devices were retrospectively studied. All patients presented non-ischemic dilated myocardiopathy and complete left bundle branch block (LBBB). Every patient went through baseline, BiV and VSR pacing while recording the 12‑lead ECG. Electrical dyssynchrony was assessed by a dyssynchrony index (DIn) obtained from correlation analysis on the 12‑lead ECG.Results: When comparing with baseline, VSR pacing improved QRS duration (178 ± 22 ms vs 158 ± 43 ms, baseline vs VSR, p < 0.05) and so did BiV pacing (178 ± 22 ms vs 142 ± 20 ms, baseline vs BiV, p < 0.05). However, electrical dyssynchrony only improved at BiV pacing (2.86±0.6 vs 0.54±0.8, baseline vs BiV, p < 0.05) while VSR showed average DIn values similar to those at baseline.Conclusions: VSR pacing did not improve the electrical synchrony while did shorten QRS duration in this sample population. Therefore, VSR paced beats would fall in the category of inefficient BiV and may not be the preferred alternative in patients with CRT and AF. [ABSTRACT FROM AUTHOR]

Right ventricular (RV) pacing causes changes in the heart's electrical and mechanical activation patterns. The QRS duration is a useful surrogate marker of electrical dyssynchrony; a longer QRS duration during RV pacing indicates poor prognosis. However, the mechanisms underlying a longer QRS duration during RV pacing remain unclear; hence, we investigated factors predicting QRS prolongation during RV pacing. We enrolled 211 patients who underwent catheter ablation for supraventricular tachyarrhythmia and showed no bundle branch block. Three-dimensional mapping for the QRS duration during RV pacing from the RV outflow to RV apex was performed, and differences in the QRS duration were analyzed. The predisposing factors causing QRS > 160 ms during RV apical pacing were also analyzed. The QRS durations at baseline and during RV pacing from the RV outflow and at the RV apex were 85.0 ± 7.5 ms, 163.7 ± 17.1 ms, and 156.2 ± 16.1 ms, respectively. With respect to the QRS duration, there was a significant correlation between RV outflow and RV apical pacing (r = 0.658, p < 0.001). Difference in the QRS duration between the RV outflow and RV apex in each patient was only 12.5 ± 10.4 ms. Logistic multivariable regression analysis identified baseline QRS duration [odds ratio (OR) 1.24, 95% confidence interval (CI) 1.15–1.33, p < 0.01], interventricular septum thickness (OR 1.20, 95% CI 1.02–1.40, p = 0.025), left atrial diameter (OR 1.08, 95% CI 1.01–1.16, p = 0.024), and E/e' (OR 1.23, 95% CI 1.12–1.35, p < 0.01) as significant predictors of QRS prolongation during RV apical pacing. The QRS duration during RV pacing largely depends not on the pacing site, but on the underlying structural heart diseases. [ABSTRACT FROM AUTHOR]

Background: Cardiac resynchronization therapy (CRT) uses left ventricular (LV) pacing to restore rapid synchronized LV activation when it is delayed in patients with myocardial disease. Objective: Although intrinsic LV activation delays are understood, little is known about reactions to LV stimulation and whether they are affected by QRS duration (QRSd), morphology, LV substrate, or choice of electrode pair. The purpose of this study was to test these interactions. Methods: In 120 heart failure patients with left bundle branch block (LBBB) and QRS >120 ms receiving CRT with quadripolar LV leads, device-based measurements of intrinsic activation delay (qLV) and paced inter- (and intra-) LV conduction times were evaluated at the proximal and distal LV bipoles. Results: During intrinsic conduction, qLV varied little between the proximal and distal pairs in patients with LBBB (n = 120; age 68 ± 11 years; 63% male; ejection fraction 25% ± 7%; 33% ischemic cardiomyopathy; QRSd 162 ± 19 ms). A minority (30%) had conduction barriers (ie, gradients) (ΔqLV 29 ± 8 ms vs 9 ± 5 ms in patients without gradients; P

[Display omitted] [ABSTRACT FROM AUTHOR]

Background: Left ventricular mechanical dyssynchrony has been shown to provide significant clinical values for chronic heart failure (HF) and cardiac resynchronization therapy (CRT). The purpose of this study was to evaluate whether electrical dyssynchrony combined with mechanical dyssynchrony has an incremental benefit over electrical dyssynchrony or mechanical dyssynchrony alone to predict clinical events in patients with acute heart failure (AHF). Methods: Ninety-six AHF patients who received standard 12-lead ECG, gated single-photon emission computed tomography (SPECT) myocardial perfusion imaging (MPI), and echocardiography were enrolled. Thirty-two normal subjects were collected as the control group to get the normal database of mechanical dyssynchrony. The end point is the composite of all-cause death and heart transplantation. Electrical dyssynchrony was defined as QRS duration > 120 ms. Mechanical dyssynchrony was defined as > mean + 2 × SD phase standard deviation (PSD) or phase bandwidth (PBW) based on our normal database. Results: During the follow-up of 28 ± 10 months, complete data were obtained in 92 patients. 26 (28.3%) Patients who reached the end point were classified into the event group. There were no significant differences in PSD or PBW between the event and non-event groups. However, PBW > 77.76° was independently associated with the end point in the univariate and multivariate analysis (hazard ratio 2.92, 95% confidence interval 1.00-8.47, P =.049; hazard ratio 3.89, 95% confidence interval 1.01-14.97, P =.048). The Kaplan-Meier curve with a log-rank test showed that the end point rate was significantly higher in the patients with PBW > 77.76° (log-rank P =.039). Moreover, the ROC curve analysis showed that the area under the curve (AUC) for predicting end point events by the integrative analysis of QRS > 120 ms and PBW > 77.76° was significantly improved compared to QRS duration > 120 ms (AUC: 0.75 vs 0.68, P =.001) or PBW > 77.76° (AUC: 0.75 vs 0.62, P =.049), respectively. The model of combined electrical and mechanical dyssynchrony yielded a further significantly improved risk prediction for adverse events in the global χ2. Conclusions: The combination of QRS duration > 120 ms and PBW > 77.76° was an independent predictor of all-cause death and heart transplantation in AHF patients. The integrative analysis of electrical and mechanical dyssynchrony provides incremental prognostic value for clinical use. [ABSTRACT FROM AUTHOR]

Background: Novel metrics of electrical dyssynchrony based on multi-electrode mapping and ECG-based markers of fusion are better predictors of cardiac resynchronization therapy (CRT) response than QRS duration.Objective: To describe a new methodology for measuring electrical synchrony based on wavefront fusion and electrocardiographic cancellation in patients with CRT and its potential for CRT optimization.Methods: Patients with left bundle branch block (LBBB) type conduction and CRT (n = 84) were studied at multiple device settings using an ECG belt (53 anterior and posterior electrodes). The area between combinations of anterior and posterior curves (AUC) was calculated and cardiac resynchronization index (CRI) defined as percent change in AUC compared to LBBB.Results: In 14 patients with complete heart block or atrial fibrillation, CRI at optimal ventriculo-ventricular delay (VVD) (40 ± 19 ms) was significantly higher than with simultaneous biventricular pacing (BiVp) (90 ± 8.6% vs. 54.2 ± 24.2%, p < 0.001). In all 70 patients paced LV-only, LV-paced wavefront was ahead of native wavefront at short atrio-ventricular delay (AVD) and CRI increased with increase in AVD, peaked, and then decreased. Optimal CRI during LV-only pacing was significantly better than optimal CRI with simultaneous BiVp (89.6 ± 8% vs. 64.4 ± 22%, p < 0.001), and occurred at AVD 68 ± 22 ms less than the atrial-RV sensed interval. With sequential BiVp, best CRI was 83.9 ± 13% (with LV preactivation of 40 ± 20 ms). Best CRI at any setting was markedly better than CRI at standard setting (91.6 ± 7.7% vs. 52.7 ± 23.3, p < 0.001).Conclusion: We describe a novel non-invasive investigational tool that quantifies wavefront fusion and electrical dyssynchrony, and may allow for individualized CRT optimization. [ABSTRACT FROM AUTHOR]

Background: Right ventricular myocardial pacing leads to nonphysiological activation of heart ventricles. Contrary to this, His bundle pacing preserves their fast activation. Ultra-high-frequency electrocardiography (UHF-ECG) is a novel tool for ventricular depolarization assessment.Objective: The purpose of this study was to describe UHF-ECG depolarization patterns during myocardial and His bundle pacing.Methods: Forty-six patients undergoing His bundle pacing to treat bradycardia and spontaneous QRS complexes without bundle branch block were included. UHF-ECG recordings were performed during spontaneous rhythm, pure myocardial para-Hisian capture, and His bundle capture. QRS duration, QRS area, depolarization time in specific leads, and the UHF-ECG-derived ventricular dyssynchrony index were calculated.Results: One hundred thirty-three UHF-ECG recordings were performed in 46 patients (44 spontaneous rhythm, 28 selective His bundle, 43 nonselective His bundle, and 18 myocardial capture). The mean QRS duration was 117 ms for spontaneous rhythm, 118 ms for selective, 135 ms for nonselective, and 166 ms for myocardial capture (P < .001 for nonselective and myocardial capture compared to each of the other types of ventricular activation). The calculated dyssynchrony index was shortest during spontaneous rhythm (12 ms; P = .02 compared to selective and P = .09 compared to nonselective), and it did not differ between selective and nonselective His bundle capture (16 vs 15 ms; P > .99) and was longest during myocardial capture of the para-Hisian area (37 ms; P < .001 compared to each of the other types of ventricular activation).Conclusion: In patients without bundle branch block, both types of His bundle, but not myocardial, capture preserve ventricular electrical synchrony as measured using UHF-ECG. [ABSTRACT FROM AUTHOR]

Identifying electrical dyssynchrony is crucial for cardiac pacing and cardiac resynchronization therapy (CRT). The ultra-high-frequency electrocardiography (UHF-ECG) technique allows instantaneous dyssynchrony analyses with real-time visualization. This review explores the physiological background of higher frequencies in ventricular conduction and the translational evolution of UHF-ECG in cardiac pacing and CRT. Although high-frequency components were studied half a century ago, their exploration in the dyssynchrony context is rare. UHF-ECG records ECG signals from eight precordial leads over multiple beats in time. After initial conceptual studies, the implementation of an instant visualization of ventricular activation led to clinical implementation with minimal patient burden. UHF-ECG aids patient selection in biventricular CRT and evaluates ventricular activation during various forms of conduction system pacing (CSP). UHF-ECG ventricular electrical dyssynchrony has been associated with clinical outcomes in a large retrospective CRT cohort and has been used to study the electrophysiological differences between CSP methods, including His bundle pacing, left bundle branch (area) pacing, left ventricular septal pacing and conventional biventricular pacing. UHF-ECG can potentially be used to determine a tailored resynchronization approach (CRT through biventricular pacing or CSP) based on the electrical substrate (true LBBB vs. non-specified intraventricular conduction delay with more distal left ventricular conduction disease), for the optimization of CRT and holds promise beyond CRT for the risk stratification of ventricular arrhythmias.

Background: Pulmonary arterial hypertension (PAH) leads to myocardial remodeling, manifesting as mechanical dyssynchrony (M-dys) and electrical dyssynchrony (E-dys), in both right (RV) and left ventricles (LV). However, the impacts of layer-specific intraventricular M-dys on biventricular functions and its association with E-dys in PAH remain unclear., Methods: Seventy-nine newly diagnosed patients with PAH undergoing cardiac magnetic resonance scanning were consecutively recruited between January 2011 and December 2017. The biventricular volumetric and layer-specific intraventricular M-dys were analyzed. The QRS duration z -scores were calculated after adjusting for age and sex., Results: 77.22 % of patients were female (mean age 30.30 ± 9.79 years; median follow-up 5.53 years). Further, 29 (36.71 %) patients succumbed to all-cause mortality by the end of the study. At the baseline, LV layer-specific intraventricular M-dys had apparent transmural gradients compared with RV in the radial and circumferential directions. However, deceased patients lost the transmural gradients. The LV longitudinal strain rate time to late diastolic peak in the myocardial region (LVmyoLSRTTLDP intra ) predicted long-term survival. The Kaplan-Meier curve revealed that patients with PAH with LVmyoLSRTTLDP intra <20.01 milliseconds had a worse prognosis. Larger right ventricle (RV) intraventricular M-dys resulted in worse RV ejection fraction. However, larger LV intraventricular M-dys in the late diastolic phase indicated remarkable exercise capacity and higher LV stroke volume index. E-dys and intraventricular M-dys had no direct correlations., Conclusions: The layer-specific intraventricular M-dys had varying impacts on biventricular functions in PAH. PAH patients with LVmyoLSRTTLDP intra <20.01 milliseconds had a worse prognosis. LV intraventricular M-dys in the late diastolic phase needs more attention to precisely evaluate LV function., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2023 The Authors. Published by Elsevier Ltd.)

Highlights • Electrical dyssynchrony (ED) was associated with left ventricular (LV) remodeling. • ED after aortic valve replacement (AVR) was associated with LV diastolic dysfunction. • ED after AVR was linked to clinical adverse events. Abstract Background Electrical dyssynchrony (ED) is one of the important contributing mechanisms in the progression of heart failure. We hypothesized that ED would interfere with cardiac reverse remodeling and affect prognosis after aortic valve surgery. Methods A total of 411 consecutive patients (233 males, mean age 65 ± 11 years) who underwent aortic valve surgery were retrospectively analyzed. The patients were divided into two groups according to the presence of ED [Group 1: no ED (n = 382, 93%), Group 2: ED (n = 29, 7%)]. ED was defined as either left ventricular bundle branch block, or electrical pacing rhythm. Cardiac reverse remodeling was assessed at 1 year after surgery by the changes in left ventricular ejection fraction (LVEF), LV end-systolic volume (LVESV), and left atrial volume index (LAVI). The primary endpoint was a composite of hospitalization for heart failure, and all-cause mortality. Results At 1 year after surgery, group 2 showed lower LVEF (58 ± 15% vs. 64 ± 9%, p = 0.044), and higher LAVI (42 ± 18 ml/m2 vs. 33 ± 13 ml/m2, p = 0.018) than group 1. However, LVESV values (55 ± 38 ml vs. 42 ± 24 ml, p = 0.076) were not significantly different. In particular, in patients with reduced preoperative LVEF, the LVEF was markedly increased in group 1 but not in group 2 after 1 year. During a median follow-up of 39 months, group 2 showed a worse clinical outcome than group 1 (20.7% vs. 7.6%, p = 0.031). After adjusting for confounding factors in the multivariate analyses, age [hazard ratio (HR) 1.11, 95% confidence interval (CI) 1.06–1.16, p < 0.001] and the presence of ED (HR 2.43, 95% CI 1.01–5.89, p = 0.046) were found to be independent predictors of clinical outcomes. Conclusions ED after aortic valve surgery negatively affected cardiac remodeling and prognosis. [ABSTRACT FROM AUTHOR]

Background: The recently developed quadripolar left ventricular (LV) leads have been developed to increase the benefit of cardiac resynchronization therapy (CRT). These leads offer the option to stimulate the LV on multiple sites (multipoint pacing, MPP). Invasive haemodynamic measurements have shown that MPP increases haemodynamic response.Purpose: To investigate whether the beneficial effect of MPP can be explained by better electrical resynchronization.Methods: Different LV lead locations were tested during biventricular (BiV) pacing and MPP in 29 CRT candidates. The 12-lead electrocardiogram (ECG) and the invasive LV pressure curves were measured simultaneously. The Kors matrix was used to convert the ECG into a vectorcardiogram (VCG). The acute haemodynamic benefit of MPP was compared with the reduction in QRS duration and VCG-derived QRS area.Results: Out of the 29 patients, three patients were excluded due to missing LV pressures or ECG measurements. In the remaining 26 patients MPP resulted in a significant haemodynamic improvement compared to BiV pacing without a significant change in QRS duration and QRS area. In only 5 out of the 26 patients the QRS area decreased during MPP compared to BiV pacing. In 17 patients MPP did not change QRS duration and significantly increased QRS area but moved the direction of the maximal QRS vector (azimuth) more opposite from baseline compared to BiV pacing. In 4 patients the QRS area was small during baseline, indicating limited electrical dyssynchrony.Conclusion: The acute haemodynamic benefit of MPP over BiV pacing is achieved by either electrical resynchronization (reduction in QRS area) or by a rotation of the maximal QRS vector, indicating a more LV dominated activation sequence. The latter property was found in two-thirds of the cohort studied. [ABSTRACT FROM AUTHOR]

Background Electrical and right ventricular (RV) mechanical dyssynchrony has been previously described in pediatric pulmonary arterial hypertension (PAH), but less is known about the relationship between electrical dyssynchrony and biventricular function. In this study we applied cardiac magnetic resonance (CMR) imaging to evaluate biventricular size and function with a focus on left ventricular (LV) strain mechanics in pediatric PAH patients with and without electrical dyssynchrony. Methods Fifty-six children with PAH and comprehensive CMR evaluation were stratified based on QRS duration z -score, with electrical dyssynchrony defined as z -score ≥2. Comprehensive biventricular volumetric, dyssynchrony, and strain analysis was performed. Results Nineteen PAH patients had or developed electrical dyssynchrony. Patients with electrical dyssynchrony had significantly reduced RV ejection fraction (35% vs 50%, p = 0.003) and greater end-diastolic (168 vs 112 ml/m 2 , p = 0.041) and end-systolic (119 vs 57, ml/m 2 , p = 0.026) volumes. Patients with electrical dyssynchrony had reduced RV longitudinal strain (–14% vs –19%, p = 0.007), LV circumferential strain measured at the free wall (–19% vs –22%, p = 0.047), and the LV longitudinal strain in the septal region (–10% vs –15%, p = 0.0268). LV mechanical intraventricular dyssynchrony was reduced in patients with electrical dyssynchrony at the LV free wall (43 vs 19 ms, p = 0.019). Conclusions The electrical dyssynchrony is associated with the reduced LV strain, enlarged RV volumes, and reduced biventricular function in children with PAH. CMR assessment of biventricular mechanical function with respect to QRS duration may help to detect pathophysiologic processes associated with progressed PAH. [ABSTRACT FROM AUTHOR]

Background: Electrical synchronization is likely improved by cardiac resynchronization therapy (CRT), but is difficult to quantify with 12-lead ECG. We aimed to quantify changes in electrical synchrony and potential for optimization with CRT using a body-surface activation mapping (BSAM) system.Methods: Standard deviation of activation times (SDAT) was calculated in 94 patients using BSAM at baseline CRT (CRTbl), native, and different CRT configurations.Results: SDAT decreased 20% from native to CRTbl (p<0.01) and an additional 26% (p<0.01) at optimal CRT (CRTopt), the minimal SDAT setting. Patients with LBBB and patients with QRS duration ≥150ms had higher native SDAT and greater decrease with CRTbl (p<0.01); however, the improvement from CRTbl to CRTopt was similar in all four groups (range: 24-28%). CRTopt was achieved with biventricular pacing in 52% and LV-only pacing in 44%. We propose that improved wavefront fusion demonstrated by BSAMs contributed substantially to the improved electrical synchrony.Conclusion: Optimization potential is similar regardless of pre-CRT QRS morphology or duration. BSAM could possibly improve CRT response by individualizing device programming to minimize electrical dyssynchrony. [ABSTRACT FROM AUTHOR]

Aims To evaluate coronary sinus single-site (CSSS) left ventricular pacing in adult patients with normal left ventricular ejection fraction (LVEF) when traditional right ventricular lead implantation is not feasible or is contraindicated. Methods and results We performed a retrospective analysis of 23 patients with tricuspid valve surgery/disease who received a CSSS ventricular pacing lead to avoid crossing the tricuspid valve. Two matched control populations were obtained from patients receiving (i) conventional right ventricular single-site (RVSS) leads and (ii) coronary sinus leads for cardiac resynchronization therapy (CSCRT). Main outcomes of interest were lead stability, electrical lead parameters and change in LVEF during long-term follow-up. Successful CSSS pacing was accomplished in all 23 patients without any procedural complications. During the 5.3 ± 2.8-year follow-up 22/23 (95.7%) leads were functional with stable pacing and sensing parameters, and 1/23 (4.3%) was extracted for unrelated reasons. Compared to CSSS leads, the lead revision/abandonment was similar with RVSS leads (Hazard ratio (HR) 0.87, 95% confidence interval (CI) 0.03, 22.0), but was higher with CSCRT leads (HR 7.41, 95% CI 1.30, 139.0). There was no difference in change in LVEF between CSSS and RVSS groups (–2.4 ± 11.0 vs. 1.5 ± 12.8, P =  0.76), but LVEF improved in CSCRT group (11.2 ± 16.5%, P =  0.002). Fluoroscopy times were longer during implantation of CSSS compared to RVSS leads (25.6 ± 24.6 min vs. 12.3 ± 18.6 min, P =  0.049). Conclusion In patients with normal LVEF, single-site ventricular pacing via the coronary sinus is a feasible, safe and reliable alternative to right ventricular pacing. [ABSTRACT FROM AUTHOR]

Aims: Left ventricular (LV) epicardial pacing (LVEpiP) in human myopathic hearts does not decrease global epicardial activation delay compared with right ventricular (RV) endocardial pacing (RVEndoP); however, the effect on transmural activation delay has not been evaluated. To characterize the transmural electrical activation delay in human myopathic hearts during RVEndoP and LVEpiP compared with global epicardial activation delay.Methods and results: Explanted hearts from seven patients (5 male, 46 ± 10 years) undergoing cardiac transplantation were Langendorff-perfused and mapped using an epicardial sock electrode array (112 electrodes) and 25 transmural plunge needles (four electrodes, 2 mm spacing), for a total of 100 unipolar transmural electrodes. Electrograms were recorded during LVEpiP and RVEndoP, and epicardial (sock) and transmural (needle) activation times, along with patterns of activation, were compared. There was no difference between the global epicardial activation times (LVEpiP 147 ± 8 ms vs. RVEndoP 156 ± 17 ms, P = 0.46). The mean LV transmural activation time during LVEpiP was significantly shorter than that during RVEndoP (125 ± 44 vs. 172 ± 43 ms, P < 0.001). During LVEpiP, of the transmural layers endo-, mid-myocardium and epicardium, LV endocardial layer was often the earliest compared with other transmural layers.Conclusion: In myopathic human hearts, LVEpiP did not decrease global epicardial activation delays compared with RVEndoP. LV epicardial pacing led to early activation of the LV endocardium, revealing the importance of the LV endocardium even when pacing from the LV epicardium. [ABSTRACT FROM AUTHOR]

Background: Dual-site right ventricular pacing (Dual RV) has been proposed as an alternative for patients with heart failure undergoing cardiac resynchronization therapy (CRT) with a failure to deliver a coronary sinus (CS) lead. Only short-term hemodynamic and echocardiographic results of Dual RV are available. We aimed to assess the long-term results of Dual RV and its impact on survival. Methods: Multicenter retrospective assessment of all CRT implants during a 12-year period. Patients with failed CS lead implantation, treated with Dual RV, were followed and assessed for the primary endpoint of all-cause mortality and/or heart transplant. A control group was obtained from contemporary patients using propensity matching for all available baseline variables. Results: Ninety-three patients were implanted with Dual RV devices and compared with 93 matched controls. During a median of 1,273 days (interquartile range 557-2,218), intention-totreat analysis showed that all-cause mortality and/or heart transplant was higher in the Dual RV group (adjusted hazard ratio [HR] = 1.66, 95% confidence interval [CI] 1.12-2.47, P = 0.012). Astreated analysis yielded similar results (HR = 1.97, 95% CI 1.31-2.96, P = 0.001). Cardiac devicerelated infections occurred seven times more frequently in the DualRVsite group (HR=7.60,95% CI 1.51-38.33, P=0.014). Among DualRVnonresponders, four had their apical leads switched off, five required an epicardial LVlead insertion, a transseptal LVlead was implanted in two, and in nine patients, after reviewing the CS venogram, a new CS lead insertion was successfully attempted. Conclusion: Dual RV pacing is associated with worse clinical outcomes and higher complication rates than conventional CRT. [ABSTRACT FROM AUTHOR]

Cardiac resynchronization therapy has emerged as the gold standard for heart failure patients with left ventricular systolic dysfunction and electrical dyssynchrony from an intrinsic intraventricular conduction delay or right ventricular pacing. However, the limits imposed by the coronary sinus venous anatomy restrict the applicability of the technology for many potential recipients. Furthermore, conventional resynchronization, by virtue of utilizing a single site of epicardial origin for left ventricular activation, is non-physiological. Several technologies on the horizon, including multisite pacing, left ventricular endocardial, and leadless devices, and direct His-bundle pacing are aimed at improving the response rate of cardiac resynchronization and extending candidacy to patients ineligible for conventional therapy. In this review, we discuss the limitations of the present technology and the role for these new therapies. [ABSTRACT FROM AUTHOR]

In the chronic complete atrioventricular (AV) block dog (CAVB) model, both bradycardia and altered ventricular activation due to the uncontrolled idioventricular rhythm contribute to ventricular remodeling and the enhanced susceptibility to Torsade de Pointes (TdP) arrhythmias. We investigated the effect of permanent bradycardic right ventricular apex (RVA) pacing on mechanical and electrical remodeling and TdP. In 23 anesthetized dogs, serial experiments were performed at sinus rhythm (SR), acutely after AV block (AAVB) and 3 weeks of remodeling CAVB at a fixed pacing rate of 60/min. ECG, and left (LV) and right ventricular (RV) monophasic action potentials durations (MAPD) were recorded; activation time (AT) and activation recovery interval (ARI) were determined from ten distinct LV electrograms; interventricular mechanical delay (IVMD) and time-to-peak strain (TTP) of the LV septal and lateral wall (ΔTTP: lateral wall minus septal wall) were obtained echocardiographically. Dofetilide (25 μg/kg/5 min) was infused to study TdP inducibility. In baseline AAVB, in comparison to SR, RVA bradypacing acutely increased QT interval, LV, and RVMAPD. Echocardiographic IVMD and ΔTTP were initially increased, which was partially corrected after 3 weeks of RVA pacing (IVMD: 22 ± 13 vs. 42 ± 11 vs. 31 ± 6 ms; ΔTTP: −2 ± 47 vs. −114 ± 38 vs. −36 ± 22 ms). QT interval (362 ± 23 vs. 373 ± 29 ms), LVMAPD (245 ± 18 vs. 253 ± 22 ms), RVMAPD (226 ± 26 vs. 238 ± 31 ms), and mean LV-ARI (268 ± 5 vs. 267 ± 6 ms) were not significantly changed after 3 weeks of RVA pacing. During AAVB, dofetilide increased mean LV-ARI (381 ± 11 ms) with largest increases in the later activated basal areas (slope AT-ARI: +0.96). In contrast with acute RVA pacing, 3 week pacing increased TdP inducibility (0/13 vs. 11/21) and mean LV-ARI (484 ± 18 ms), while the slope of AT-ARI responded differently on dofetilide (−2.37), with larger APD increases in the early region. The latter was supported at the molecular level: reduced RNA expressions of three repolarization-related ion channel genes in early (KCNQ1, KCNH2, and KCNJ2) versus two in late regions (KNCQ1 and KCNJ2). In conclusion, bradycardic RVA pacing acutely induced LV intra- and interventricular mechanical dyssynchrony, which was partially reversed after 3 weeks of pacing (remodeling). The latter occurred without apparent baseline electrical effects. However, dofetilide clearly unmasked (region-specific) arrhythmic consequences of remodeling. [ABSTRACT FROM AUTHOR]

Background: Pacing at sites of longest interventricular delay has been associated with greater reverse remodeling in cardiac resynchronization therapy (CRT). However, the effects of pacing at such sites on clinical outcomes is less well studied., Objective: The purpose of this study was to assess the association between interventricular delay and clinical outcomes in CRT patients implanted with quadripolar left ventricular (LV) leads., Methods: RALLY-X4 was a registry study of the Acuity X4 quadripolar LV leads. Interventricular delay was measured during unpaced basal rhythm from the right ventricular (RV) lead to the LV lead electrode (E1 to E4) chosen for CRT pacing. Patients were stratified by median RV-LV delay (80 ms) into short and long delay groups; they also were analyzed by multivariable modeling. The primary composite outcome measure was all-cause mortality and heart failure hospitalization (HFH) at 18 months., Results: A total of 581 patients had complete RV-LV delay data. Mean LV ejection fraction was 27%, and 73% had typical left bundle branch block. Predictors of long RV-LV delay included female sex, left bundle branch block, and QRS duration >150 ms. Survival free of the primary outcome at 18-month follow-up was 87% in the long activation delay group compared with 77% in the short delay group (P = .0042). Multivariate analysis showed that RV-LV delay was an independent predictor of survival free of HFH (P = .028)., Conclusion: Among CRT patients with quadripolar LV pacing leads, longer baseline interventricular activation delay was significantly associated with the composite endpoint of all-cause mortality and HFH., (Copyright © 2022 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

Background Although response to cardiac resynchronization therapy (CRT) has been conventionally assessed with left ventricular volume reduction, ventricular arrhythmias (ventricular tachycardia/ventricular fibrillation [VT/VF]) are of critical importance associated with unfavorable outcomes even in the 'superresponders' to therapy. We evaluated the predictors of VT/VF and the association of residual dyssynchrony during follow-up. Methods Ninety-five patients receiving CRT were followed-up for 9 ± 3 months. Post-CRT dyssynchrony was defined as a prolonged QRS duration (QRSd) for persistent electrical dyssynchrony (ED), and a Yu index ≥ 33 ms for persistent mechanical dyssynchrony. The first VT/VF episode, including nonsustained VT detected on device interrogation and/or appropriate antitachycardia pacing or shock for VT/VF, were the end points of the study. Results Forty-five patients who reached the study end points had significantly lower mean ΔQRS (baseline QRSd - post-CRT QRSd) values than those without VT/VF (-20.8 ± 28.9 ms vs -6.6 ± 30.7 ms, P = 0.022). Both the baseline and post-CRT QRSds, along with the Yu index values, were not different in two groups. Patients with VT/VF were statistically more likely to have persistent ED (38% vs 9%, P = 0.021). Kaplan-Meier curves showed that a negative ΔQRS was associated with a higher incidence of VT/VF during follow-up (P = 0.016). A multivariate Cox model revealed that QRS prolongation was an independent predictor of VT/VF after CRT (P = 0.029). Conclusions A negative ΔQRS, also called persistent ED, is associated with VT/VF. Narrowest possible QRSd might be a reliable goal of both implantation and optimization of devices to reduce arrhythmic events after CRT. [ABSTRACT FROM AUTHOR]

Introduction Predicting reverse remodeling after cardiac resynchronization therapy (CRT) remains challenging and different etiologies of heart failure might hamper identification of predictors. Objective Assess the incremental value of mechanical dyssynchrony besides electrical dyssynchrony for predicting CRT response. Methods 227 patients (51% ischemic) received CRT. Response was defined as ≥ 15% left ventricular end systolic volume decrease after six months. Prediction models were developed comprising clinical parameters and electrical dyssynchrony (Model A), subsequently complemented with mechanical dyssynchrony (Model B). Models were compared by area under the receiver-operating curve (AUC), net reclassification index (NRI) and integrated discrimination improvement (IDI) for the complete cohort, ischemic (ICM) and non-ischemic (NICM) subpopulations. Results Model B performed significantly better than Model A supported by AUC, NRI and IDI. Furthermore, model B significantly better predicted response for NICM than ICM. Conclusion Electrical dyssynchrony and mechanical dyssynchrony are essential to predict CRT response. Nevertheless, response prediction for ICM remains challenging. [ABSTRACT FROM AUTHOR]

Background The use of vectorcardiography (VCG) has regained interest, however, original Frank-VCG equipment is rare. This study compares the measured VCGs with those synthesized from the 12-lead electrocardiogram (ECG) in patients with heart failure and conduction abnormalities, who are candidate for cardiac resynchronization therapy (CRT). Methods In 92 CRT candidates, Frank-VCG and 12-lead ECG were recorded before CRT implantation. The ECG was converted to a VCG using the Kors method (Kors-VCG) and the two methods were compared using correlation and Bland–Altman analyses. Results Variables calculated from the Frank- and Kors-VCG showed correlation coefficients between 0.77 and 0.90. There was a significant but small underestimation by the Kors-VCG method, relative bias ranging from − 1.9% ± 4.6% (QRS-T angle) to − 9.4% ± 20.8% (T area). Conclusion The present study shows that it is justified to use Kors-VCG calculations for VCG analysis, which enables retrospective VCG analysis of previously recorded ECGs in studies related to CRT. [ABSTRACT FROM AUTHOR]

Background Left bundle branch block (LBBB) leads to prolonged left ventricular (LV) total activation time (TAT) and ventricular electrical uncoupling (VEU; mean LV activation time minus mean right ventricular [RV] activation time); both have been shown to be preferential targets for cardiac resynchronization therapy (CRT). Whether right ventricular apical pacing (RVAP) produces similar ventricular activation patterns has not been well studied. Objective The purpose of this study was to compare electrical ventricular activation patterns during RVAP and LBBB. Methods We performed ECG mapping during sinus rhythm, RVAP, and CRT in 24 patients with LBBB. Results We observed differences in the electrical activation pattern with RVAP compared to LBBB. During LBBB, RV activation occurred rapidly; in contrast, RV activation was prolonged during RVAP (46 ± 21 ms vs 69 ± 17 ms, P <.001). There was no significant difference in LVTAT; however, differences in conduction pattern were observed. During LBBB, LV activation was circumferential, whereas with RVAP, LV activation proceeded from apex to base. Differences in the number, size, and orientation of lines of slow conduction also were observed. With LBBB, VEU was nearly twice as long as during RVAP (73 ± 12 ms vs 38 ± 21 ms, P <.001). CRT resulted in a greater reduction in VEU relative to LBBB activation (P <.001). Conclusion RVAP produces significant differences in ventricular activation characteristics compared to LBBB. Significantly less VEU occurs with RVAP, and as a result CRT produces a smaller relative reduction in VEU. This may explain the finding that CRT appears to be more effective in patients with LBBB than in those who were upgraded because of high percentages of RV pacing. [ABSTRACT FROM AUTHOR]

Up to one-third of patients who undergo cardiac resynchronisation therapy (CRT) are not responders. To identify potential responders to CRT may be sometimes difficult and time-consuming. Forty-five patients who had undergone CRT implantation for standard indications were evaluated. Electrical left ventricular (LV) lead location was assessed by left ventricular activation time (LVAT), LV lead electrical delay (LVLED), and RV-LV interlead electrical delay (RVsense-LVsense). Anatomic LV pacing location was assessed as basal or mid-ventricular between 3:00 to 5:00 (traditionally optimal site), and all the other positions (traditionally non-optimal site). CRT response was defined as a decrease in LV end-systolic volume (LVESV) exceeding 15% at six months. LVLED was larger in the responder group than that in the non-responder group (67.3±8.5% vs. 55.3±8.1%, P < 0.001). In the multivariate analysis, LVLED and cLBBB morphology were the two independent predictors of positive echocardiographic response to CRT (OR=1.180, P =0.003; OR=7.497, P =0.04, respectively). A cutoff value of LVLED> 54.82% predicted responders with 96.3% sensitivity and 75.2% specificity and the area under the receiver operating characteristic (ROC) curve was 0.844 for LVLED ( P =0.002). No relationship was found between the anatomic LV pacing sites and response to CRT ( P =0.188). The larger left ventricular lead electrical delay may predict response to cardiac resynchronisation therapy. [ABSTRACT FROM AUTHOR]