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

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

Long‐Term Nonoutflow Septal Versus Apical Right Ventricular Pacing: Relation to Left Ventricular Dyssynchrony

Background: Right ventricular (RV) apical pacing deteriorates left ventricular (LV) function. RV nonoutflow (low) septal pacing may better preserve ventricular performance, but this has not been systematically tested. Our aim was to assess (1) whether long‐term RV lower septal pacing is superior to RV apical pacing regarding LV volumes and ejection fraction (EF), and (2) if the changes in LV dyssynchrony imposed by pacing are related to the long‐term changes in LV volumes and EF. Methods: In thirty‐six patients with atrioventricular (AV) block, a dual‐chamber pacemaker was implanted. The ventricular electrode was placed either at the apex or at the lower septum, in a randomized sequence. Twenty‐four to 48 hours following implantation, we measured LV volumes, EF, and LV dyssynchrony (by tissue Doppler imaging), both with and without pacing. Patients were reassessed echocardiographically after 12 months. Results: Lower septal pacing induced a more synchronized pattern of LV contraction changes (P < 0.05). Following 12 months, differences were observed between groups regarding LV volumes and EF. EF increased within the septal group (from 52 ± 3.3% to 59 ± 3.0%, P < 0.05). A significant inverse relation was documented between changes in LV dyssynchrony and changes in EF (r =?0.64, P < 0.05). Conclusions: In patients with AV block, RV nonoutflow septal pacing represents an attractive alternative, since it preserves better and may even improve LV volumes and EF. Late changes in EF are associated with the changes in LV dyssynchrony imposed by pacing.     

The Effects of Ventricular Pacing on Left Ventricular Geometry,Function, Myocardial Oxygen Consumption,and Efficiency of Contraction in Conscious Dogs

The effects of ventricular pacing on left ventricular (LV) dynamic geometry, function, and myocardial oxygen consumption (MVO₂) were measured in 12 conscious dogs using sonomicrometry, micromanometry, ultrasonic flow probes, and oximetry catheters during right atrial (A-) and right ventricular (V-) pacing at 150 beats/mm. Systolic function was quantified using slopes (M_w) and volume-intercepts (V_w) of linear relationships between end-di-astolic volume (EDV) and stroke work (SW) for data obtained during vena caval occlusion. V-pacing shifted SW-EDV relationships downward (M_w decreased from 97 ± 21 to 81 ± 21 Kerg/mL) and to the right (V_w increased from 14 ± 11 to 20 ± 12 mL) in comparison with A-pacing (P < 0.05). These functional changes correlated with altered contractile geometry manifest as early shortening in the septal free wall relative to anterior-posterior dimension (increased minor axis mid-wall eccentricity at end-diastole and begin-ejection). Steady-state LV power output decreased from 802 ± 213 mW during A-pacing to 514 ± 170 mW during V-pacing (P < 0.05), while MVO₂ remained relatively unchanged during V-pacing (10 ± 3 mL O₂/min vs 11 ± 3 mL O₂/min during A-pacing, P = NS). As a result, overall LV efficiency decreased from 0.24 ± 0.08 during A-pacing to 0.16 ± 0.06 during V-pacing (P < 0.05). These data illustrate the impact of V-pacing on dynamic LV geometry and function, including impaired LV work output at all physiological levels of preload. Most importantly, the relationship between LV work output and MVO₂ is depressed during V-pacing, emphasizing the interaction between LV mechanics and pump efficiency in intact subjects. As a result, measures taken to restore normal contractile geometry might improve LV efficiency and performance when V-pacing is necessary.     

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

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

Effect of pacing-induced ventricular dyssynchrony on right ventricular function

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

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

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

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

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

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

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

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

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

Stimulation rate and the optimal interventricular interval during cardiac resynchronization therapy in patients with chronic atrial fibrillation

Background: Optimization of cardiac resynchronization therapy (CRT) with respect to the interventricular (V‐V) interval is mainly limited to pacing at a resting heart rate. We studied the effect of higher stimulation rates with univentricular and biventricular (BiV) pacing modes including the effect of the V‐V interval optimization. Methods: In 36 patients with heart failure and chronic atrial fibrillation (AF), the effects of right ventricular (RV), left ventricular (LV), simultaneous BiV, and optimized sequential BiV (BiVopt) pacing were measured. The effect of the pacing mode and the optimal V‐V interval was determined at stimulation rates of 70, 90, and 110 ppm using invasive measurement of the maximum rate of left ventricular pressure rise (LV dP/dt_max). Results: The average LV dP/dt _max for all pacing modalities at stimulation rates of 70, 90, and 110 ppm was 781 ± 176, 833 ± 197, and 884 ± 223 mmHg/s for RV pacing; 893 ± 178, 942 ± 186, and 981 ± 194 mmHg/s for LV pacing; 904 ± 179, 973 ± 187, and 1052 ± 206 mmHg/s for simultaneous BiV pacing; and 941 ± 186, 1010 ± 198, and 1081 ± 206 mmHg/s for BiVopt pacing, respectively. In BiVopt pacing, the corresponding optimal V‐V interval decreased from 34 ± 29, 28 ± 28, and 21 ± 27 ms at stimulation rates of 70, 90, and 110 ppm, respectively . In two individuals, LV dP/dt_max decreased when the pacing rate was increased from 90 to 110 ppm. Conclusion: In patients with AF and heart failure, LV dP/dt_max increases for all pacing modalities at increasing stimulation rates in most, but not all, patients. The rise in LV dP/dt_max with increasing stimulation rates is higher in biventricular (BiV and BiVopt) than in univentricular (LV and RV) pacing. The optimal V‐V interval at sequential biventricular pacing decreases with increasing stimulation rates.     

The hemodynamic effect of right ventricle (RV), RT3DE targeted left ventricle (LV) and biventricular (BIV) pacing in the early postoperative period after cardiac surgery

Background: Congestive heart failure negatively impacts the prognosis in patients after cardiac surgery. The aim of our study was to assess the value of targeted cardiac resynchronization therapy (CRT) within 72 hours after cardiac surgery in patients with mechanical dyssynchrony, who had an ejection fraction ≤ 35%, QRS ≥150 ms or between 120 and 150 ms. Methods: A prospective randomized trial based on three‐dimensional echocardiography (RT3DE) and optimized sequential dual‐chamber (DDD ) pacing in patients after cardiac surgery. DDD epicardial pacing (Medtronic coaxial epicardial leads 6495) was provided by a modified Medtronic INSYNC III Pacemaker (Medtronic Inc., Minneapolis, MN, USA). Summary of results: The study included 21 patients with ischemic heart disease (HD) or valvular HD (16 men, 5 women, average age 69 years) with left ventricle (LV) dysfunction after cardiac surgery . Patients with biventricular (BIV) (CO 6.7 ± 1.7 L/min, CI 3.5 ± 0.8 L/min/m²) and LV (CO 6.2 ± 1.5 L/min, CI 3.2 ± 0.7 L/min/m²) pacing had statistically significantly higher CO and CI than patients with right ventricular (RV) (CO 5.4 ± 1.4 L/min, CI 2.8 ± 0.6 L/min/m²) pacing (BIV vs RV P ≤ 0.001; LV vs RV P ≤ 0.05; BIV vs LV P ≤ 0.05). Conclusions: RT3DE targeted and optimized CRT in the early postperative period after cardiac surgery provided better hemodynamic results than RV pacing. (PACE 2011; 34:1231–1240)     

Relationship between P-wave duration and atrial electromechanical delay assessed by tissue Doppler echocardiography

Background: The aim of the study was to assess the relationship between P‐wave duration on the surface electrocardiogram (ECG) and echocardiographic parameters of atrial electromechanical delay (EMD), as well as contraction synchrony during different atrial pacing modalities. Methods: In 57 patients with sinus node disease and prolonged sinus P‐wave duration treated with multisite atrial pacing (MSAp), the EMD was measured by tissue Doppler in several left and right atrial sites during sinus rhythm, MSAp, and single‐site pacing at right atrial appendage (RAAp), Bachmann's bundle (BBp) region, and coronary sinus (CSp) ostium. Regional atrial synchrony was calculated on the basis of EMD. Results: P‐wave duration was 141 ± 16, 120 ± 17, 138 ± 17, 144 ± 16, and 160 ± 19 ms during sinus rhythm, MSAp, BBp, CSp, and RAAp, respectively (P < 0.001 RAAp and MSAp vs other). P‐wave duration correlated with all atrial EMDs as well as interatrial and intraleft atrial parameters of dyssynchrony. In multivariate analysis, the EMD in lateral left atrial wall was the strongest predictor of P‐wave duration (β 0.41; P < 0.001). The relationship between P‐wave duration and the atrial EMDs was most prominent during RAAp (all left atrial walls r > 0.51; P < 0.01) and BBp (all atrial walls r > 0.42; P < 0.05), while during sinus rhythm and CSp, only weak correlation between echo and ECG was found. Neither of the tissue Doppler parameters correlated with P‐wave duration during MSAp. Interatrial dyssynchrony correlated with P‐wave duration during sinus rhythm and RAAp and intraleft atrial dyssynchrony only during sinus rhythm. Conclusions: P‐wave duration of the surface ECG is highly correlated with the atrial EMD, the relationship is specific for each pacing modality. (PACE 2011; 23–31)     

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

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

Comparison of the efficacy of two surgical alternatives for cardiac resynchronization therapy: trans-apical versus epicardial left ventricular pacing

Background: Epicardial pacing lead implantation is the currently preferred surgical alternative for left ventricular (LV) lead placement. For endocardial LV pacing, we developed a fundamentally new surgical method. The trans‐apical lead implantation is a minimally invasive technique that provides access to any LV segments. The aim of this prospective randomized study was to compare the outcome of patients undergoing either trans‐apical endocardial or epicardial LV pacing. Methods: In group I, 11 end‐stage heart failure (HF) patients (mean age 59.7 ± 7.9 years) underwent trans‐apical LV lead implantation. Epicardial LV leads were implanted in 12 end‐stage HF patients (group II; mean age 62.8 ± 7.3 years). Medical therapy was optimized in all patients. The following parameters were compared during an 18‐month follow‐up period: LV ejection fraction (LVEF), LV end‐diastolic diameter (LVEDD), LV end‐systolic diameter, and New York Heart Association (NYHA) functional class. Results: Nine out of 11 patients responded favorably to the treatment in group I (LVEF 39.7 ± 12.5 vs 26.0 ± 7.8%, P < 0.01; LVEDD 70.4 ± 13.6 mm vs 73.7 ± 10.5 mm, P = 0.002; NYHA class 2.2 ± 0.4 vs 3.5 ± 0.4, P < 0.01) and eight out of 12 in group II (LVEF 31.5 ± 11.5 vs 26.4 ± 8.9%, P = < 0.001; NYHA class 2.7 ± 0.4 vs 3.6 ± 0.4, P < 0.05). During the follow‐up period, one patient died in group I and three in group II. There was one intraoperative LV lead dislocation in group I and one early postoperative dislocation in each group. None of the patients developed thromboembolic complications. Conclusions: Our data suggest that trans‐apical endocardial LV lead implantation is an alternative to epicardial LV pacing. PACE 2012; 35:124–130)     

Transseptal left ventricular endocardial pacing reduces dispersion of ventricular repolarization

Background: Cardiac resynchronization therapy (CRT) may be proarrhythmic in some patients. This may be due to the effect of left ventricular (LV) epicardial pacing on ventricular repolarization. The purpose of this study was to evaluate the effect of endocardial versus epicardial LV biventricular pacing on surface electrocardiogram (ECG) parameters that are known markers of arrhythmogenic repolarization. Methods: ECG markers of repolarization (QT dispersion, QTD; T peak to end, T_peak‐end; T_peak‐end dispersion, T_peak‐endD; QTc) were retrospectively measured before and after CRT in seven patients with transseptal LV endocardial leads (TS group), 28 matched patients with coronary sinus (CS) LV leads (CS group), and eight patients with surgical LV epicardial leads (SUR group). All ECGs were scanned and analyzed using digital callipers. Results: Compared to the CS group, the TS group CRT was associated with a significant postpacing reduction in QTD (?45.2 ± 35.6 vs ?4.3 ± 43.6 ms, P = 0.03) and T_peak‐end (?24.2 ± 22.1 vs 3.4 ± 26.7 ms, P = 0.02). There was a nonsignificant post‐CRT reduction in both T_peak‐endD (?11.3 ± 31.0 vs 2.4 ± 28.9 ms, P = 0.27) and QTc (?50.0 ± 46.4 vs 4.4 ± 70.2 ms, P = 0.06) in the TS versus the CS group. In contrast, there were no differences between the SUR and CS groups in terms of the effect of CRT on these repolarization parameters. Conclusions: CRT with (atrial transseptal) endocardial LV lead placement is associated with repolarization characteristics that are considered to be less arrhythmogenic than those generated by CS (epicardial) LV lead placement. Further work is needed to determine whether these changes translate to a reduction in proarrhythmia. (PACE 2011; 34:1258–1266)     

Performance Evaluation of a Right Atrial Automatic Capture Verification Algorithm using Two Different Sensing Configurations

Background: This acute data collection study evaluated the performance of a right atrial (RA) automatic capture verification (ACV) algorithm based on evoked response sensing from two electrode configurations during independent unipolar pacing. Methods: RA automatic threshold tests were conducted. Evoked response signals were simultaneously recorded between the RA_Ring electrode and an empty pacemaker housing electrode (RA_Ring→Can) and the electrically isolated Indifferent header electrode (RA_Ring→Ind). The atrial evoked response (AER) and the performance of the ACV algorithm were evaluated off‐line using each sensing configuration. An accurate threshold measurement was defined as within 0.2 V of the unipolar threshold measured manually. Threshold tests were designed to fail for small AER (< 0.35 mV) or insufficient signal‐to‐artifact ratio (SAR < 2). Manual threshold measurements were obtained during RA unipolar and bipolar pacing and compared across device indications. Results: Data were collected from 38 patients with RA bipolar leads from four manufacturers. AER signals were analyzed from 34 patients who were indicated for a pacemaker (five), implantable cardioverter‐defibrillator (11), or cardiac resynchronization therapy pacemaker (six) or defibrillator (12). The minimum AER amplitude was larger (P < 0.0001) when recorded from RA_Ring→Can (1.6±0.9 mV) than from RA_Ring→Ind (1.3±0.8 mV). The algorithm successfully measured the pacing threshold in 96.8% and 91.0% of tests for RA_Ring→Can and RA_Ring→Ind, respectively. No statistical difference between the unipolar and bipolar pacing threshold was observed. Conclusions: The RA_Ring→Can AER sensing configuration may provide a means of implementing an independent pacing/sensing method for ACV in the RA. RA bipolar pacing therapy based on measured RA unipolar pacing thresholds may be feasible.     

An animal model for ectopy-induced cardiomyopathy

Background: Ectopy‐induced cardiomyopathy is an increasingly recognized cause of reversible left ventricular (LV) dysfunction. The underlying mechanisms remain unknown. Our goal was to create an animal model for ectopy‐induced cardiomyopathy. Methods: Eleven mongrel dogs underwent the implantation of a dual‐chamber pacemaker. Four dogs served as the control group and seven as the paced group. In the paced group, the pacemaker was connected to two endocardial right ventricular leads, one inserted into the atrial port and the other one into the ventricular port with an atrioventricular delay adjusted to ensure the presence of coupled pacing simulating ventricular bigeminy. Echocardiographic measurements of LV size (LV end‐diastolic diameter [LV‐EDD], LV end‐systolic diameter [LV‐ESD]), LV ejection fraction (LVEF), and mitral regurgitation (MR) were obtained at baseline and after 4 weeks of monitoring or pacing in all dogs except one who had lead dislodgement. Results: In the control group (n = 4), no significant changes in LV dimensions or function were noted. In the paced group (n = 6), LV‐EDD and LV‐ESD increased from 3.58 ± 0.65 cm and 2.47 ± 0.55 cm to 4.15 ± 0.59 cm and 3.21 ± 0.47 cm, respectively (P < 0.01). In addition, LVEF decreased from 60 ± 7% to 46 ± 9% (P < 0.05). No changes in MR were noted. Conclusion: We have shown that coupled pacing simulating ventricular bigeminy was feasible and resulted in increased LV dimensions and decreased LV function. By controlling the percentage of pacing, the coupling interval and the location of the pacing lead, this new model will allow the assessment of the relative roles of these variables in the development of ectopy‐induced cardiomyopathy. (PACE 2011; 34:291–295)     

Effects of pacing rates on global and regional myocardial blood flow

Background: Information is scarce on the effects of right ventricular apical (RVA) pacing on regional and global myocardial blood flow (MBF). The purpose of this study was to assess the relationship between pacing rate and both regional and global MBF. Methods: Four patients with exclusive atrial pacing and six patients with exclusive RVA pacing underwent three consecutive H₂¹⁵O positron emission tomography scans at 60, 90, and 130 pulses per minute (ppm). For each pacing rate, regional and global MBF was determined. In all patients, the left ventricular (LV) function was normal. Results: By varying the atrial pacing rate from 60 to 130 ppm, the mean global MBF increased from 0.94 to 1.40 mL/g/min, whereas the mean septal to lateral MBF ratio decreased from 1.09 to 0.83. In ventricular‐paced patients at corresponding rates, the mean global MBF also increased from 1.07 to 1.52 mL/g/min but here the mean septal to lateral MBF ratio increased from 0.83 to 1.0. Conclusions: During both acute atrial and RVA pacing, regional and global MBF increases with higher pacing rates. However, the septal to lateral MBF ratio decreases with atrial pacing and increases with RVA pacing in patients with normal LV function. In RVA pacing, these different rate‐dependent effects on regional MBF can be considered as a favorable factor that helps to understand why in some long‐term paced patients, LV function is preserved. (PACE 2011; 34:587–592)     

Relationship of myocardial mechanics and regional volume change in patients with left ventricular systolic dysfunction

The contraction and rotation of left ventricular (LV) segments in a synchronous fashion is vital for cardiac pump function. However, no data exist regarding the relationship of LV segmental mechanics and regional volume change in patients with LV systolic dysfunction. Thirty-two patients with EF < 50% and fifty-two normal subjects were enrolled. The radius strain and rotation were assessed in six segments at three short axis views using speckle tracking imaging. The mean and standard deviation (SD) of the strain peak time index (SPTI%) and the rotation peak time index (RPTI%) for each view were calculated as representing myocardial segmental synchrony. The mean and the SD of the 4-D mini-volume time index (VMTI, %) from 16 regions were calculated as representing regional volume change using real-time three-dimensional echocardiography (RT-3DE). The SD for each time index was averaged as the systolic dyssynchrony index (SDI) in both groups. The differences of the SPTI and the RPTI to the VMTI (T_sv and T_rv) were calculated as dyssynchrony between myocardial segmental mechanics and regional volume change. The time interval of the RPTI between apical and basal rotation (T_abrot) was also calculated. The relationship of T_sv, T_rv and T_abrot to LV ejection fraction (EF) was then analyzed. In patients with LV systolic dysfunction, both peak strain and peak rotation occurred later than the regional minimum volume (55.3 ± 11.1% vs. 45.9 + 5.5%; 50.4 ± 8.7% vs. 45.9 ± 5.5% (both P < 0.05) as compared with normal subjects (41.1 ± 6.6% vs. 40.3 ± 3.8%; 44.1 ± 7.5% vs. 40.3 ± 3.8%). The SDI in each time index is also significantly wider than in normal subjects (P < 0.001). In addition, there was a negative correlation between T_sv, T_rv and T_abrot with EF, respectively (P < 0.05). In patients with abnormal LV systolic function the rotation occurs significantly later than regional volume change as compared with normal subjects. There is a negative correlation between this time delay and LVEF. Thus, the relationship of myocardial segmental change and regional volume change could provide insight into intraventricular dyssynchrony in patients with LV systolic dysfunction.