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.     

Improvement in right ventricular systolic function after cardiac resynchronization therapy correlates with left ventricular reverse remodeling

Background: Cardiac resynchronization therapy (CRT) improves left ventricular (LV) systolic function in heart failure (HF). However, the effects of CRT on right ventricular (RV) systolic function are not fully understood. Objective: We aimed to determine echocardiographic correlates of improvement in RV systolic function after CRT. Methods: Fifty‐four patients (61.9 ± 10.5 years; 43 men; LV ejection fraction 24.6 ± 4.0%; QRS duration > 120 ms) with HF were enrolled. Standard echocardiography, strain rate (SR), and tissue Doppler imaging were performed in all patients before and 6 months after CRT. Pulsed‐wave TDI‐derived systolic indices of RV included systolic (RV_S) and isovolumic velocity (RV_IVV) and isovolumic acceleration (RV_IVA). Response to CRT was defined as decline in LV end‐systolic volume (LVESV) ≥ 10%. Results: When indices of RV systolic function were assessed between responders and nonresponders, in responders (38 patients, 70.4%) RV end‐diastolic diameters (RVD1–3), mid‐RV strain, and mid‐RV SR improved significantly (P < 0.01, for all). RV_S (10.77 ± 4.29 vs 12.62 ± 4.10 cm/sec, P = 0.005), RV_IVV (14.71 ± 5.88 vs 18.52 ± 6.62 cm/sec, P < 0.001), and RV_IVA (1.69 ± 0.70 vs 2.39 ± 0.77 m/sec², P < 0.001) significantly increased among responders. There was no significant change in these parameters among nonresponders. Pearson's analyses revealed moderate positive correlations between reduction of LVESV and ΔRV_IVV (r = 0.467, P = 0.001) and ΔRV_IVA (r = 0.473, P = 0.001), respectively. Conclusions: RV diameters and systolic indices after CRT improved only in the responder group. Improvement in RV systolic performance after CRT is correlated with the reduction of LVESV. (PACE 2011; 34:200–207)     

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))     

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.     

Ventricular activation sequence during left ventricular pacing promotes QRS complex oversensing in the atrial channel

Background: Left ventricular (LV)‐only pacing has a significant effect on delay in depolarization of parts of the ventricles that are likely oversensed in the right atrial channel. The study aimed to assess the impact of ventricular activation sequence on QRS oversensing and far‐field endless‐loop pacemaker tachycardia (ELT) in patients who received cardiac resynchronization therapy (CRT) devices. Methods: The study examined 102 patients with CRT devices. Oversensing artifacts in the atrial channel were inspected on intracardiac electrograms, and their timing with respect to the beginning of QRS was determined during DDD‐right ventricular (RV), DDD‐LV, DDD‐biventricular (BiV), and AAI pacing modes. The occurrence of ELT during DDD‐LV pacing with a postventricular atrial refractory period (PVARP) of 250 ms was also assessed. Results: The timing of oversensing artifacts (in relation to the beginning of surface QRS) was dependent on ventricular activation sequence, occurring promptly following intrinsic activation via the right bundle branch (47.1 ± 26.4 ms), later during RV pacing (108.7 ± 22.5 ms) or BiV pacing (109.4 ± 23.1 ms), and significantly later, corresponding to the final part of the QRS, during LV pacing (209.6 ± 40.0 ms, range: 140–340 ms, P < 0.001). Oversensing was significantly more frequent during LV than during RV pacing (35.3% vs 22.5%, P < 0.001). Far‐field ELT was observed in six patients. Conclusions: Oversensing artifacts in the atrial channel are likely caused by depolarization of the basal part of the right ventricle. The novel mechanism of QRS oversensing outside PVARP, caused by a reversed ventricular activation sequence during LV‐only pacing, may be important in some CRT patients. (PACE 2011; 34:1682–1686)     

Insights into the Effects of Contraction Dyssynchrony on Global Left Ventricular Mechano-Energetic Function

Background: The effects of dyssynchrony on global left ventricular (LV) mechanics have been well documented; however, its impact on LV energetics has received less attention. Objective: To assess the effects of LV contraction dyssynchrony on global LV mechano‐energetic function in a pacing‐induced acute model of dyssynchrony. Methods: Using blood‐perfused isolated rabbit heart preparations (n = 11), LV pressure, coronary flow, and arteriovenous oxygen content difference were recorded for isovolumic contractions under right atrial (RA) pacing (control) and simultaneous RA and right ventricular outflow tract (RVOT) pacing (dyssynchrony). LV mechanical function was quantified by the end‐systolic pressure‐volume relationship (ESPVR). Myocardial oxygen consumption‐pressure‐volume area (MVO₂‐PVA) relationship quantified LV energetic function. Internal PVA for MVO_{2 RVOT} was calculated based on the MVO₂‐PVA relationship for RA pacing. Thus, lost PVA (internal PVA–PVA_RVOT) represents the mechanical energy not observable at the global level. Results: Compared to RA pacing, RVOT pacing depressed LV mechanics as indicated by a rightward shift of ESPVR (i.e., increase in V_d from 0.58 ± 0.10 to 0.67 ± 0.10 mL, P < 0.05). Despite depressed mechanics, RVOT pacing was associated with greater MVO₂ such that the MVO₂‐PVA relationship intercept was markedly increased from 0.025 ± 0.003 to 0.029 ± 0.003 mL?O₂/beat/100gLV (P < 0.05). Excess MVO₂ (i.e., MVO_{2 RVOT}– MVO_{2 RA}) significantly correlated with lost PVA (R²= 0.54, P < 0.001). Conclusion: A potential mechanism explaining the observed increase in MVO₂ with dyssynchrony may be that the measured PVA at the global level underestimates the internal PVA at the cellular level, which is likely to be the true determinant of MVO₂.     

The impact of the right ventricular lead position on response to cardiac resynchronization therapy

Introduction: Left ventricular (LV) lead placement to the latest contracting area (concordant LV lead) is associated with better response to cardiac resynchronization therapy (CRT) compared to a discordant LV lead. However, the effect of the right ventricular (RV) lead site on CRT response is unclear. We investigated the relationship of the RV and LV lead positions on CRT response. Methods: In 131 CRT patients, the LV lead was positioned preferentially in a lateral or posterolateral vein and the RV lead to either the RV septum (RVS, n = 55) or RV apex (RVA, n = 76). The latest site of contraction was determined with two‐dimensional speckle tracking radial strain imaging and patients had a concordant LV lead position if pacing the latest segment, and discordant if not. Response was defined as ≥15% reduction in LV end systolic volume (LVESV) at 6‐month follow‐up. Results: There were no significant differences in mean reduction of LVESV at follow‐up (RVS vs RVA: ?23.3 ± 16% vs 22.1 ± 18%, P = 0.70) or rate of responders (58.2% vs 57.9%, P = 0.97) between the two groups. In patients with a concordant LV lead (n = 71), the response rate was significantly higher than those with a discordant lead (76.1% vs 36.7%, P < 0.001). There were no differences in outcomes in patients with a concordant or discordant LV lead according to the RV lead location. Conclusion: The extent of LV reverse remodeling following CRT is not related to the RV lead position, but is significantly higher in patients with a concordant LV lead. (PACE 2011; 34:467–474)     

Impact of right ventricular dyssynchrony on left ventricular performance in patients with pulmonary hypertension

Pulmonary hypertension has been associated with right ventricular (RV) dyssynchrony which may induce left ventricular (LV) dysfunction and dyssynchrony through ventricular interdependence. The present study evaluated the influence of RV dyssynchrony on LV performance in patients with pulmonary hypertension. One hundred and seven patients with pulmonary hypertension (age 63 ± 14 years, systolic pulmonary arterial pressure 60 ± 19 mmHg) and LV ejection fraction (EF) >35 % were evaluated. Ventricular dyssynchrony was assessed with speckle tracking echocardiography and defined as the standard deviation of the time to peak longitudinal strain of six segments of the RV (RV-SD) and the LV (LV-SD) in the apical 4-chamber view. Mean RV-SD and LV-SD assessed with longitudinal strain speckle tracking echocardiography were 51 ± 28 and 47 ± 21 ms, respectively. The patient population was divided according to the median RV-SD value of 49 ms. Patients with RV-SD ≥49 ms had significantly worse NYHA functional class (2.7 ± 0.7 vs. 2.3 ± 0.7, p = 0.004), RV function (tricuspid annular plane systolic excursion: 16 ± 4 vs. 19 ± 4 mm, p < 0.001), LVEF (50 ± 10 vs. 55 ± 8 %, p = 0.001), and larger LV-SD (57 ± 18 vs. 36 ± 18 ms, p < 0.001). RV-SD significantly correlated with LV-SD (r = 0.55, p < 0.001) and LVEF (r = ?0.23, p = 0.02). Multiple linear regression analysis showed an independent association between RV-SD and LV-SD (β = 0.35, 95 %CI 0.21–0.49, p < 0.001). RV dyssynchrony is significantly associated with LV dyssynchrony and reduced LVEF in patients with pulmonary hypertension.     

Assessment of left ventricular systolic function using tissue Doppler imaging in children after successful repair of aortic coarctation

Aim: Assessment of left ventricular systolic function in children after the successful repair of aortic coarctation using tissue Doppler imaging (TDI). Methods: The study group consisted of 32 patients (mean age 12·0 ± 4·2 years) after the aortic coarctation repair. The TDI parameters and the conventional echocardiographic endocardial and midwall indices of the left ventricular systolic function were analysed and compared with the results obtained from 34 healthy children. Results: The systolic mitral annulus motion velocity, systolic myocardial velocity of the medial segment of the left ventricular septal wall, left ventricular strain and Strain Rate (SR) in the study group were significantly higher than in the control group, respectively: 6·92 ± 0·75 cm s^?1 versus 6·45 ± 0·83 cm s^?1; 5·82 ± 1·03 cm s^?1 versus 5·08 ± 1·11 cm s^?1; ?28·67 ± 6·04% versus ?22·53 ± 6·44% and ?3·20 ± 0·76 s^?1 versus ?2·39 ± 0·49 s^?1. Except midwall shortening fraction the conventional endocardial and midwall echocardiographic indices in the study group were significantly higher in comparison to the healthy controls. The left ventricular systolic meridional fibre stress and end‐systolic circumferential wall stress did not differ between the examined groups. There were no differences of the TDI or conventional parameters between hypertensive and normotensive patients. Conclusions: Left ventricular systolic performance in children after the surgical repair of aortic coarctation reveals tendency to rise in late follow‐up despite a satisfactory result after surgery. Higher systolic strain and SR in children treated due to coarctation of the aorta may suggest the increased preserved left ventricular performance despite normalization of afterload.     

Adverse effects of long-term right ventricular apical pacing and identification of patients at risk of atrial fibrillation and heart failure

In patients needing a pacemaker (PM) for bradycardia indications, the amount of right ventricular (RV) apical pacing has been correlated with atrial fibrillation (AFib) and heart failure (HF) in both DDD and VVI mode. RV pacing was linked with left ventricular (LV) dyssynchrony in almost 50% of patients with PM implantation and atrioventricular (AV) node ablation for AFib. In patients with normal systolic function needing a PM, apical RV pacing resulted in LV ejection fraction (LVEF) reduction. These negative effects were prevented by cardiac resynchronization therapy (CRT). Algorithms favoring physiological AV conduction are possible useful tools able to maintain both atrial and ventricular support and limit RV pacing. However, when chronic RV pacing cannot be avoided, it appears necessary to reconsider the cut-off value of basic LVEF for CRT. In HF patients, RV pacing can induce greater LV dyssynchrony, enhanced by underlying conduction diseases. In this context, a more deleterious effect of RV pacing in implantable cardioverter-defibrillator (ICD) patients with low LVEF can be expected. In some major ICD trials, DDD mode was correlated with increased mortality/HF. This negative impact was attributed to unnecessary RV pacing >40-50%, virtually absent in VVI-40 mode. However, some data suggest that avoiding RV pacing may also not be the best option for patients requiring an ICD. In patients with impaired LV function, AV synchrony should therefore be ensured. The best pacing mode in ICD patients with HF should be defined on an individual basis.     

Alternate site right ventricular pacing: defining template scoring

Background: Prolonged right ventricular (RV) apical pacing produces dysynchronous ventricular contraction, which may result in left ventricular (LV) dysfunction, whereas septal pacing sites might reflect a more synchronous LV activation. This study examined a method of evaluating alternate RV pacing sites using a template scoring system based on measuring the angle of lead attachment in the 40^o left anterior oblique (LAO) fluoroscopic view and its effect on altering the loop of lead in the RV. Methods: Twenty‐three consecutive patients for RV pacing were enrolled. Conventional active fixation leads were positioned in either the RV outflow tract (RVOT) or mid RV using a stylet designed for septal placement (Model 4140, St. Jude Medical, St. Paul, MN, USA). Using LAO cine fluoroscopy, a generous loop of lead was inserted into the RV chamber and the change in angle of attachment determined. Results: Successful positioning of pacing leads at the RVOT septum (18 patients) and mid‐RV septum (five patients) was achieved. With introduction of more lead into the RV chamber, the angle of attachment in the LAO projection altered over a range of 6^o–32^o for all patients with a mean of 14.6 ± 6.6^o. In 87% of patients, the range was predominantly within the same template score with only minor overlap into another zone. Conclusions: This study shows that the angle of lead attachment in the RV is altered by introducing more lead, but in most cases, the template score remains the same. Further studies are required to determine the accuracy and efficacy of the templates. (PACE 2011; 34:1080–1086)     

Biventricular upgrading in patients with conventional pacing system and congestive heart failure: results and response predictors

BACKGROUND: There are few studies on cardiac resynchronization therapy (CRT) in heart failure (HF) patients with preexisting right ventricular (RV) pacing. The purpose of this study was to determine the efficacy of CRT upgrading in RV-paced patients and the predictivity of electromechanical dyssynchrony parameters (EDP) evaluated by standard echocardiography (ECHO) and tissue Doppler imaging (TDI). METHODS: Thirty-eight consecutive patients with HF [New York Heart Association (NYHA) class III or IV, LVEF < 35%], prior continuous RV pacing, and absence of atrial fibrillation were enrolled in the presence of a paced QRS > or = 150 ms and evaluated by ECHO and TDI. A responder was defined as a patient with a favorable change in NYHA class and neither HF hospitalization nor death, plus an absolute increase of LVEF > or = 10 units. RESULTS: At six-months follow-up, the whole study population had significant improvement in symptoms, systolic function, and QRS duration (P < 0.001); 32 (84%) patients had a favorable clinical outcome, 25 (66%) were considered responders according to the previous definition. Postimplant QRS was similarly reduced in both responders and nonresponders, whereas EDP had a significant improvement only in responders (P < 0.05). Using EDP, 23 (79%) patients were responders compared with 2 (22%) patients without mechanical dyssynchrony (P = 0.002). CONCLUSIONS: In HF patients with previous RV pacing, CRT is effective to improve clinical, functional outcome, and LV performance and to reduce electromechanical dyssynchrony in a large proportion of patients. Dyssynchrony evaluated by standard and TDI ECHO can be useful for CRT selection of paced patients.     

Acute effects of right ventricular apical pacing on left atrial remodeling and function

Background : The acute effects of right ventricular apical (RVA) pacing on left atrial (LA) function in patients with normal ejection fraction are not clear. Methods : A total of 94 patients (age 68.1 ± 11.1 years, 26 men) with implanted RVA‐based dual‐chamber pacemakers were recruited into this study. Patients who were pacemaker‐dependent, in persistent atrial fibrillation or left ventricular ejection fraction <45% were excluded. Echocardiography (iE33, Philips, Andover, MA, USA) was performed during intrinsic ventricular conduction (V‐sense) and RVA pacing (V‐pace) with 15 minutes between switching modes. The total maximal LA volume (LAV_max), preatrial contraction volume (LAV_pre), and minimal volume (LAV_min) were assessed by area‐length method. Peak systolic, early diastolic, and peak late diastolic (atrial contractile) velocity (Sm‐la, Em‐la, and Am‐la) and strain (?s‐la, ?e‐la, and ?a‐la) were measured by color‐coded tissue Doppler imaging (TDI) in four mid‐LA walls at apical four‐ and two‐chamber views. Results : During V‐pace, LA volumes increased significantly compared with V‐sense (LAV_max: 52.0 ± 18.8 vs 55.2 ± 21.1 mL, P = 0.005; LAV_pre: 39.8 ± 16.4 vs 41.3 ± 16.6 mL, P = 0.014; LAV_min: 27.4 ± 14.0 vs 29.1 ± 15.1 mL, P = 0.001). TDI parameters showed significant reduction in Sm‐la and Em‐la. Furthermore, ?s‐la, ?e‐la, and ?a‐la decreased significantly, especially in patients with preexisting diastolic dysfunction (all P < 0.01). Conclusions: RVA pacing acutely induced LA enlargement and impaired atrial contractility. Patients with preexisting diastolic dysfunction may be more vulnerable to develop LA dysfunction and remodeling after acute RVA pacing. (PACE 2011;XX:1–7)     

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)     

Right ventricular long-axis function in relation to left ventricular systolic function

A decrease in left ventricular (LV) systolic function is accompanied by a decrease in maximal relaxation velocity in LV long‐axis direction, but is it also accompanied by a decrease in right ventricular (RV) long‐axis function? To study this 35 consecutive patients were examined by echocardiography. Ejection fraction (LVEF) and mitral annulus motion (MAM) were used as indices of LV systolic function and tricuspid annulus motion (TAM), that is the systolic shortening in RV long‐axis direction, was used as an index of RV systolic long‐axis function. In the same way the maximal relaxation velocity in LV long‐axis direction, that is the maximal diastolic velocity of MAM (MDV MAM), has been suggested as an index of LV diastolic function the maximal diastolic velocity of TAM (MDV TAM) can be supposed to be an index of RV diastolic function measuring the maximal relaxation velocity in the RV long‐axis direction. A significant positive correlation was found between MDV TAM and MAM (r = 0·64, P<0001) and LVEF (r = 0·54, P = 0·001) and between TAM and the two studied indices of LV systolic function, with the highest correlation to MAM (r = 0·68, P<0·001) and the lowest to LVEF (r = 0·57, P<0·001). Thus, a decrease in LV systolic function is accompanied by a decrease in both systolic and diastolic RV long‐axis function, findings that probably are due to the close anatomical connection between the ventricles and to changes that occur in afterload of the RV secondary to LV systolic dysfunction.     

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

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

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

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

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)