Permanent Right Ventricular Pacing Research Articles

Acute right systolic ventricular dysfunction in permanent cardiac pacing. Insight from RV PACE trial (Right Ventricular function assessment in Permanent cArdiac paCing by Echography)

Permanent right ventricular (RV) pacing is now clearly linked to heart failure and decrease in LVEF, in non neglected proportion. Several trials and observations reported the worse impact of this heart pacing mode on left ventricular functions, but rare are those that studied RV systolic function. In this observational prospective trial, we evaluate echographic systolic RV function, before and immediately after cardiovascular implantable electronic device (CIED) implantation and at 6 months of follow-up. In this intermediate analysis, we report impact of RV pacing on systolic RV function. Between February 2020 and February 2021, we enrolled 174 [114 (65%) male, 38 (21%) with AF] consecutive patients underwent RV permanent pacing (CRT, Hisian and left bundle branch pacing excluded) in prospective study for evaluation of echographic parameters of RV systolic function (TAPSE, RV S’, RV global longitudinal strain and RV free wall strain) and severity of tricuspid regurgitation (TR). Transthoracic echography (TTE) was performed (by 3 physicians) at baseline (just before procedure) and immediately after implantation. At baseline, mean LVEF was 56% ± 15.6. TAPSE (22.8 ± 6.29 vs. 19.3 ± 5.47 mm; P < 0.001) and tissue Doppler on lateral tricuspid annular (RV S’) (12.1 ± 3.28 vs. 11.2 ± 3.28 cm/s; P < 0.001) measured before and immediately after implantation show a significant decrease in RV function. The same finding is reported for Global RV Strain (−20 ± 0.6 vs. −18 ± 0.5%; P < 0.001) and RV free wall strain (−25 ± 0.7 vs. −23 ± 0.6%; P < 0.001). TR after CEID implantation is more severe in comparison with basal echography [TR stage 1/2: 132 (89%) vs. 110 (79%); P < 0.01] (Fig. 1). Permanent RV pacing immediately decrease RV systolic function assessed traditional echocardiographic parameters and RV strain. TR also gets worsened.

Assessment of QT interval in ventricular paced rhythm: Derivation of a novel formula

ObjectiveThe objective of the study was to determine the optimal formula to estimate QT interval adjusting for QRS prolongation during right ventricular (RV) pacing. MethodsThis observational study included individuals (n = 43) with a newly implanted permanent ventricular pacemaker, who had a narrow QRS complex before pacemaker insertion. QT interval with RV pacing was related to QT interval before pacemaker implantation. The validation cohort (n = 442) had permanent RV pacing in DDD mode. ResultsA new QTc formula was derived utilizing the constants from the relationship between the spline heart rate QT correction (QTcRBK) before and after pacing; specifically, QTcRBKPACED = QTcRBK × 0.86. The JT interval from paced complexes was highly heart rate (HR) dependent and was not accurate for QT assessment. Previous, QTc formula for paced complexes were not highly correlated with QT before pacing unless a robust HR correction is added. Formulae subtracting a fixed amount from QTcPACED markedly overestimated QTc before pacing. ConclusionWe proposed a new, simple formula for QT estimation in RV pacing. JT interval in paced complexes is highly HR dependent and is not accurate for QT assessment. The new spline approach for HR correction for the QT, once incorporated into some previously proposed formulae, blunts HR dependency and improves prediction of QT before pacing. QTcRBKPACED*0.86 and QTcRBKPACED – (QRS*0.5) demonstrated the best balance of relatively strong correlation to QTc before pacing and accurate QTc prolongation identification. Abnormal QT for QTcRBKPACED*0.86 as defined by the 97.5th and 99th percentile are 469 and 479 ms respectively.

Should all patients with heart block receive biventricular pacing? All heart block patients with a pacemaker indication should receive biventricular pacing: one move, double the gains?

Conventional right ventricular (RV) pacing can cause left ventricular (LV) dysfunction and even heart failure (HF) particularly if ventricular pacing is frequent.1 New onset HF has been observed in approximately one third of patients receiving RV pacing for acquired second- or third-degree atrioventricular block (AVB) after a median follow-up of nearly 8 years.2 An elegant study has shown recently that apparent pacing induced cardiomyopathy could occur even if the accumulative pacing percentage was <40%.1 Although there has been rapid progress in medication and device therapy for HF, it is still a burden on the public health systems and better prevention remains important.3 Avoiding the use of a potentially harmful device when a good alternative is available is a matter of serious consideration. Response by Arenas et al on p 729 Single- or dual-chamber pacemakers with RV pacing are undoubtedly the main therapy for symptomatic AVB. With increasing evidence of potential adverse effects of permanent RV pacing mainly because of systolic dyssynchrony,4,5 other pacing modalities or pacing modes are being considered. Biventricular pacing is one of the options and has been shown to be potentially superior to RV pacing even for those who require pacing but do not have a conventional indication for biventricular pacing.6,7 Biventricular pacing is emerging as a realistic treatment option to prevent RV pacing induced LV dysfunction for symptomatic patients with advanced AVB. Despite the lack of accurate epidemiology data for AVB, it is clear that it is not uncommon in both apparently healthy populations and those with overt heart disease. Approximately 1% to 2% of normal subjects have first-degree AVB which increases to 5% in men over the age of 60 with cardiac diseases.8–10 The prevalence of second-degree AVB for Mobitz II block …

Heart Failure Associated with Pacemaker-Induced Dyssynchrony

Heart failure (HF) is a devastating disease that significantly affects patient morbidity and mortality. Recent research has shown that permanent right ventricular (RV) pacing is causally linked to HF. Permanent RV pacing is thought to cause inter- and intraventricular dyssynchrony, which leads to a decreased systolic contraction and a decreased ejection fraction. Primary care nurse practitioners (NPs) should be cognizant of the signs and symptoms of HF in this patient population to diagnose and treat HF as a result of pacemaker-induced dyssynchrony.

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

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

Speckle-Tracking Radial Strain Reveals Left Ventricular Dyssynchrony in Patients With Permanent Right Ventricular Pacing

Speckle-tracking strain analysis was used to assess the effects of permanent right ventricular (RV) pacing on the heterogeneity in timing of regional wall strain and left ventricular (LV) dyssynchrony. Recent studies have shown detrimental effects of RV pacing, possibly related to the induction of LV dyssynchrony. Fifty-eight patients treated with His bundle ablation and pacemaker implantation were studied. To assess the effect of RV pacing on time-to-peak radial strain of different LV segments, we applied speckle-tracking analysis to standard LV short-axis images. In addition, New York Heart Association (NYHA) functional class, LV volumes, and systolic function were assessed at baseline and after long-term RV pacing. At baseline, similar time-to-peak strain for the 6 segments was observed (mean 371 +/- 114 ms). In contrast, after a mean of 3.8 +/- 2.0 years of RV pacing, there was a marked heterogeneity in time-to-peak strain of the 6 segments. In 33 patients (57%), LV dyssynchrony, represented by a time difference > or =130 ms between the time-to-peak strain of the (antero)septal and the posterolateral segments, was present. In these patients, a deterioration of LV systolic function and NYHA functional class was observed. In 11 patients, an "upgrade" of the conventional pacemaker to a biventricular pacemaker resulted in partial reversal of the detrimental effects of RV pacing. Speckle-tracking analysis revealed that permanent RV pacing induced heterogeneity in time-to-peak strain, resulting in LV dyssynchrony in 57% of patients, associated with deterioration of LV systolic function and NYHA functional class. Biventricular pacing may reverse these adverse effects of RV pacing.

Transoesophageal left ventricular pacing in heart failure patients with permanent right ventricular pacing

Previous studies of biventricular (BV) pacing for treatment of heart failure (HF) patients with left bundle branch block (LBBB) evaluated responders to BV pacing with acute transvenous left ventricular (LV) pacing and arterial pulse pressure (PP). The aim of this study was to assess transoesophageal LV pacing in evaluation of the haemodynamic response with a view to upgrading responders from permanent right ventricular (RV) pacing to BV pacing. Ten HF patients (age 62+/-8 years; one female, nine males) in NYHA III, LV ejection fraction 24+/-9% and permanent RV pacing by means of an implanted pacemaker or ICD were tested using transoesophageal LV pacing and PP. Permanently RV-paced HF patients were analysed with transoesophageal atrial sensed LV pacing in VAT mode with a different AV delay (n = 6) and with transoesophageal LV pacing in V00 mode during atrial fibrillation (n = 4). In five responders, PP was higher during transoesophageal LV pacing than PP during RV pacing (74+/-42 versus 57+/-31 mmHg, P = 0.015). Responders were upgraded by means of an LV lead via the coronary sinus in the posterior (n = 1) or posterolateral (n = 4) walls and after attaining a high LV pacing threshold with an epicardial LV lead on the anterior (n = 1) or anterolateral (n = 1) walls. NYHA class improved from 3 to 2+/-0.3 (P = 0.003) during 204+/-120 days follow-up and cardiac output increased from 4.4+/-1.5 to 5.6+/-1.7 l/min (P = 0.027) when comparing BV pacing and optimal AV delay with RV pacing. In five nonresponders, PP was not higher during transoesophageal LV pacing than during RV pacing. Transoesophageal LV pacing may be a useful technique to detect responders to BV pacing in permanently RV-paced HF patients.

Influence of Permanent Right Ventricular Pacing on Cardiorespiratory Exercise Parameters in Chronic Heart Failure Patients With Implanted Cardioverter Defibrillators

Patients with chronic heart failure and implanted cardioverter-defibrillators (ICDs) may have a higher incidence of new-onset or worsening heart failure requiring hospitalization with dual-chamber ICDs compared with single-chamber ICDs. The purpose of this study was to show the impact of permanent right ventricular (RV) pacing on exercise capacity and related cardiorespiratory parameters in patients with chronic heart failure and ICDs. Seventeen patients with chronic heart failure and a dual-chamber ICD performed cardiopulmonary exercise testing (CPX) on 3 different days. After CPX 1, patients were randomized either to back-up pacing or permanent RV pacing. After 3 months, CPX 2 was performed and patients changed groups (crossover design); CPX 3 was performed after 3 additional months. Maximal values for workload (108 +/- 46 W vs 117 +/- 48 W, p < 0.01), oxygen uptake (Vo(2)) [21.0 +/- 5.3 mL/min/kg vs 22.5 +/- 6.4 mL/min/kg, p < 0.05], oxygen pulse (13 +/- 3.7 mL vs 14 +/- 4.0 mL, p < 0.05), and metabolic equivalent (6.0 +/- 1.5 vs 6.4 +/- 1.8, p < 0.05) were significantly lower with permanent RV pacing compared to back-up pacing. Workload, Vo(2), and oxygen pulse were significantly reduced at the ventilatory anaerobic threshold, while workload and Vo(2) were significantly lower at the respiratory compensation point. No differences were found for maximal heart rate, minute ventilation Ve, and respiratory exchange ratio. The Ve/carbon dioxide production slope was significantly steeper with permanent RV pacing compared to back-up pacing. Permanent RV pacing significantly reduced maximal and submaximal measures of exercise. For patients with chronic heart failure and sufficient atrioventricular conduction, every effort should be made to minimize permanent right ventricular pacing.