Introduction Chronic RV pacing has been recognised as being harmful to cardiac function. Patients undergoing a de novo pacemaker implant with even mild LV impairment are recommended to instead receive a physiological pacing strategy (biventricular or conduction system pacing [CSP]). No corresponding guideline recommendation exists for patients who already have a pacemaker. Methods We undertook a random-effects meta-analysis of all RCTs and observational studies covering device upgrade to biventricular pacing or conduction system pacing. Results 6 RCTs assessing effect of upgrade to BiV pacing randomising 161 patients were eligible for analysis. Eligible observational studies included 46 of BiV upgrade and 7 of CSP upgrade totalling 2795 patients. Mean LVEF improved by +8.3% from 34.4% in BiV upgrade RCTs (p=0.001) and +8.3% from 25.7% in BiV upgrade observational studies (p<0.001). In observational studies of upgrade to CSP, LVEF increased by +10.1% from 38.4% (p=0.001) despite less severe LV impairment at baseline (p=0.004 vs mean EF in BiV RCTs and p<0.0001 vs mean EF in BiV observational studies). LVESV decreased significantly by −25.4 ml, −23.7 ml, and −19.8 ml in BiV RCTs, BiV observational studies and CSP observational studies. Significant changes were also seen in NYHA class (decreased by −0.4, −0.8 and −1.0 respectively). Minnesota Heart Failure Score (−6.9 points) and peak oxygen uptake (+1.1 ml/kg/min) increased significantly in RCTs of BiV upgrade. This was also seen in observational studies of BiV upgrade (−21.0 points and +2.63 ml/kg/min respectively). Conclusions RCTs and observational studies of upgrade to BiV pacing show significant physiological and symptomatic benefit. Observational studies of CSP upgrade show similar benefit with significant improvements in LVEF, LVESV and NYHA class in patients with an even milder degree of baseline LV impairment. Funding Acknowledgement Type of funding sources: None.
Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): British Heart Foundation Background; Left bundle area pacing is a novel technique that provides direct stimulation of cardiac conduction tissue in order to deliver physiological ventricular activation. The approach for left bundle area pacing is transseptal lead implantation, where the lead is advanced from the right ventricular side of the septum to the left ventricular side to capture the proximal left bundle. Observational data suggests that whilst this is a safe and feasible method, implant success rate is not 100%, and appears to be lower in patients with a cardiac resynchronization therapy (CRT) indication rather than a bradycardia indication for pacing. The mechanisms for failure to advance the lead through the ventricular septum are not well understood. Purpose; We used pre-procedural CMR to determine whether there are features which can help identify patients where lead implantation may be challenging. We assessed whether the extent and location of septal late gadolinium enhancement identified patients in whom left bundle area pacing will be challenging. We hypothesized that the presence of extensive scar in the septum impedes advancing the lead to the left ventricular septum and prevents capture of the left bundle. Methods; Patients underwent cardiac MRI including motion corrected free-breathing late gadolinium enhancement imaging1 before implantation. Scar was quantified using the full height half maximum method and expressed as the overall proportion of myocardial mass in the basal anteroseptal and basal inferoseptal segments, as shown in Figure 1. Left bundle area pacing was then attempted in patients with a CRT indication for pacing. We compared the extent of septal scar between patients in whom left bundle area pacing was achieved and those where there was failure to advance the lead deep into the septum. Results; 12 patients (11 male, 1 female), with average age 72 (IQR 63 to 78) and LVEF 30% (IQR 26 to 33) were studied. There was failure to advance the lead deep into the septum in 4 patients. There was a significantly higher basal septal scar burden in those patients where there was failure to advance the left bundle lead compared to those in which left bundle capture was achieved as shown in Figure 2 (median 55% and 5% respectively, p-value 0.02 by Wilcoxon signed rank test). Conclusion; The presence and extent of late gadolinium enhancement in the basal septum appears to be an important determinant of successful implantation of left bundle pacing lead using current implant technology. This may be because extensive septal scar prevents advancement of the pacing lead through the septum. Cardiac MRI before left bundle area pacing is likely to be useful in procedural planning.
Funding Acknowledgements Type of funding sources: Public Institution(s). Main funding source(s): British Heart Foundation Background: His bundle pacing can be achieved in two ways selective His bundle pacing, where the His bundle is captured alone, and non-selective His bundle pacing, where local myocardium is also captured resulting a pre-excited ECG appearance. We assessed the impact of this ventricular pre-excitation on left and right ventricular dys-synchrony. Methods We recruited patients who displayed both selective and non-selective His bundle pacing. We performed non-invasive epicardial electrical mapping to determine left and right ventricular activation times and patterns. Results In the primary analysis (n = 20, all patients), non-selective His bundle pacing did not prolong LVAT compared to select His bundle pacing by a pre-specified non-inferiority margin of 10ms (LVAT prolongation: -5.5ms, 95% confidence interval (CI): -0.6 to -10.4, non-inferiority p < 0.0001). Non-selective His bundle pacing did not prolong right ventricular activation time (4.3ms, 95%CI: -4.0 to 12.8, p = 0.296) but did prolong QRS duration (22.1ms, 95%CI: 11.8 to 32.4, p = 0.0003). In patients with narrow intrinsic QRS (n = 6), non-selective His bundle pacing preserved left ventricular activation time (-2.9ms, 95%CI: -9.7 to 4.0, p = 0.331) but prolonged QRS duration (31.4ms, 95%CI: 22.0 to 40.7, p = 0.0003) and mean right ventricular activation time (16.8ms, 95%CI: -5.3 to 38.9, p = 0.108) compared to selective His bundle pacing. Activation pattern of the left ventricular surface was unchanged between selective and non-selective His bundle pacing. Non-selective His bundle pacing produced early basal right ventricular activation, which was not observed with selective His bundle pacing. Conclusions Compared to selective His bundle pacing, local myocardial capture during non-selective His bundle pacing produces right ventricular pre-excitation resulting in prolongation of QRS duration. However, non-selective His bundle pacing preserves the left ventricular activation time and pattern of selective His bundle pacing. When choosing between selective and non-selective His bundle pacing, left ventricular dyssynchrony is not an important factor. Abstract Figure: Selective vs Non-Selective HBP
Funding Acknowledgements Type of funding sources: Other. Main funding source(s): BRAVO trial: BHF SP/10/002/28189, FS/10/038, FS/11/92/29122, FS/13/44/30291) National Institute for Health Research Imperial Biomedical Research Centre. HOPE-HF trial: British Heart Foundation (CS/15/3/31405, FS/13/44/30291, FS/15/53/31615, FS/14/27/30752, FS/10/038). Introduction The optimal atrioventricular (AV) delay for implantable cardiac devices can be derived by echocardiography or beat-by-beat blood pressure measurements. However, both of these approaches are labour intensive and neither could be incorporated into an implantable cardiac device for frequent repeated optimisations. Laser Doppler perfusion monitoring (LDPM) measures blood flow through tissue. LDPM has been miniaturised ready to be incorporated into future implantable cardiac devices. Purpose We studied if LDPM is a clinically reliable alternative method to blood-pressure measurements to determine optimal AV delay. Methods Data from 58 patients undergoing 94 clinical AVD optimisations using LDPM and simultaneous non-invasive beat-by-beat blood pressure was obtained. The optimal AV delay for each method and for each optimisation was determined using a curve of haemodynamic response to switching from AAI (reference state) to DDD (test state) at a series of AV delays (40, 80, 120, 160, 200, 240 ms). We then compared the derived optimal AV delays between the two measurement approaches. We also assessed the impact of the paced heart-rate on agreement between laser Doppler and Blood-Pressure derived optimal AV delays. Results The AV delay derived using LDPM was not clinically significant different from that derived by blood pressure changes. The median difference was -9ms (IQR -26 to 7, p = 0.05). Variability between the two methods was low (median absolute deviation 17ms). Optimisations performed at higher heart-rates resulted in a non-significant smaller difference between the LDPM and blood-pressure derived AV delays (median absolute deviation 12 vs 22 ms, p = 0.11). Conclusions Optimal AVDs derived from non-invasive blood-pressure or laser Doppler perfusion methods are clinically equivalent. The addition of laser Doppler to future implantable cardiac devices may enable devices to dynamically and reliably optimise AV delays. Abstract Figure 1
Funding Acknowledgements Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): NIHR Imperial Biomedical Research Centre Introduction Implantable Cardioverter-Defibrillators (ICDs) cannot distinguish between ventricular tachycardia (VT) with haemodynamic compromise from haemodynamically tolerated VT to ensure that therapies are delivered only when necessary. Currently, unnecessary therapies are reduced by longer duration thresholds and higher rate thresholds. This can result in ICDs withholding or delaying therapies during haemodynamically compromising VT while potentially still providing therapies during rapid or prolonged VT that is haemodynamically well tolerated. Laser doppler perfusion monitoring (LDPM) allows assessment of peripheral blood flow as a surrogate for haemodynamic status. We have previously demonstrated that laser doppler perfusion signals, analysed using an electro-mechanical coupling algorithm (SafeShock), can reliably identify loss of perfusion during ventricular fibrillation (VF), as well as discriminate VF from simulated lead fractures and T wave over-sensing. The utility of LDPM signals in VT, however, has not been established. Purpose In this study we assessed the utility of LDPM using the SafeShock algorithm to discriminate haemodynamically tolerated VT from VT with haemodynamic compromise. Methods Recruited participants underwent a rapid ventricular pacing protocol to simulate VT at different rates. Pacing was performed using the right ventricular lead of an implanted pacing device or a temporary pacing wire in the right ventricular apex. 3-lead ECG, blood pressure (either invasively using a radial artery catheter or non-invasively using beat-by-beat finometry) and LDPM signal were continuously recorded during the protocol. LDPM signals during simulated VT were analysed using the SafeShock electro-mechanical algorithm and compared to blood pressure change from baseline intrinsic rhythm to simulated VT. Results We obtained 588 recordings of simulated VT in 56 patients at rates of 100 bpm, 120 bpm, 140 bpm, 160 bpm, 180 bpm and 200 bpm. Percentage change in systolic blood pressure from baseline to VT correlated with LDPM-derived perfusion value during VT (Spearman’s Rho = 0.7786, p < 0.0001). Using a cut-off of 5 units, perfusion value predicted a 20% drop in systolic blood pressure in VT with an accuracy of 89.4% (sensitivity 94.8%, specificity 83.6%, p value <0.0001). Conclusions Peripheral perfusion measurements, analysed using an electro-mechanical algorithm, can accurately discriminate haemodynamically tolerated VT from VT with haemodynamic compromise. ICDs with integrated LDPM sensors and algorithms could make therapy decisions based on the circulatory status of patients with arrhythmias not just rate and duration parameters. This could reduce unnecessary therapies while facilitating prompt treatment of compromising arrhythmias. Abstract Figure 1
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