High-rate atrial pacing to reduce left-sided filling pressures: a combined computational and clinical pilot study

T Van Loon, P Boerdonk,K Sack,R Cornelussen,T Jackson, T Delhaas,D Linz, J Luermans, K Vernooy,J Lumens

EP Europace(2022)

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Abstract Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): This work was supported by the Netherlands Organisation for Scientific Research (NWO- ZonMw, VIDI grant 016.176.340 to J.L.) and the Dutch Heart Foundation (ERA-CVD JTC2018 grant 2018T094; Dr. Dekker Program grant 2015T082 to J.L.) Background In heart failure patients, interventions to reduce elevated left ventricular (LV) filling pressure improve symptoms and reduce the risk of hospitalization. In this combined computational-clinical study, we explore high-rate atrial pacing as an alternative intervention to reduce LV filling pressure. Methods First, the theoretical basis was explored in a computational model of reduced LV compliance and various fixed atrioventricular delays. Second, an explorative clinical study was conducted in 19 paroxysmal atrial fibrillation (AF) patients undergoing pulmonary vein isolation (PVI) with sinus rhythm at the beginning of the procedure. Prior to the PVI, atrial pacing rate was gradually increased from resting heart rate to Wenckebach point with 10bpm increments. LA pressure was continuously monitored with a fluid-filled transseptal catheter. Results Computational modelling demonstrated a parabolic relationship between atrial pacing rate and LA pressure depending on atrioventricular delay (Figure A). In patients (Figure B), intermediately increased rates (60bpm[60-70], median[IQR], to 90bpm[73-100], respectively) reduced LA pressure from 16.0mmHg[14.0-20.5] to 14.0mmHg[10.8-16.8]. Highly increased rates (130bpm[120-140]) significantly increased LA pressure to 26.0mmHg[21.5-27.8]. Conclusions Both the model simulations and the subsequent clinical pilot study support the hypothesis that high-rate atrial pacing can reduce left-sided filling pressure. However, inter-patient variability of response to high-rate pacing was observed, to which simulations identified atrioventricular conduction to be a potential source.
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