Pediatric/Adult Congenital Heart Disease -> Translational D-AB15 - Pacing in Patients with Congenital Heart Disease (ID 44) Abstract

D-AB15-03 - Epicardial Leadless Pacemaker In A Lamb Model (ID 1410)


Background: Current pacemaker therapy in newborns and small toddlers requires epicardial lead fixation with the pulse generator most commonly implanted abdominally. During growth, lead fracture can occur due to tension or mechanical strain.
Objective: Aim of the study was to investigate the feasibility of epicardial pacing with a commercially available leadless pacemaker in an animal model.
Methods: 16 lambs (median body weight 24 kg) underwent epicardial implantation of a Micra TPS pacemaker (Medtronic Inc, Minneapolis, USA). After lateral thoracotomy, the Micra was placed through a purse-string suture in the LV pericardium in 10 animals trapping the pacemaker´s tines and the electrode between the pericardium and epicardium. In 6 lambs the devices were fixated with the 4 tines within the myocardium of the left atrial appendage. Pacemakers were programmed to AAI/VVI 30/min. After a follow-up of 31 weeks (median body weight 50 kg) animals were sacrificed and pacemakers and hearts were explanted for histological analysis.
Results: After implantation, median intrinsic P/R amplitude was 4.25/5.5 mV, median impedance (atrial/ventricular) was 1155/1065 Ω while the median pacing threshold was 1.125/1.9 V at 0.24 ms. After 31 weeks, median P/R wave amplitude was 3.3/4.2 mV and median impedance had dropped to 570/660 Ohms. Median atrial pacing threshold was 0.5 V at 0.24 sec. 8/10 ventricular pacemakers had lost capture at 0.24 ms pulse width. At explanation, firm attachment of the non-electrode end of the device at the thoracic wall due to fibrous tissue was found in 8/10 ventricular devices.
Conclusion: Our results suggest that use of the Micra TPS pacemaker for epicardial pacing is feasible with the tines at the tip of the device firmly fixated within the myocardium allowing for adequate electrode-tissue contact and avoiding firm attachment to the thoracic wall. In the present study this result was achieved at atrial myocardium while all devices implanted at ventricular level finally lost their function due to improper electrode-tissue contact. In order to improve the performance of the epicardially implanted leadless pacemaker, it seems to be important to modify the device body with special respect to electrode position and fixation.