Using the Sinoatrial Node to Induce Pulsatility in Mechanical Circulatory Support Devices

Purpose Mechanical Circulatory Support (MCS) devices such as ventricular assist devices (VADs) are increasingly important in managing patients with end-stage heart failure. Current generation VADs, such as the HVAD operate on a continuous flow basis. Many authors have identified the lack of pulsatility as a limitation. We tested the feasibility of using a signal from ex-vivo tissue of rabbit sinoatrial node (SAN) to induce pulsatility in an HVAD as well as the BiVACOR total artificial heart through synchronous speed variation. Methods Seven different rabbits had SAN tissue extracted, placed in a tissue bath and superfused with Krebs-Ringer solution. An extracellular fine metal electrode was placed into the tissue preparation for activity capture. The rate of spontaneous SAN activity was modulated by changing the temperature of the superfusing solution. Electrical activity was captured and identified using a data acquisition system and custom-made software. This was used to trigger a stepwise speed change in an HVAD as well as the BiVACOR running in a mock circulatory loop. Signal capture was tested across a range of heart rates. Results Electrogram signals were successfully recorded for all tissue extracts. To simulate physiological settings, we implemented a 100ms delay between capture and effect, as well as a speed change duration of 30% per cycle (obtained from beat-to-beat variation). HVAD motor speed was successfully increased from 2500RPM to 2800RPM in synchronicity with the firing of the SAN. We were also able to achieve a speed reduction from 2500RPM to 2000RPM in synchronicity with the firing of the SAN. The BIVACOR was similarly able to undergo motor speed increase and decrease in synchrony with the SAN at the lower heart rate setting. Conclusion We successfully captured electrical activity from the SAN, then relayed it to both an HVAD and the BiVACOR controller, in doing so we were able to induce pulsatility through speed variation in synchrony with SAN activity. This has the potential to change MCS haemodynamics.