P1488Autonomic nervous system optimized cardiac resynchronization therapy

Introduction. Traditional Cardiac Resynchronization Therapy, CRT, relies on bi-ventricular, bi-V, pacing. For left bundle branch block, LBBB, patients with good atrial-right ventricular conduction, A-RVc, alternatives have been proposed that use left-ventricular only pacing, LVoP, with adaptive atrio-ventricular delay, AVD, that is updated every minute from A-RVc measurements. The key advantage is extended device longevity since the RV pacing pulse is not emitted. Purpose. In this paper we present a CRT alternative using fixed AVD LVoP + RV sense trigger (an LV pulse is triggered when an RV depolarization is sensed), RVsT, that can be used with LBBB patients with good A-RVc. Intrinsic RV depolarization is used. The longevity of the device is expected to approach that of a dual chamber device since AVD adaption is not needed. Method. 5 CRT patients with LBBB and good A-RVc, previously programmed to bi-V pacing, were reprogrammed to fixed AVD LVoP + RVsT. The devices are standard CRT pacemakers, CRT-P, with RVsT. They are normally operated in LVoP mode. In response to atrial tachycardia, mode switching to bi-V will be required. So, 3 chamber devices are still required. Results. Nightly at about 02:00 the CRT-P collects Ax-Vs (Ax = As & Ap) statistics for 35 consecutive heart cycles with AVD of 300 ms, while the patient is asleep. A typical plot of these timing statistics at the time of reprogramming to LVoP is shown in Fig. 1. After a self-training period of 2 weeks to 9 months, these statistics coalesce in a narrow range of values, 20 ms wide, as illustrated in Fig. 2 for our super responder (2 weeks). This 20 ms wide pattern persisted for the next 9 months. In the case of the index patient this lasted 3+ years. This persistent A-RVc pattern across all 5 patient can only be explained by a tight dromotropic control by the Autonomic Nervous System, ANS. Fig. 3 illustrates RVsT. As the RVs arrives earlier than the LVp, there is no longer synchronicity improvement since the LVp now follows the RVs immediately. In Fig. 4, we see long periods with high %RVs associated with high heart rates. Increased hemodynamic demand can only be met by increased contractility. Thus inotropic modulation by the ANS is now active and effective. The patients were put on remote monitoring with nightly follow-ups. Over a period of 6.5 months RVs (pre LVp) statistics were collected. A daily median of 11% was reported for this patient. On a particular day, it can be as high as 50%. Dromotropic action to pull in the RVs cannot be explained without concurrent inotropic modulation. Conclusions. Traditional CRT leads to ineffective ANS modulation due to bi-V pacing for >95-98% of the cycles. In our 5 patients the fixed AVD LVoP + RVsT program has allowed nervous system remodeling and the ANS is back in control of hemodynamics. Thus we have ANS optimized CRT! It is an attractive CRT alternative for LBBB patients with good A-RVc since device longevity is also improved. Abstract Figure. Fixed delay LV-only + RVs trigger