Rick Schreurs

ABSTRACT Introduction The SonR system is an algorithm that uses data froman accelerometer in the right atrial (RA) or right ventricular (RV) pacing lead that is used to automatically optimize atrioventricular (AV) and interventricular [1] delay in patients receiving cardiac resynchronization therapy. This animal study aims to investigate the influence of cardiac contractility, atrioventricular coupling and interventricular dyssynchrony on the amplitude of the first heart sound (SonR1), in order to better understand and possibly improve the algorithm. Methods and results Studies were performed in 9 anesthetized dogs with left bundle branch block or total atrioventricular (AV) block with right ventricular (RV) pacing, using tachypacing or isoflurane to induce heart failure. Invasive left (LV) and RV pressures and RA and RV SonR1 signals were measured during biventricular [2] and LV pacing at various AV-delays and compared to baseline values of intrinsic conduction. The animals were divided in a non-responding (NResp, N=4) and responding (Resp, N=5) group based on a >10% increase of LV dP/dt max during LV or BiV pacing. Dobutamine induced improvement of cardiac contractility in 3 animals revealed strong correlations between LV and RV dP/dt max­ and RA and RV SonR1. During BiV pacing at various AV-delays no consistent changes in LV pressures, LV and RV dP/dt max , mechanical interventricular dyssynchrony (MIVD) and SonR1 amplitudes were found in NResp animals. in Resp animals BiV and LV pacing increased systolic LV pressure and LV dP/dt max at the optimal AV-delay (AV opt ) compared to baseline (BL) values, along with an increase in RA (and to a lesser extent RV) SonR1. During pacing at short AV delays SonR1 values were at least as high as during AV opt , despite lower hemodynamic benefit, indicating an effect of atrio-ventricular interaction on SonR1. Moreover, LV pacing at AV short revealed similar SonR1 values as during BiV pacing, although MIVD was significantly larger during LV pacing. Conclusions The SonR1 amplitude is influenced by changes in cardiac contractility and time interval between atrial and ventricular contraction, while interventricular dyssynchrony plays a minor role. Placement of the SonR sensor in the RA seems to assess cardiac function better than an RV-placed sensor.