Rick Schreurs

85 SonR for AV-optimization INTRODUCTION Cardiac resynchronization therapy (CRT) is a well-established therapy for treatment of patients with heart failure and conduction abnormalities, coinciding with a wide QRS complex, especially left bundle branch block (LBBB) [3]. CRT employs (almost) simultaneous stimulation of the right (RV) and left ventricle (LV), usually with a certain delay with respect to the sensed or paced atrial activity. A large number of hemodynamic studies (reviewed in [4]) have shown that optimization of the delays between atrial and ventricular stimulation (AV-delay) and between RV and LV stimulation (VV-delay) leads to the best hemodynamic improvement. However, such echocardiographic optimization is performed in a recumbent, resting position, whereas patients may especially need the optimal stimulation setting when exercising. Moreover, the optimal delays may not be constant over time. To this purpose, the SonR system has been introduced, which contains a sensor embedded in the right ventricular (RV) or right atrial (RA) pacing lead to record and amplify myocardial vibrations during the entire cardiac cycle. Until now, most attention has been paid to the vibrations, associated with the first heart sound (S1) and is referred to as peak endocardial acceleration (PEA) or, more recently, SonR1. Although the exact origin of the heart sounds are not entirely clear, currently the most accepted mechanism is the one introduced by Rushmer [5]. He suggested that the acceleration and deceleration of the blood in the ‘cardiohemic’ system induces the heart sound vibrations. These velocity changes could be abrupt cessation of backflow of blood in the atrial and ventricular cavities, creating vibrations in the valve, the column of blood and myocardial structures surrounding it. Along the lines of this hypothesis, more forceful contractions, as during increased contractility dobutamine stress testing, showed good correlations between SonR1 recorded in the RV or right atrium (RA) and LV and RV dP/ dt max [6-8] in healthy pigs and sheep. However, more complex behavior of SonR1 may be expected during CRT. Firstly, CRT aims at increasing contractility by reducing atrioventricular and interventricular asynchrony, which may lead to a larger S1 amplitude. Moreover, the S1 amplitude is affected by the interplay between ventricular and atrial pressures. S1 is smaller at long AV-delays, when the mitral valve is able to close gently at the moment of reversal of the transmitral AV pressure gradient. In contrast, at shorter AV-delays, end-diastolic filling flow is abruptly interrupted by ventricular contraction onset at a time when left atrial (LA) pressure is still high, generating high amplitude vibrations resulting in a louder S1 [9]. Since the S1 and the SonR1 component share many characteristics, the SonR1 may behave similarly when changing AV-delay [10]. Finally, the heart sounds contain components of closure of the RV and LV valves. In case of a dyssynchronous heart these components may not be 5