Rick Schreurs

94 Chapter 5 vs 97±9mmHg respectively, P=0.024). The parabolic pattern of LV dP/dt max that was visible during BiV pacing was also observed during LV pacing (second row figure 2 and 3 ). At AV opt LV dP/dt­ max was, by definition, significantly elevated compared to BL values (+15.1±5.0%, p=0.013). No significant differences were observed between BiV and LV pacing for the aforementioned parameters. Pacing at AV short , and thereby fully capturing of LV and BiV pacing, led to positive MIVD values during LV pacing (+30±7ms), indicating LV preexcitation, whereas BiV pacing created MIVD values close to zero (-6±8ms, P=0.043 compared to LV pacing). MIVD at AV short (+30±7ms) and AV opt (-2±5ms) differed significantly to BL values (-33±3ms, P=0.001 for AV short and P=0.000 for AV opt ) during LV pacing. The behavior of RA SonR1 amplitude was similar between BiV and LV pacing, with a sigmoid curve ( Figure 2 ) and a maximal increase during LV pacing at AV short (279±23mG at AV short vs 174±30mG at BL, P=0.012, figure 3 bottom right panel). During AV opt and AV short both RA and RV SonR1 were not significantly different between BiV and LV pacing, despite a significant difference in MIVD between these pacing modes. DISCUSSION This experimental study shows that the amplitude of SonR1 is determined by contractility and time between atrial and ventricular contraction. During BiV pacing at intermediate AV-delays, SonR1 increases in parallel with an increase in systolic LV pressure and LV dP/dt max and distinguishes between animals responding and not responding to CRT. Interventricular dyssynchrony is not a major determinant of SonR1, because during LV and BiV pacing similar LV dP/dt max and SonR1 changes occurred while MIVD was clearly different. In hemodynamic responders, SonR1 continues to increase during BiV and LV pacing at shorter AV-delays, despite a reduction in LV pressure and LV dP/dt max . The latter increase in SonR1 seems caused by a short time interval between atrial and ventricular contraction. These data support the use of the inflection point of the AV-delay – SonR1 curve for automatic programming of AV-delay in CRT. Although absolute values of RA SonR1 were smaller than those of RV SonR1, RA SonR1 appears more sensitive to find the hemodynamic optimum. SonR1 and cardiac contractility The dobutamine stress data in this study support previous data that SonR1 reflects contractility in hearts when activation pattern and AV-delay were kept constant. Bordachar et al . showed that during dobutamine infusion in pigs with normal and ischemia-induced decreased LV function changes of transcutaneous SonR1 amplitude correlated with LV dP/ dt max [14]. Similar results were found with an accelerometer embedded in the atrial pacing lead [8, 15-17]. Our data also support earlier findings in patients and sheep that in the setting of dobutamine stress test the SonR1 amplitude reflects both LV and RV contractility [6]. The contribution of both ventricles can be explained by the fact that both ventricles are