Rick Schreurs

91 SonR for AV-optimization Hemodynamic effects of BiV pacing in Resp and NResp animals To investigate the effect of AV-delay on SonR1, data of NResp and Resp animals were compared during BiV pacing protocols. Values during the entire range of AV-delays are presented for representative NResp and Resp animals in figure 2 whereas values for all animals at AV short and AV opt are shown in figure 3 . In Resp animals BiV pacing tended to increase LVP max at AV opt , while a non-significant decrease was seen during short AV-delays. LV end diastolic pressure remained relatively stable with changing AV-delays, with a trend to decrease at AV short . In contrast, BiV pacing in the NResp animals did not change LVP max at AV opt and revealed a decrease at AV short , while no alteration in LV end diastolic pressure was observed (upper row figure 2 and 3 ). In the Resp group all animals showed, by definition, an increase in LV dP/dt max­ compared to BL values during BiV pacing at AV opt (1101±103mmHg/s vs 987±117mmHg/s, respectively, p=0.025, second row figure 2 ), whereas NResp animals showed small and inconsistent changes (second row of figures 2 and 3 ). Peak increase of LV dP/dt max in Resp animals occurred at intermediate AV-delays (60-150ms), while in NResp animals the highest (least decreased) values were observed at the longest AV-delays and a consistent decrease was seen at the shortest AV-delays. RV dP/dt max showed a less reproducible pattern, especially in the Resp group. In the NResp group a slight increase was observed at AV- delays ranging from 60-105ms (example in second row figure 2 ). BiV pacing at short AV-delays consistently decreased RV dP/dt max in all animals. No changes in MIVD occurred when varying AV-intervals in BiV pacing in NResp animals (example in third row figure 2 , group data in figure 3 ). In contrast, MIVD values became close to zero when shortening the AV-delay in Resp animals. A significant reduction in MIVD was observed at AV opt during BiV pacing in de Resp group 5