Rick Schreurs

26 Chapter 2 replicate the low ejection fraction, increased LV wall stress and end-systolic volume, and impaired myocardial relaxation as seen in LBBB patients [20]. Electrophysiological effects of CRT The basic idea behind CRT is to resynchronize the late and more slowly activated LV by individually pacing both ventricles. Figure 1 shows that RV pacing alone results in an activation pattern that resembles the intrinsic activation pattern of LBBB and leads to a QRS duration of 250ms in this example. At a short AV-delay LV pacing increases QRS duration, but with a completely reversed activation pattern compared to LBBB and RV pacing. With BiV pacing the left and right activation wavefronts fuse in the LV, which accelerates its activation, and consequently result in a shorter QRS duration of 150ms. In dogs simultaneous RV and LV pacing shortens TAT and QRS duration compared to the LBBB situation and immediately improves hemodynamics [10]. However, note that BiV pacing does not necessarily reduce QRS duration [6, 7] or TAT [15], which can be explained by prolonged activation of the RV that is not intrinsically activated anymore (i.e. slower cell-to-cell conduction instead of activation through the Purkinje network; compare intrinsic conduction and RV pacing in figure 1 ). Moreover, in dogs it has been shown that hemodynamic improvement can even occur when the QRS duration has not shortened because of CRT [1]. In responders, CRT reduces LV dyssynchrony, measured as LV TAT or as the electrical dyssynchrony index (ED; figure 1 ; lowest for BiV pacing) [13]. CRT reduces the difference in the onset of electrical activation between LV and RV [21]. Ultimately, the intra- and interventricular resynchronization will improve pump function. Acute hemodynamic effects of CRT In dogs with LBBB acute BiV pacing raises dP/dt max almost back to pre-LBBB levels, without affecting LV end systolic or end diastolic pressures. In dogs with LBBB and tachypacing induced heart failure the relative increase in LV dP/dt max is larger than in non-failing LBBB hearts, but the absolute increase is comparable [16]. In patients the onset of BiV pacing immediately increases LV dP/dt max compared to LBBB or RV pacing and this increase typically ranges from 10-30% [6, 7, 22]. LV dP/dt max has become an important variable for hemodynamic studies in CRT, but also pulse pressure and cardiac index increase during BiV stimulation [6, 22, 23]. Pressure- volume loop analysis in dogs with heart failure and LBBB shows an increase in stroke volume and stroke work in BiV pacing compared to baseline measurements [7]. It has been suggested that stroke work is a more reliable measure than increased LV dP/dt max , since stroke work takes the complete systolic phase into account and comprises of both pressure and volume changes, whereas LV dP/dt max only reflects the isovolumic contraction