心力衰竭的非药物及起搏治疗-教学课件，幻灯，.ppt

normal LV function. During normal SR the electrical impulse travels from the His-bundle towards the apex, but this first part of ventricular activation concerns the rapid conduction system, not the working myocardium. In the LV the working myocardium is activated first at the LV endocardium in low septal and anterior free-wall regions, which are very close to the LV apex and LV septal endocardium (23,24). From these exits of the Purkinje system, the LV activation wavefront travels from apex to base (23,24). Pacing at the LV apex and the lower LV septal Figure 2. Echocardiographic strain images from the four-chamber view and two-chamber view, with corresponding time-strain plots from sites adjacent to papillary muscles before and after cardiac resynchronization therapy. Baseline plots demonstrate late peak strain occurring in the anterolateral papillary muscle site compared with the posteromedial papillary muscle site. Peak strain is aligned after cardiac resynchronization therapy in these sites. But, now there may be some compelling reasons to change – a previous slide showed the snowball effect of RV apical pacing on LV function. Here’s its effect on the myocardial cells, although these are thankfully actually taken from an animal study. In normal heart muscle, cells align in parallel as the picture on the left shows you. However, after six months of RV apical pacing, you can see that the cells are no longer aligned – that is, some are going horizontal and some vertical. From a histological standpoint, the difference is pretty dramatic. So, based on the hemodynamic changes in the previous slide and the histologic changes in this side, you can see that RV apical pacing should not be considered to be “physiologic”. So the question is: if not from the RV apex, then where? Interestingly, although Medtronic is mainly targeting MVP in patients with Sinus Node Dysfunction, we are also seeing a reduction in cumulative V-Pacing in many patients with intermittent AV B