Ventricular pacing caused a threefold difference in myofiber work within the LV wall, with total mechanical work in remote regions reaching 125% during RV apex pacing and 171% during LV base pacing.
Does ventricular pacing alter the spatial distribution of myocardial strain and work in an anesthetized dog model?
Ventricular pacing induces significant regional heterogeneity in myocardial work, with reduced work near the pacing site and increased work in remote regions, which is more pronounced with RV apical compared to LV basal pacing.
p-value: p=<0.05
OBJECTIVES: The purpose of this study was to determine the spatial distribution of myocardial function (myofiber shortening and work) within the left ventricular (LV) wall during ventricular pacing. BACKGROUND: Asynchronous electrical activation, as induced by ventricular pacing, causes various abnormalities in LV function, perfusion and structure. These derangements may be caused by abnormalities in regional contraction patterns. However, insight into these patterns during pacing is as yet limited. METHODS: In seven anesthetized dogs, high spatial and temporal resolution magnetic resonance-tagged images were acquired in three orthogonal planes. Three-dimensional deformation data and LV cavity pressure and volume were used to determine midwall circumferential strain and external and total mechanical work at 192 sites around the left ventricle. RESULTS: During ventricular pacing, systolic fiber strain and external work were approximately zero in regions near the pacing site, and gradually increased to more than twice the normal value in the most remote regions. Total mechanical work, normalized to the value during right atrial pacing, was 38 +/- 13% (right ventricular apex RVapex pacing) and 61 +/- 23% (left ventricular base LVbase pacing) close to the pacing site, and 125 +/- 48% and 171 +/- 60% in remote regions, respectively (p < 0.05 between RVapex and LVbase pacing). The number of regions with reduced work was significantly larger during RVapex than during LVbase pacing. This was associated with a reduction of global LV pump function during RVapex pacing. CONCLUSIONS: Ventricular pacing causes a threefold difference in myofiber work within the LV wall. This difference appears large enough to regard local myocardial function as an important determinant for abnormalities in perfusion, metabolism, structure and pump function during asynchronous electrical activation. Pacing at sites that cause more synchronous activation may limit the occurrence of such derangements.
Prinzen et al. (1999) studied Ventricular pacing (n=7). Ventricular pacing (RV apex and LV base) vs. Right atrial pacing was evaluated on Total mechanical work normalized to right atrial pacing (p=<0.05). Ventricular pacing caused a threefold difference in myofiber work within the LV wall, with total mechanical work in remote regions reaching 125% during RV apex pacing and 171% during LV base pacing.
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