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.
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.
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.
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.
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.