Mapping of regional myocardial strain and work during ventricular pacing: experimental study using magnetic resonance imaging tagging

Abstract

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.

Figure 1

Examples of MRI tagging images, acquired during LVbase pacing. Presented are short-axis images at the papillary level, with taglines oriented at an angle of 0 (SA 0) and 90° (SA 90) with the circumference and long-axis images with taglines at an angle of 90° with the long axis (LA 90). In plane, resolution was 1.25 mm (readout direction) × 3 mm (phase encoding direction) and slice thickness was 7 mm. Images were taken every 20 ms, frame 0 being the time when taglines were parallel. Note the inward bending of taglines at the LV anterior wall and the outward bending in the septum in the SA0 image of frame 4, indicating early systolic shortening and stretching in these regions, respectively.

Figure 2

Schematic of the calculation of local work during normal and abnormal activation. Simplified fiber stress-fiber length (σ-L) relations in regions with early, normal and late activation are presented. PE = potential energy, EW = external work. External work is determined as the area of the σ-L loop, and potential work is the area of the triangle delineated by the origin, the end systolic fiber length-stress point and the end systolic fiber length point. Fiber length was defined as L/L₀ (see Methods). Total work is the sum of PE and EW.

Figure 3

Midwall circumferential strain as a function of time in a high papillary cross-section of one experiment. The “tracings” are displayed according to the anatomy of the LV, as if the LV was cut open along the mid septum. Only every other material point is shown (12 out of the 24 in circumferential direction; see Methods). The approximate pacing site is indicated by an asterisk, and was actually 2 cm below this cross-section during RVapex pacing and slightly above it during LVbase pacing. Zero strain is the length at the time of placing the taglines (time = 0 ms). The ejection phase is indicated by the broken lines.

Figure 4

Midwall fiber stress-fiber length diagrams in the same regions and the same experiment as presented in Figure 3. Fiber length = 1, is defined as the length at estimated zero cavity volume (see Methods). Actual values were calculated according to eq. 2. Format is the same as in Figure 3.

Figure 5

Systolic circumferential strain (top), external work (middle) and total work (bottom) during RA, LVbase and RVapex pacing, as measured at two sites: RVapex (striped bars) and LVbase (closed bars). Mean values ± SD from seven experiments are presented. *p < 0.05 compared with the same site during RA pacing, †p < 0.05 compared with the same site during pacing at the RVapex and #p < 0.05 compared with the opposite region during pacing at the same site.

Figure 6

Maps of local external work during RA, RVapex and LVbase pacing (from top to bottom) from the same experiment as presented in Figures 3 and 4. External work values are presented as gray levels, zero being black (see scale bar). The LV wall is represented as a circle with the base located at the outer contour and the apex in the middle. Location of septum, anterior and lateral wall are indicated.

Figure 7

Cumulative histograms of midwall external work in the LV wall. For each experiment values from all 192 sites of the LV were normalized to the mean value during RA pacing (=1). Presented are the mean curved from the seven experiments. Thin horizontal lines indicate SD of the 0.1 through 0.9 values during each mode of pacing. Solid line = RA pacing, dotted line = RVapex pacing and broken line = LVbase pacing. *p < 0.05 as compared with RA pacing, #p < 0.05 between RVapex and LVbase pacing.