Transmural mechanics at left ventricular epicardial pacing site

Abstract

Left ventricular (LV) epicardial pacing acutely reduces wall thickening at the pacing site. Because LV epicardial pacing also reduces transverse shear deformation, which is related to myocardial sheet shear, we hypothesized that impaired end-systolic wall thickening at the pacing site is due to reduction in myocardial sheet shear deformation, resulting in a reduced contribution of sheet shear to wall thickening. We also hypothesized that epicardial pacing would reverse the transmural mechanical activation sequence and thereby mitigate normal transmural deformation. To test these hypotheses, we investigated the effects of LV epicardial pacing on transmural fiber-sheet mechanics by determining three-dimensional finite deformation during normal atrioventricular conduction and LV epicardial pacing in the anterior wall of normal dog hearts in vivo. Our measurements indicate that impaired end-systolic wall thickening at the pacing site was not due to selective reduction of sheet shear, but rather resulted from overall depression of fiber-sheet deformation, and relative contributions of sheet strains to wall thickening were maintained. These findings suggest lack of effective end-systolic myocardial deformation at the pacing site, most likely because the pacing site initiates contraction significantly earlier than the rest of the ventricle. Epicardial pacing also induced reversal of the transmural mechanical activation sequence, which depressed sheet extension and wall thickening early in the cardiac cycle, whereas transverse shear and sheet shear deformation were not affected. These findings suggest that normal sheet extension and wall thickening immediately after activation may require normal transmural activation sequence, whereas sheet shear deformation may be determined by local anatomy.

Fig. 1

A: schematic representation of the left ventricle (LV). X₁, circumferential axis; X₂, longitudinal axis; X₃, radial axis; LAD, left anterior descending; LCx, left circumflex; D₁, D₂, first and second diagonal branch of LAD, respectively. B: schematic representation of local fiber-sheet axes. Fiber angle (α) was measured in the X₁–X₂ plane at each wall depth with reference to positive X₁. Sheet angle (β) was measured in the plane perpendicular to the fiber angle at each wall depth with reference to positive X₃. X_f, fiber axis, X_s, sheet axis, X_n, axis oriented normal to the sheet plane. The X_f, X_s, and X_n axes present a Cartesian system (for details, see Ref. 2).

Fig. 2

Three cardiac phases are shown. dP/dt_max, LV peak positive developed pressure over time; EC, early contraction phase; Ejection, ejection phase; ER, early relaxation phase; ED, end diastole; ES, end systole; LVP_min, minimum LV pressure.

Fig. 3

Temporal sequence of each strain component. Values are means ± SE (n = 5). Subepicardium, midwall, and subendocardium represents 25%, 50%, and 75% wall depth from the epicardial surface, respectively. The reference state for strain calculation was end diastole for both atrial pacing (peak of the ECG R-wave) and LV epicardial pacing (V-spike). Note different scales for shear and normal strains. A: Cardiac strains; B: fiber-sheet strains.

Fig. 4

Transmural delay in mechanical activation time (t_m). Values are means ± SE (n = 5). Subepicardium and subendocardium refer to 25% and 75% wall depth, respectively. End diastole was used as the reference state (time 0) for both atrial pacing and LV epicardial pacing. Maximum fiber shortening in atrial pacing and LV epicardial pacing was found near end systole and dP/dt_max, respectively. *P < 0.05 vs. subepicardium of the same pacing mode; †P < 0.05 vs. subepicardium of atrial pacing.