Endocardial versus epicardial electrical synchrony during LV free-wall pacing

Abstract

Cardiac resynchronization therapy has been most typically achieved by biventricular stimulation. However, left ventricular (LV) free-wall pacing appears equally effective in acute and chronic clinical studies. Recent data suggest electrical synchrony measured epicardially is not required to yield effective mechanical synchronization, whereas endocardial mapping data suggest synchrony (fusion with intrinsic conduction) is important. To better understand this disparity, we simultaneously mapped both endocardial and epicardial electrical activation during LV free-wall pacing at varying atrioventricular delays (AV delay 0-150 ms) in six normal dogs with the use of a 64-electrode LV endocardial basket and a 128-electrode epicardial sock. The transition from dyssynchronous LV-paced activation to synchronous RA-paced activation was studied by constructing activation time maps for both endo- and epicardial surfaces as a function of increasing AV delay. The AV delay at the transition from dyssynchronous to synchronous activation was defined as the transition delay (AVt). AVt was variable among experiments, in the range of 44-93 ms on the epicardium and 47-105 ms on the endocardium. Differences in endo- and epicardial AVt were smaller (-17 to +12 ms) and not significant on average (-5.0 +/- 5.2 ms). In no instance was the transition to synchrony complete on one surface without substantial concurrent transition on the other surface. We conclude that both epicardial and endocardial synchrony due to fusion of native with ventricular stimulation occur nearly concurrently. Assessment of electrical epicardial delay, as often used clinically during cardiac resynchronization therapy lead placement, should provide adequate assessment of stimulation delay for inner wall layers as well.

Fig. 1

Fluoroscopic image of instrumented heart. A, right atrial (RA) pacing electrodes. B, localization marker. C, endocardial basket array. D, left ventricular (LV) pacing electrodes. E, epicardial sock wires.

Fig. 2

Example of electrical activation delay magnitude (EADM) plotted as a function of atrioventricular (AV) delay. At low AV delay values, corresponding to LV paced activation, EADM is at the top asymptote [highly dyssynchronous (dyssync) region]. At high AV delay values, corresponding to intrinsic activation from the RA pacing stimulus, electrical activation delay magnitude (EADM) is close to lower asymptote (synchronous region). The transition region represents fusion of the two activation patterns. The transition AV delay is defined as the AV delay at which the curve fit to the data crosses through the midpoint between the two asymptotes. Example epicardial electrical activation time maps are shown for each region, where blue is early and yellow is late. In the dyssynchronous region, maps demonstrate early activation near the LV pacing site and late activation of the RV. In the transition region, maps demonstrate fusion between the LV stimulus and Purkinje activation. In the synchronous region, the heart is activated synchronously and almost entirely through the Purkinje system.

Fig. 3

Endocardial and epicardial electrical activation maps for LV pacing at increasing AV delay and RA pacing. For both the epicardial and endocardial surface maps, the view is from the outside of the heart toward the inside. The broad black lines on the epicardial maps indicate the insertion of the RV as digitized. Endocardial and epicardial maps are centered about the earliest activation point for AV delay = 0. The small “+” symbols show the locations of the epicardial electrodes. Color transitions are in steps of 10 ms (see color bar on the right). Times are referenced to the LV pacing stimulus for LV pacing and to the RA pacing stimulus for RA pacing. A–F, different AV delays for left ventricular pacing in a single representative animal; F indicates right atrial pacing in same animal.

Fig. 4

Electrical activation delay magnitude (EADM) normalized and plotted as a function of AV delay for the endocardium (□) and epicardium (●) for each animal (A–F). As AV delay is increased, endocardial and epicardial synchrony transition from the top (dyssynchronous) asymptote to the bottom (synchronous) asymptote. The endocardial (■) and epicardial (▲) transition AV delays (AV_t) are shown.

Fig. 5

Maximum rate of developed pressure over time (dP/dt) shown for each experiment (○) evaluated under dyssynchronous electrical activation (Dyssync), pacing at the transition AV delay (Trans), and synchronous activation (Sync). For each condition, the average value (●) is shown ± SE.

Fig. 6

Example of computed EADM values for the endocardium and epicardium overlaid on the actual endocardial and epicardial EADM values for one animal.