Abstract
Funding Acknowledgements
WT 203148/Z/16/Z; MR/N011007/1; RE/08/003; PG/15/91/31812; PG/16/81/32441
Background
Endocardial pacing has been shown to improve response to cardiac
resynchronization therapy (CRT) in comparison to conventional epicardial pacing and the
physiological activation, endocardium to epicardium, is proposed to make it less arrhythmogenic.
However, the relative arrhythmic risk of endocardial and epicardial pacing has not been
systematically investigated. Pacing in proximity to scar increases susceptibility to arrhythmogenesis
during epicardial pacing. Whether this is also the case during endocardial pacing is currently
unknown.
Purpose
We investigate 1) whether endocardial pacing is less arrhythmogenic than epicardial
pacing, 2) whether pacing location relative to scar plays a role in arrhythmogenesis during
endocardial pacing, and 3) whether these findings could be explained by the direction of the
transmural action potential duration (APD) gradient.
Methods
We used computational models of ischemic heart failure and patient-specific (n = 24) left ventricular anatomy and scar morphology to simulate repolarization during endocardial and
epicardial pacing. Pacing locations were selected 0.2-3.5cm from a scar. We ran simulations with a
20ms transmural APD gradient, as found in heart failure, from the epicardium to endocardium
(physiological) and with this gradient inverted. We computed the volume of high
(>3ms/mm) repolarization gradients (HRG) within 1cm around a scar, as a surrogate for arrhythmia
risk, and analysed these with ANOVA and Tukey-Kramer post-hoc tests.
Results
Simulations with a physiological APD gradient predict that endocardial pacing creates a
smaller (34%) volume of HRG around (1cm) a scar compared to epicardial pacing when
pacing 0.2cm from scar (Figure 1-A). The volume of HRG decreases (P < 0.05) with distance
from scar for epicardial pacing but not endocardial pacing (Figure 1-A). Inverting the
transmural APD gradient, inverts the trend observed with a physiological gradient. In this case, the
volume of HRG is unaffected by pacing location during epicardial pacing, whereas it decreases (19%)
with the distance from scar for endocardial pacing. This is illustrated
in the regions highlighted in yellow in Figure 1 for endocardial pacing at 0.2 and 3.5cm from a scar
with a physiological (B) and an inverted (C) gradient.
Conclusions
Endocardial pacing is less arrhythmogenic (purpose 1) than conventional epicardial
pacing when pacing in proximity to scar and is also less susceptible to pacing location relative to scar
(purpose 2). The direction of the transmural APD gradient offers a mechanistic explanation for
reduced susceptibility to arrhythmogenesis during endocardial pacing compared to epicardial pacing
(purpose 3). Endocardial pacing is an attractive alternative to conventional epicardial pacing in
patients with scar, as it allows pacing in proximity to scar while avoiding increasing arrhythmogenic
risk in patients with ischemic heart failure.
Abstract Figure.
Left ventricular endocardial pacing is less arrhythmogenic than conventional epicardial pacing when pacing in proximity to scar
