P532Endocardial pacing is less arrhythmogenic than conventional epicardial pacing when pacing in proximity to scar in patients with ischemic heart failure
Authors: Mendonca Costa C , Neic A , Gillette K , Porter B , Gould J , Sidhu B , Chen Z , Elliott M , Mehta V , Plank G , Rinaldi C A , Bishop M J , Niederer S A 
Published: June 2020

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

(&gt;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 &lt; 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.