Quantifying the determinants of decremental response in critical ventricular tachycardia substrate

Mohammadali Beheshti; Sachin Nayyar; Karl Magtibay; Stéphane Massé; Andreu Porta-Sanchez; Shouvik Haldar; Abhishek Bhaskaran; Edward Vigmond; Kumaraswamy Nanthakumar

doi:10.1016/j.compbiomed.2018.05.025

Quantifying the determinants of decremental response in critical ventricular tachycardia substrate

Comput Biol Med. 2018 Nov 1:102:260-266. doi: 10.1016/j.compbiomed.2018.05.025. Epub 2018 May 28.

Authors

Mohammadali Beheshti¹, Sachin Nayyar¹, Karl Magtibay¹, Stéphane Massé¹, Andreu Porta-Sanchez¹, Shouvik Haldar¹, Abhishek Bhaskaran¹, Edward Vigmond², Kumaraswamy Nanthakumar³

Affiliations

¹ The Hull Family Cardiac Fibrillation Management Laboratory, Toronto General Hospital, University Health Network, Toronto, ON, Canada.
² IHU L'Institut de RYthmologie et Modélisation Cardiaque, University of Bordeaux, Pessac, France. Electronic address: edward.vigmond@u-bordeaux.fr.
³ The Hull Family Cardiac Fibrillation Management Laboratory, Toronto General Hospital, University Health Network, Toronto, ON, Canada. Electronic address: kumar.nanthakumar@uhn.ca.

PMID: 29871758
DOI: 10.1016/j.compbiomed.2018.05.025

Abstract

Background: Decremental response evoked with extrastimulation (DEEP) is a useful tool for determining diastolic return path of ventricular tachycardia (VT). Though a targeted VT ablation is feasible with this approach, determinants of DEEP response have not been studied OBJECTIVES: To elucidate the effects of clinically relevant factors, specifically, the proximity of the stimulation site to the arrhythmogenic scar, stimulation wave direction, number of channels open in the scar, size of the scar and number of extra stimuli on decrement and entropy of DEEP potentials.

Methods: In a 3-dimensional bi-domain simulation of human ventricular tissue (TNNP cell model), an irregular subendocardial myopathic region was generated. An irregular channel of healthy tissue with five potential entry branches was shaped into the myopathic region. A bipolar electrogram was derived from two electrodes positioned in the centre of the myopathic region. Evoked delays between far-field and local Electrogram (EGM) following an extrastimulus (S1-S2, 500-350 ms) were measured as the stimulation site, channel branches, and inexcitable tissue size were altered.

Results: Stimulation adjacent to the inexcitable tissue from the side opposite to the point-of-entry produces longest DEEP delay. The DEEP delay shortens when the stimulation point is farther away from the scar, and it decreases maximally when stimulation is done from a site beside a conduction barrier. Entropy increases with S2 when stimulation site is from farther away. An unprotected channel structure with multiple side-branch openings had shorter DEEP delay compared to a protected channel structure with a paucity of additional side-branch openings and a point-of-entry on the side opposite to the pacing source. Addition of a second shorter extrastimulus did not universally lead to higher DEEP delay CONCLUSIONS: Location and direction of the wavefront in relation to scar entry and size of scar determine the degree of evoked response while the number of extrastimuli has a small additional decremental effect.

Keywords: Cardiac modeling; DEEP; Mapping.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Arrhythmias, Cardiac / physiopathology
Catheter Ablation / methods
Electrocardiography
Electrophysiologic Techniques, Cardiac / methods*
Heart
Heart Conduction System / physiopathology*
Heart Ventricles / physiopathology
Humans
Tachycardia, Ventricular / diagnosis
Tachycardia, Ventricular / physiopathology*

Grants and funding

MOP 142272/CIHR/Canada