Vulnerability to electric shocks in the regionally-ischemic ventricles
Blanca Rodríguez1, Brock Tice, Robert Blake
1Oxford University, UK. blanca@comlab.ox.ac.uk
Insights
Defibrillation in ischemic hearts shows unchanged upper limit of vulnerability (ULV) but an expanded vulnerable window (VW). This increased cardiac vulnerability post-LAD occlusion is due to slow conduction and dispersion of refractoriness.
Area of Science:
- Cardiovascular Physiology
- Computational Biology
- Electrophysiology
Background:
- Defibrillation is crucial for treating cardiac arrhythmias, yet its efficacy in ischemic heart disease remains poorly understood.
- Ischemic heart disease significantly alters cardiac electrical properties, potentially impacting defibrillation success.
Purpose of the Study:
- To investigate the impact of regional ischemia on cardiac vulnerability to defibrillation shocks.
- To understand the mechanisms behind defibrillation failure in the early stages of ischemia following Left Anterior Descending (LAD) occlusion.
Main Methods:
- Development of a 3D anatomically accurate, electrophysiologically detailed bidomain model of the ischemic ventricles.
- Simulation of ventricular pacing and application of monophasic shocks to determine the upper limit of vulnerability (ULV) and vulnerable window (VW).
- Comparison of ULV and VW in normoxia versus 10 minutes post-LAD occlusion.
Main Results:
- The ULV remained unchanged 10 minutes post-LAD occlusion, as virtual electrode polarization and post-shock behavior were unaffected by ischemia at high shock strengths.
- The VW significantly increased from 60 ms in normoxia to 90 ms at 10 minutes post-occlusion.
- Increased cardiac vulnerability in regional ischemia is linked to slow conduction and dispersion of refractoriness, promoting reentrant circuit formation.
Conclusions:
- Early regional ischemia does not alter the ULV but significantly expands the VW, increasing susceptibility to defibrillation failure.
- The findings highlight the complex electrophysiological changes during ischemia that enhance vulnerability to arrhythmias.
- This study provides crucial insights into defibrillation challenges in ischemic heart disease, guiding future therapeutic strategies.
Abstract:
Although the majority of patients undergoing defibrillation suffer from coronary heart disease, little is known about defibrillation in the setting of ischemic disease. The goal of this study is to aid understanding of defibrillation failure in ischemic hearts by studying changes in cardiac vulnerability to electric shocks the first 10 min following LAD occlusion. To do so, a 3D anatomically-accurate electrophysiologically-detailed bidomain model of the regionally ischemic ventricles following LAD occlusion was developed based on experimental data. The ventricles were paced at the apex and truncated exponential monophasic shocks were applied over a range of coupling intervals to determine the upper limit of vulnerability (ULV) and the vulnerable window (VW) in normoxia and 10 min post-occlusion. Simulation results demonstrate that, despite the profound electrophysiological changes in the ischemic region, the ULV remains unchanged 10 min post-occlusion because following high shock strengths gesULV virtual electrode polarization and postshock behavior remain unaffected by ischemia. However, the range of coupling intervals comprising the VW increases from spanning 60 ms in normoxia to 90 ms at 10 min post-occlusion. The increased in vulnerability in regional ischemia stems from the fact that slow conduction and increased dispersion of refractoriness in the ischemic region increase the likelihood of the establishment of a reentrant circuit following shocks of strength
Related Concept Videos
Dysrhythmias III: Characteristics of Dysrhythmias
Disturbances in Heart Rhythm
Arrhythmias are categorized by their speed, rhythm, and origin. A slow heart...
Dysrhythmias I: Introduction
Dysrhythmias IV: Characteristics of Bradyarrhythmias
Electrophysiology of Normal Cardiac Rhythm
Dysrhythmias II: Classification of Tachyarrhythmias


