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Three‐dimensional mechanisms of increased vulnerability to electric shocks in myocardial infarction: Altered virtual electrode polarizations and conduction delay in the peri‐infarct zone
Author(s) -
Rantner Lukas J.,
Arevalo Hermenegild J.,
Constantino Jason L.,
Efimov Igor R.,
Plank Gernot,
Trayanova Natalia A.
Publication year - 2012
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2012.229088
Subject(s) - border zone , cardiology , medicine , myocardial infarction , infarction , shock (circulatory) , bidomain model , vulnerability (computing) , defibrillation , optical mapping , neuroscience , psychology , computer science , computer security
Key points• Defibrillation is known to be less efficient in infarcted than in healthy hearts. • In a rabbit model of myocardial infarction, altered 3D distribution of virtual electrodes and propagation delay in the peri‐infarct zone caused increased vulnerability to electric shocks in infarcted hearts. • The infarct scar alone – without the presence of a peri‐infarct zone – did not cause an increase in vulnerability. • The results help us to understand the mechanisms of increased vulnerability and decreased defibrillation efficacy in infarcted hearts.Abstract Defibrillation efficacy is decreased in infarcted hearts, but the mechanisms by which infarcted hearts are more vulnerable to electric shocks than healthy hearts remain poorly understood. The goal of this study was to provide insight into the 3D mechanisms for the increased vulnerability to electric shocks in infarcted hearts. We hypothesized that changes in virtual electrode polarizations (VEPs) and propagation delay through the peri‐infarct zone (PZ) were responsible. We developed a microanatomically detailed rabbit ventricular model with chronic myocardial infarction from magnetic resonance imaging and enriched the model with data from optical mapping experiments. We further developed a control model without the infarct. The simulation protocol involved apical pacing followed by biphasic shocks. Simulation results from both models were compared. The upper limit of vulnerability (ULV) was 8 V cm −1 in the infarction model and 4 V cm −1 in the control model. VEPs were less pronounced in the infarction model, providing a larger excitable area for postshock propagation but smaller transmembrane potential gradients to initiate new wavefronts. Initial post‐shock transmural activation occurred at a later time in the infarction model, and the PZ served to delay propagation in subsequent beats. The presence of the PZ was found to be responsible for the increased vulnerability.