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Cardiac vulnerability to electric shocks during phase 1A of acute global ischemia
Blanca Rodríguez1, Brock M Tice, James C Eason
1Tulane University, New Orleans, Louisiana 70118, USA. blanca@tulane.edu
Objectives:
The purpose of this study is to characterize the changes in vulnerability to electric shocks during phase 1A of global ischemia in the rabbit ventricles and to determine the mechanisms responsible for these changes.
Background:
Mechanisms responsible for the changes in cardiac vulnerability over the course of ischemia phase 1A remain poorly understood. The lack of understanding results from the rapid ischemic change in cardiac electrophysiologic properties, which renders experimental evaluation of vulnerability difficult.
Methods:
To examine dynamic changes in vulnerability to electric shocks over the course of acute global ischemia phase 1A, this study used a three-dimensional anatomically accurate bidomain model of ischemic rabbit ventricles. Monophasic shocks are applied at various coupling intervals to construct vulnerability grids in normoxia and at various stages of ischemia phase 1A.
Results:
Our simulations demonstrate that 2 to 3 minutes after the onset of ischemia, the upper limit of vulnerability remains at its normoxic value (12.75 V/cm); however, arrhythmias are induced at shorter coupling intervals. As ischemia progresses, the upper limit of vulnerability decreases, reaching 6.4 V/cm in the advanced stage of ischemia phase 1A, and the vulnerable window shifts towards longer coupling intervals.
Conclusions:
Changes in the upper limit of vulnerability result from an increase in the spatial extent of the shock-end excitation wavefronts and the slower recovery from shock-induced positive polarization. Shifts in the vulnerable window stem from decreases in local repolarization times and the occurrence of postshock conduction failure caused by prolonged postrepolarization refractoriness.
Insights
Cardiac vulnerability to electric shocks changes during global ischemia. Early ischemia shortens arrhythmia induction intervals, while later stages decrease the shock threshold and widen the vulnerable window.
Area of Science:
- Cardiovascular Physiology
- Computational Electrophysiology
- Cardiac Electrophysiology
Background:
- Understanding cardiac vulnerability during ischemia is crucial but challenging due to rapid electrophysiological changes.
- Previous research has not fully elucidated the mechanisms behind altered vulnerability during phase 1A global ischemia.
Purpose of the Study:
- To characterize changes in rabbit ventricular vulnerability to electric shocks during phase 1A global ischemia.
- To identify the underlying mechanisms responsible for these dynamic vulnerability shifts.
Main Methods:
- Utilized a 3D anatomically accurate bidomain model of ischemic rabbit ventricles.
- Simulated monophasic shocks at various coupling intervals to create vulnerability grids under normoxic and ischemic conditions.
Main Results:
- Early ischemia (2-3 min) maintained the upper limit of vulnerability but induced arrhythmias at shorter intervals.
- As ischemia progressed, the upper limit of vulnerability decreased significantly, and the vulnerable window shifted to longer coupling intervals.
Conclusions:
- Increased shock-induced excitation wavefronts and slower recovery from positive polarization alter the upper limit of vulnerability.
- Decreased repolarization times and prolonged refractoriness contribute to vulnerable window shifts and post-shock conduction failure.
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