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Ventricular activation during sympathetic imbalance and its computational reconstruction
M P Nash1, J M Thornton, C E Sears
1University Laboratory of Physiology, Oxford OX1 3PT, United Kingdom. martyn.nash@physiol.ox.ac.uk
Journal of Applied Physiology (Bethesda, Md. : 1985)
|January 3, 2001
Summary
Norepinephrine infusion triggered ventricular arrhythmias by causing abnormal electrical activation originating from the infusion site. Computational models suggest calcium overload in this region contributes to triggered automaticity, offering targets for arrhythmia prevention.
Area of Science:
- Cardiology
- Electrophysiology
- Computational Biology
Background:
- Ventricular arrhythmias pose significant clinical challenges.
- Understanding the triggers of sudden cardiac events is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the epicardial activation sequence during norepinephrine-induced ventricular arrhythmias in pigs.
- To identify factors modulating these arrhythmias and their underlying mechanisms.
Main Methods:
- Characterization of epicardial activation using in vivo animal models.
- Hemodynamic monitoring and electrophysiological recordings.
- Computational modeling of cardiac cell behavior and calcium handling.
Main Results:
- Norepinephrine infusion induced rapid ventricular arrhythmias with altered QRS morphology.
- Earliest epicardial activation shifted to the NE infusion site, preceding atrial activation.
- Arrhythmias were reversed by stopping NE, prevented by propranolol, and abolished by nerve stimulation.
- Computational models implicated abnormal intracellular calcium handling in the arrhythmogenesis.
Conclusions:
- Adrenergic stimulation can induce ventricular arrhythmias via triggered automaticity originating from a focal region.
- Computational reconstruction highlights the role of calcium overload in this process.
- Reducing spatial inhomogeneities in intracellular calcium may prevent such arrhythmias.