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Early afterdepolarizations (EAD's) are irregularities of the cardiac action potential that interrupt or retard repolarization. EAD's have been linked to the development of specific types of cardiac arrhythmias, however, the mechanism underlying the development of these arrhythmias remains unclear. The authors implemented a two-element kinetic model of the ventricular action potential to investigate a potentially arrhythmogenic form of triggered activity. By approximating EAD's by a sinusoidal driving force, the authors were able to study the effects of interelement coupling resistivity and sinusoidal frequency and amplitude on the triggering of action potentials. They demonstrated EAD's in a ventricular action potential model by altering the potassium and calcium channels to simulate experimental conditions under which EAD's occur. They also found that triggered activity depends critically on the frequency and amplitude of the driving force and also on the degree of cellular uncoupling between the elements. The authors' results suggest that triggered activity (due to EAD's) may be suppressed by drugs that improve coupling in unhealthy tissue, or ones that prevent EAD formation by inhibiting calcium channels.
Date of Publication: Oct. 1995