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Electrophysiologic mechanisms of ventricular arrhythmias

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In this work the electrophysiologic mechanisms of ventricular arrhythmias have been briefly summarized. Ventricular arrhytmias can be caused either by pacemaker activity or by reentrant excitation. Enhancement of normal automaticy can generate a parasystolic rhythm in normal fibers. Abnormal automaticity may arise fom fibers in which maximum diastolic potential has been reduced by a variety of interventions. Triggered activity is caused by either an early (EAD) or delayed (DAD) afterdepolarization and requires a prior normal action potential for initiation. While there is growing evidence that EAD-induced triggered activity plays a significant role in the Long QTU syndrome and Torsade de Pointes, no clinical arrhythmias has definitely been ascribed to DADs, although DADs have been recorded in man after acute digoxin intoxication.

Ventricular arrhytmias can be also caused by reentrant excitation, which can be subdivided into reflection or circus movement reentry (CMR). In the reflection model impulses in both directions are transmitted over the same pathway. In the CMR three models can be differentiated: the ring model, which requires a fixed anatomical obstacle; the figure-eight model and the leading circle model, where functional rather than fixed anatomical obstacles are involved.

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circus movement reentry


delayed afterdepolarization


early afterdepolarization




left ventricle


monophasic action potential


muscle fiber


Purkinje fiber


right ventricle


Torsade de Pointes


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Correspondence to Nabil El-Sherif.

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El-Sherif, N. Electrophysiologic mechanisms of ventricular arrhythmias. Int J Cardiac Imag 7, 141–150 (1991).

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Key words

  • afterdepolarization
  • circus movement reentry
  • monophasic action potential
  • reentrant excitation
  • reflection
  • ventricular arrhythmias