Spiral tip movement: The role of the action potential wavelength in polymorphic cardiac arrhythmias

Sudden cardiac death is often preceded by re-entrant (spiral wave) tachyarrhythmias associated with a prolongation of the action potential wavelength. Potassium channel blockade, hypokalemia and genetic alterations in membrane ion channels (e.g. long QT syndrome) can all lead to extension of the action potential wavelength. In experiments with cardiac cells, we have found that potassium channel blockade can also promote transient oscillation of the membrane potential which can then initiate transient or sustained rhythm disturbances. Using a simple FitzHugh-Nagumo model of an excitable cell, we observed that extending the time required for an excited cell to return to the rest state (equivalent to potassium channel blockade or hypokalemia) amplified the region of spiral tip movement (meandering). When the region of meandering was large relative to the total myocardial surface, the QRS amplitude and configuration varied from one re-entrant cycle to the next and resembled the patterns seen in the cardiac arrhythmia, torsade de pointes. By changing media parameters in order to slow conduction, the spatial wavelength of the action potential was reduced which diminished the relative size of the meandering region and increased the degree of uniformity in QRS shape, i e the peak amplitude and QRS configuration were relatively constant from cycle to cycle. Injecting a small, continuous depolarizing current near the spiral tip reduced the local threshold of excitability and reduced the size of the meandering region. These studies support a unified model for initiation and evolution of polymorphic re-entrant arrhythmias and suggest new strategies for arrhythmia management based on control of spiral tip movement.

Duke Scholars

Author Charles Franklin Starmer Computer Science