In a canine ventricular muscle model, nonuniform recovery of excitability facilitates re-entrant ventricular tachycardia induced by a premature stimulus, which can be suppressed by lidocaine.
Nonuniform recovery may facilitate reentry in canine VT models; leaves open clinical relevance and lidocaine effects in humans.
Mechanisms of ventricular tachycardia induced by local application of a properly timed premature stimulus were studied with routine microelectrode technique and extracellular recordings on a ventricular sheet. Thinly sliced preparations obtained from subepicardial muscle of the canine ventricle were used as an approximation of a two-dimensional model. On these preparations, spontaneously sustained tachycardia easily induced by a single premature stimulus. Since delayed after-depolarizations were never evoked by frequent stimulations even in the K+-free and high-Ca++ media, these tachycardias seemed to be induced by re-entrant and circus movement mechanisms. To analyse the re-entrant mechanisms, action potentials generated by normal driving stimuli were recorded from multiple points (40∼50 points) and the spreads of the depolarization and repolarization phases of the action potentials were mapped. The depolarizing wave front on the map always showed a circular or elliptical pattern. Whenever the pattern of spread of the repolarizing wave was similar to that of the depolarizing wave, sustained tachycardia was never brought about by any premature stimulus. On the other hand, when the map of the spread of the repolarizing wave was very complicated and mixed with that of the depolarizing wave, sustained tachycardia was frequently induced. From the above results, it is suggested that the nonuniform recovery of excitability plays a role in the generation of sustained tachycardia. Moreover, a portion of the unidirectional block of the premature impulse was determined by calculated using the conduction velocity of the premature impulse and the effective refractory period in each cell; then a route of re-entry for the premature impulse was simulated. In additional experiments, tachycardia was always suppressed by lidocaine, but was not suppressed by verapamil. The suppression mechanism of lidocaine appeared to be to bring nonuniform recovery of excitability to uniform recovery. Moreover, the leading circle hypothesis was evaluated on the ventricular muscle in the present experiment and diameters of the leading circle in the ventricular muscle were determined to be 8∼10 mm.
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Kamiyama et al. (1986) studied this question.
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