Mechanisms for the success and failure of pacing for termination of ventricular tachycardia: clinical and hypothetical considerations.
The effectiveness of pacing techniques for termination of ventricular tachycardia is well established, and of great value in the electrophysiologic laboratory, and, to a more limited degree, for chronic therapy using implanted anti-tachycardia devices. Although it appears that most clinical ventricular tachycardias are due to reentrant mechanisms, responses to antitachycardia pacing have often been difficult to understand. In this paper, clinical observations are correlated with hypothetical constructs and considerations, in an attempt to derive some general principles related to the success and failure of pacing for ventricular tachycardia. In these analyses, it appears that properties of conductivity and refractoriness in the myocardium are as important as the properties of the tachycardia circuit. Programmed extrastimuli or rapid pacing result in shortening of the effective refractory period of the myocardium, together with depressed conduction velocity of the stimulated wavefront. However, the changes in wavefront conductivity do not occur in step with changes in the effective refractory period; as a result, the stimulated wavefront arrives at the tachycardia circuit in a pattern which differs from the stimulation pattern. In general, it appears that termination of the tachycardia is favored when the stimulated wavefront arrives at the tachycardia circuit at a point when it cannot enter the circuit in an antegrade direction. These conditions are favored by a refractory period in the circuit which is moderately long compared to that of the myocardium. Constructions explaining the observation of a tachycardia termination zone are presented, together with explanations for failure to achieve termination, and for various patterns of acceleration.
D002304:Cardiac Pacing, Artificial; D004562:Electrocardiography; D006329:Heart Conduction System / Q000503:physiopathology; D006339:Heart Rate; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D013610:Tachycardia / Q000503:physiopathology / Q000628:therapy*