Programmed stimulation of the ventricles--back to the future.

In the inaugural issue of this journal appeared two articles describing programmed electrical stimulation of the ventricles. Fisher et al. evaluated a new method for induction of ventricular tachycardia, in “Ultrarapid Train Stimulation versus Conventional Programmed Electrical Stimulation for Induction of Ventricular Arrhythmias in Patients with Coronary Artery Disease”[1]. Wyse et al. describe the effects of a conventional programmed stimulation protocol on QT dispersion, in “Divergence of Endocardial QT Interval Components during Programmed Electrical Stimulation Including Observations during Induction of Sustained Ventricular Tachyarrhythmias”[2]. The publication of these articles, 25 years after Wellens ~rst described programmed stimulation of the ventricles in humans [3], offers an opportunity to re_ect on the status of programmed electrical stimulation in clinical electrophysiology, its utility and limitations. In order to interpret appropriately the signi~cance of these two studies, it may be useful to consider how we use programmed ventricular stimulation in practice. While programmed stimulation was initially applied to elucidate the mechanisms responsible for monomorphic sustained ventricular tachycardia, and to aid in its diagnosis [3], later investigators applied the technique to patients who had experienced syncope or survived cardiac arrest (without documentation of the initiating arrhythmia), for similar reasons that it had been utilized in patients with spontaneous sustained ventricular tachycardia [4,5]. It has been used more recently in patients who have never experienced any symptomatic arrhythmia, in order to assess their risk for sudden cardiac death [6]. Further complicating these matters, is the fact that the technique has been applied to patients with the above arrhythmias occurring in association with a variety of anatomic substrates, including coronary artery disease, cardiomyopathies, etc. Why are these factors important? It is very likely that not only are the mechanisms responsible for ventricular tachyarrhythmias dependent on the type of associated heart disease, but even within the subset of patients with coronary artery disease for example, the characteristics of tachycardias are dependent in many respects on the clinical presentation [7]. There is also evidence that within the group of patients with coronary artery disease, the site of previous myocardial infarction can in_uence the arrhythmia substrate [8,9]. In this light, I would like to review brie_y the highlights of the studies by Fisher and Wyse. Fisher and his colleagues extended their earlier studies of the termination of ventricular tachycardia by ultrarapid stimulation trains, to the potential of this technique for initiation of ventricular tachycardia [10]. By coupling ultrarapid trains (at cycle lengths of 10, 20, or 30 msec) of progressively increasing duration to a standard “drive” of seven or eight beats, they were able to deliver 1, 2, or 3 extrastimuli with the greatest possible degree of prematurity relatively quickly. Their results show a high degree of concordance for inducible ventricular tachyarrhythmias between their standard stimulation protocol, and the ultrarapid train protocol, but the train protocol reached one of the predetermined endpoints in signi~cantly less time (5.25 versus 16.1 minutes). Unfortunately, the reproducibility of tachycardia induction was evaluated in only 3 patients. Wyse and his colleagues examined the effect of programmed ventricular stimulation on the difference between the endocardial QT intervals of the last extrastimulus, recorded at the right ventricular apex and out_ow tract. By using unique and original recording technology, the investigators were able to achieve very high ~delity measures of local QT intervals. The duration of the initial portion of the QT interval bore a linear relationship to the prematurity of the extrastimulus in the control group of patients without structural heart disease. As expected, this interval shortened as the extrastimulus prematurity increased. Of interest, the terminal portions of the QT interval did not exhibit the expected rate adaptation, but rather remained constant or increased with increasing extrastimulus prematurity. In contrast, the experimental patient group, consisting of patients with prior myocardial infarction undergoing electrophysiologic studies for evaluation of spontaneous ventricular tachyarrhythmias, showed a blunting of the adaptation of the initial and total QT interval to extrastimulus prematurity. The terminal component of the QT interval in the study patients behaved in a manner similar to that of the control group. The control patients showed minimal “dispersion” of the QT intervals that displayed a _at relationship to extrastimulus prematurity. The QT “dispersion” of patients with ventricular arrhythmias Journal of Interventional Cardiac Electrophysiology 1997;1:281–285 © Kluwer Academic Publishers. Boston. Printed in U.S.A.