Long-term Reproducibility of Ventricular Tachycardia Induction in Patients With Implantable Cardioverter/Defibrillators
Serial Noninvasive Studies
Background Noninvasive electrophysiological studies (EPSs) can be performed in current implantable antitachycardia pacemaker/cardioverter/defibrillators (ICDs). Thus, these devices may be used as tools to study changes in the electrophysiological substrate and ventricular tachycardia characteristics over time.
Methods and Results Fifty-five patients receiving an ICD for treatment of sustained ventricular tachyarrhythmias underwent serial EPSs after implantation of the ICD. Studies were performed before hospital discharge and 1, 3, 5, 9, 12, 18, 24, and 36 months after ICD implantation. Sustained monomorphic ventricular tachycardia (VT) was induced in 37 patients (group 1) at the predischarge EPS, whereas no sustained arrhythmia could be induced in 18 patients (group 2) at baseline. Group 1 patients underwent 165 noninvasive EPSs after discharge. Sustained monomorphic VT was induced during 72% of the follow-up EPSs, ventricular fibrillation (VF) was induced during 11% of follow-up EPSs, and no sustained VT or VF was induced during 17% of follow-up visits. Sustained VT was induced at every follow-up EPS in 23 patients (62%), whereas no sustained VT/VF could be induced at least once during follow-up in 14 patients (38%). Clinical or electrophysiological variables did not predict noninducibility during follow-up. However, the probability that a patient would experience spontaneous VT decreased significantly over time in patients in whom VT was not inducible during at least 1 follow-up EPS (P=.05). Group 2 patients underwent 86 noninvasive EPSs after discharge. Sustained monomorphic VT was induced during 22% of follow-up EPSs, VF was induced during 19% of follow-up EPSs, and no sustained VT/VF could be induced during 68% of follow-up EPSs. No sustained VT/VF could be induced during every follow-up EPS in 9 patients (50%), whereas sustained monomorphic VT was induced at least once during follow-up in 7 patients (34%). Persistent noninducibility of VT during follow-up was associated with low probability of occurrence of spontaneous VT (11%), whereas inducibility of VT at least once during follow-up was associated with the occurrence of spontaneous VT (89%, P=.003).
Conclusions Considerable variability of VT induction is observed over a lengthy period in patients presenting with sustained VT/VF. Persistent noninducibility of VT is associated with a reduced probability of spontaneous VT. These observations suggest that the substrates for inducible and spontaneous VT change in parallel over time.
The newer generations of implantable antitachycardia pacemaker/cardioverter/defibrillators (ICDs) offer tiered therapy for the treatment of recurrent sustained ventricular tachycardia (VT) as well as improved diagnostic capabilities that optimize programming of device therapies.1 2 3 Noninvasive electrophysiological studies (EPSs) can be performed with these devices used as programmable stimulators.2 3 4 Thus, ICDs may be used to evaluate changes in the electrophysiological substrate and VT induction over time. Although some information concerning the reproducibility of VT induction over short periods of time is available,5 6 7 8 9 10 less information is available concerning the long-term reproducibility of VT induction.11 12 Moreover, little is known about changes in the electrophysiological substrate over time in patients who present with sustained ventricular tachyarrhythmias and in whom no ventricular tachyarrhythmia is inducible at baseline EPS.12 Finally, no information is available concerning the relation of VT inducibility and the occurrence of spontaneous episodes of VT. Accordingly, the purposes of the present study were (1) to evaluate the long-term reproducibility of VT induction in patients in whom monomorphic VT was induced at a baseline noninvasive EPS performed 1 week after an ICD implantation; (2) to evaluate the variability of induced VT characteristics over time in this patient population; (3) to evaluate the long-term reproducibility of noninducibility of VT in patients in whom VT was not inducible at a baseline noninvasive EPS performed 1 week after an ICD implantation; and (4) to correlate changes in VT inducibility with the spontaneous occurrence of VT or ventricular fibrillation (VF).
Fifty-five patients received a multiprogrammable tiered-therapy ICD (model 7216A, 7217B, or 7219D PCD, Medtronic) for the treatment of hemodynamically significant VT in 35 patients and out-of-hospital VF in 20 patients. Epicardial lead systems were implanted in 26 patients and transvenous-subcutaneous patch lead systems in 29 patients. Two patients underwent concomitant coronary artery bypass graft surgery. Invasive EPSs were performed before device implantation in 51 patients. At the baseline invasive drug-free EPS, sustained monomorphic VT was induced in 33 patients, VF was induced in 7 patients, nonsustained VT was induced in 4 patients, and no arrhythmia could be induced in 7 patients on completion of the EPS protocol. Forty-three patients underwent 3±2 serial electropharmacological trials before ICD implantation.
Serial noninvasive EPSs were performed at 1 week and 1, 3, 6, 9, 12, 18, 24, 36, and 48 months after ICD implantation. The patients gave written informed consent for participation in the follow-up studies as approved by the Institutional Review Boards of both participating centers. To avoid the ethical dilemma of repeated investigational inductions of VF, 2 additional patients who otherwise qualified with inducible VF at the 1-week study were excluded. If patients were on empirical antiarrhythmic drug therapy at the baseline noninvasive EPSs performed 1 week after ICD implantation, this medication was continued during the follow-up period. EPSs were performed with the ICD used as a programmable stimulator.1 4 Single, double, and triple ventricular extrastimuli were delivered after eight-beat drive trains at three ventricular pacing cycle lengths (600, 500, and 400 ms) at a pulse amplitude of 5.4 V and 1.0-ms pulse duration. Coupling intervals of ventricular extrastimuli were decreased by 10- to 20-ms intervals until ventricular refractoriness was reached or a sustained ventricular tachyarrhythmia was induced. If sustained VT or VF was induced, the study was terminated. Reproducibility of VT/VF induction was not assessed at each EPS.
The electrophysiological parameters assessed at each visit included ventricular pulse duration stimulation thresholds measured at 2.8 and 5.4 V; ventricular effective refractory periods measured at ventricular pacing cycle lengths 600, 500, and 400 ms; induced VT cycle length; morphology of the induced VT; number of extrastimuli required to induce VT; and arrhythmia induced (VT, VF, nonsustained VT, or none).
The number of episodes of spontaneous VT/VF was retrieved from device memory at each follow-up visit. The cycle length of the most recent episode of spontaneous VT/VF was also retrieved. Most devices used in this study could not store intracardiac electrograms. The nature of spontaneous events was determined after consideration of the patient symptoms, the 20 RR intervals preceding arrhythmia detection, the 10 RR intervals after therapy delivery, and ECG monitoring when available.
Pulse duration stimulation thresholds were defined as the lowest pulse width that consistently depolarized the ventricles measured to the nearest 0.03 ms.
Ventricular effective refractory period was the longest S1-S2 interval that did not depolarize the ventricles. This was measured to the nearest 10 ms.
VF was defined as rapid pleomorphic tachycardia with cycle length <200 ms. Although the PCD models 7216A, 7217B, and 7219D define VF for therapy selection as tachycardia with a cycle length <240 ms or a longer interval programmed by the electrophysiologist, the latter definition was not used to define the induced arrhythmia.
VT was defined as five or more repetitive ventricular complexes at a rate >100 beats per minute. Sustained VT activated ICD therapy. Nonsustained VT spontaneously terminated before device activation.
Noninducible meant no VT/VF induced during completion of the entire EPS protocol.
Patients were divided into two groups on the basis of the arrhythmia induced at the 1-week noninvasive EPS: those with sustained VT induced (group 1) and those in whom no sustained VT could be induced (group 2). Differences in ventricular pacing thresholds, ventricular effective refractory periods, and VT cycle lengths were compared over time. Differences in the arrhythmias induced, the morphology of the arrhythmias induced, and the number of ventricular extrastimuli required to induce an arrhythmia were also evaluated over time. Ventricular pacing thresholds and ventricular refractory periods were compared between EPSs during which sustained VT was induced and EPSs during which sustained VT was not induced.
Continuous data are presented as mean±SD. Differences in continuous data over time were compared by ANOVA for repeated measures. Differences between groups were compared by the unpaired t test or two-way ANOVA where appropriate. Differences in proportions were compared by χ2 analysis with Fisher’s exact test where appropriate. Cumulative, event-free interval curves were generated by the Kaplan-Meier method13 and were compared by means of a generalized Wilcoxon test.14 Differences were considered statistically significant if P<.05.
Sustained monomorphic VT was induced in 37 patients (group 1) at the baseline EPS performed 1 week after ICD implantation, whereas no sustained VT/VF was induced in 18 patients (group 2). The clinical characteristics of the study population are shown in Table 1⇓. Group 1 patients were more likely to have sustained a prior myocardial infarction (P<.05), they were more likely to present with VT compared with VF (P<.05), their mean left ventricular ejection fraction was lower (P<.05), they were more likely to be on antiarrhythmic drugs (P<.01), and they more frequently received an ICD system with epicardial leads (P<.05). During the follow-up period, none of the patients experienced an acute myocardial infarction or unstable angina, nor did any patient undergo myocardial revascularization procedures. Eight group 1 patients and 1 group 2 patient required changes in medical therapy for progression of congestive heart failure (P=NS).
Invasive Electrophysiological Studies
Invasive EPSs were performed in the antiarrhythmic drug–free state before ICD implantation in 34 group 1 patients. Sustained monomorphic VT was induced in 29 (85%), VF was induced in 1 (3%), and no sustained arrhythmia could be induced in 4 (12%). The mean VT cycle length was 290±64 ms. The morphology of the VT induced at the invasive EPS was concordant with the morphology induced at the baseline noninvasive EPS in 21 patients (62%). The number of extrastimuli required to induce VT at the invasive EPS was concordant with the number of extrastimuli required to induce VT at the baseline noninvasive EPS in 12 patients (35%). Invasive EPSs were performed in the antiarrhythmic drug–free state before ICD implantation in 17 group 2 patients. Sustained monomorphic VT was induced in 4 (24%), VF was induced in 6 (35%), and no sustained arrhythmia could be induced in 7 (41%). Sustained VT was less likely to be induced in group 2 patients than in group 1 patients (P<.001), and group 2 patients were more likely to have no sustained arrhythmia induced compared with group 1 patients (P<.05).
Time-Dependent Electrophysiological Variables
Ventricular pacing thresholds did not change significantly over time. Moreover, no significant differences were observed when pacing thresholds in the patients who received epicardial leads were compared with those who received endocardial leads (Table 2⇓). No significant changes in ventricular effective refractory period or VT cycle length were observed over time (Table 3⇓). Ventricular effective refractory period was similar in group 1 and group 2 patients. VT cycle length tended to be shorter in group 2 patients than in group 1 patients, but this difference approached statistical significance only at the 3-month visit (P=.05, Table 3⇓).
Serial EPSs in Group 1 Patients
Group 1 patients were followed for 16±13 months. Sustained monomorphic VT was induced in all 37 patients at the predischarge EPS. These patients underwent 165 noninvasive EPSs during follow-up. Twenty-one patients were receiving chronic empirical antiarrhythmic drug therapy during the follow-up period. Drug therapy consisted of amiodarone (n=9), quinidine (n=4), procainamide (n=1), sotalol (n=2), mexilitine (n=1), propafenone (n=1), mexilitine/quinidine combination therapy (n=1), propafenone/mexilitine combination therapy (n=1), and amiodarone/procainamide combination therapy (n=1). Of the 10 patients receiving β-adrenergic receptor blocking agents, 3 were also receiving other empirical antiarrhythmic drug therapy.
During the follow-up EPSs, sustained monomorphic VT was induced in 119 (72%), VF was induced in 18 (11%), nonsustained VT was induced in 10 (6%), and no arrhythmia was induced during 18 (11%). Thus, no sustained arrhythmia could be induced during 17% of follow-up EPSs. Sustained monomorphic VT was always induced in 20 patients during follow-up EPS. In the remaining 17 patients, VF was induced at least once in 7 patients, and no sustained ventricular arrhythmia could be induced on completion of the EPS protocol at least once in 14 patients. Changes in VT inducibility over time are shown in Fig 1⇓. At baseline, all patients had sustained VT induced. At the follow-up studies, no sustained arrhythmia could be induced in 9% of patients at 1 month, 27% at 12 months, and 31% at 24 months. The proportion of patients in whom sustained VT could be induced was significantly reduced at the 1-month follow-up visit (P<.05) and remained similar thereafter. The proportion of patients maintaining their initial EPS status as a function of time is shown in Fig 2⇓ (top). The proportion of patients with sustained VT always inducible declined progressively over time. Noninducibility of VT did not predict persistent noninducibility of VT. Sustained VT was induced at least once during a subsequent follow-up visit in 12 of the 14 patients in whom no sustained ventricular tachyarrhythmia could be induced during a follow-up EPS. The remaining 2 patients did not have further follow-up EPS (1 death, 1 refusal).
The arrhythmias induced during follow-up and the reproducibility of VT induction were similar in the 32 patients with and the 5 without coronary artery disease. The 32 patients with coronary artery disease underwent 144 follow-up EPSs, during which sustained monomorphic VT was induced in 102 (71%), VF was induced in 17 (12%), and no sustained ventricular arrhythmia could be induced in 25 (17%). Sustained monomorphic VT was always induced during follow-up EPS in 17 patients (53%). In the remaining 15 patients, VF was induced at least once in 5 patients, and no sustained ventricular arrhythmia could be induced at least once on completion of the EPS protocol in 12 patients.
The clinical characteristics of group 1 patients in whom VT always remained inducible are compared with the group 1 patients in whom sustained arrhythmia was not inducible at least once during follow-up EPS (Table 4⇓). Patients in whom VT always remained inducible tended to be older than patients in whom VT was sometimes noninducible (P=.06). Significant differences in other patient characteristics or electrophysiological parameters were not observed between the two subgroups. The dose of antiarrhythmic drug was reduced in 7 patients during follow-up, but this was not associated with changes in VT inducibility. Ventricular stimulation thresholds and ventricular effective refractory periods of the 14 group 1 patients who were sometimes noninducible were similar for episodes when sustained VT was inducible and episodes when VT was not inducible (Fig 3⇓). The data in Fig 3⇓ are derived from EPSs before and after the EPS that demonstrated noninducibility.
Variation in VT morphology was noted over time. Only 38% of patients had sustained VT with morphology similar to that of the baseline VT during all follow-up visits, whereas 59% of episodes of sustained VT during all follow-up visits were of similar morphology. The morphology of the baseline VT did not predict the likelihood of inducing VF or the likelihood that no sustained arrhythmia would be induced over time.
During the baseline EPS, sustained monomorphic VT was induced with one extrastimulus in 6 patients (16%), two extrastimuli in 11 patients (30%), and three extrastimuli in 20 patients (54%). Only 10 patients (27%) always had VT induced during follow-up visits with the same number of ventricular extrastimuli that induced VT at the baseline visit.
Spontaneous VT Characteristics in Group 1 Patients
During follow-up, 1356 episodes of spontaneous VT occurred in 35 patients. Telemetry data, including VT cycle length, were available for 138 episodes. The VT cycle length of spontaneous episodes was 356±51 ms and did not change substantially over time. Spontaneous VF, as defined by device programming, occurred 108 times in 17 patients, and telemetry data confirming VF were available for 13 episodes. The mean cycle length of spontaneous episodes of VF was 250±31 ms.
Correlation Between Inducibility of VT and Spontaneous VT in Group 1 Patients
Patients in whom VT was not inducible at least once during follow-up were less likely to experience spontaneous episodes of VT over time (Fig 4⇓, P=.05). In contrast, the probability of experiencing spontaneous VT over time did not change for patients in whom VT remained inducible at each follow-up visit (Fig 4⇓, P=NS).
Reproducibility of Noninducibility of VT Over Time in Group 2 Patients
In the 18 group 2 patients, no sustained ventricular tachyarrhythmia could be induced on completion of the predischarge EPS protocol. In 7 patients (39%), nonsustained VT was induced at this study. The 18 patients in group 2 underwent 86 noninvasive EPSs during follow-up. During the follow-up EPSs, sustained monomorphic VT was induced in 19 (22%), VF was induced in 8 (9%), nonsustained VT was induced in 9 (11%), and no ventricular arrhythmia was induced in 50 (58%). No sustained arrhythmia could be induced during all follow-up visits in 9 patients (50%). In the remaining 9 patients, sustained VT was induced at least once in 7, sustained VT was induced twice in 5, and VF was induced at least once in 4. Changes in inducibility over time are shown in Fig 5⇓. The proportion of patients persistently noninducible decreased during the first year of follow-up (P<.05). The proportion of patients maintaining their initial EPS status as a function of time is shown in Fig 2⇑ (bottom). The proportion of patients with sustained VT always noninducible declines progressively over time. The clinical characteristics of the group 2 patients in whom VT always remained noninducible are compared with the group 2 patients in whom sustained VT was inducible at least once during follow-up EPS (Table 5⇓). Significant differences were not observed between the two subgroups.
Correlation Between Noninducibility of VT and Spontaneous VT in Group 2 Patients
During follow-up, 389 episodes of spontaneous VT/VF occurred in 9 patients. In another 3 patients, spontaneous events with RR intervals less than the tachycardia detection interval were documented to be sinus tachycardia in 2 patients and atrial flutter in the third patient. The proportion of group 2 patients experiencing spontaneous VT during follow-up was significantly lower in patients in whom VT/VF remained noninducible over time (11%) compared with the group 2 patients in whom VT or VF was induced during at least one follow-up EPS (89%, P=.003). The probability of experiencing spontaneous VT/VF over time is shown for the two subgroups in Fig 6⇓. The probability of experiencing spontaneous VT/VF was substantially lower in patients with VT always noninducible than in those in whom VT could be induced sometimes (Fig 6⇓, P=.002).
This study assessed patients with inducible sustained VT at baseline and showed considerable variability of VT induction over a period of 24 months. Although many patients have no sustained arrhythmia induced during at least one follow-up EPS, this observation does not predict persistent noninducibility of VT over time. However, the occurrence of noninducibility of VT is associated with a reduced probability that spontaneous VT or VF will occur subsequently. This study also assessed patients in whom sustained VT or VF was not inducible at the noninvasive baseline EPS. They also showed variability of VT induction over 24 months. Importantly, persistent noninducibility was associated with a very low occurrence of spontaneous VT or VF in this group, whereas inducibility of VT/VF at least once during follow-up identified patients who were more likely to experience spontaneous VT or VF.
Inducibility of VT at Baseline
Patients with sustained VT inducible at the baseline noninvasive EPS were more likely to have sustained a prior myocardial infarction and had more impaired left ventricular function than group 2 patients. Thus, group 1 patients were more likely to have the substrate required for initiation of VT than group 2 patients. The lower left ventricular ejection fraction observed in group 1 patients may have been a factor contributing to the higher proportion of group 1 patients requiring epicardial patches compared with group 2 patients.
Reproducibility of VT Induction
A number of investigators have evaluated the reproducibility of VT induction over short periods of time. During invasive EPS, the immediate reproducibility of VT induction ranges from 77% to 100%.8 9 10 Greater variability of VT induction has been reported when investigators compare the day-to-day reproducibility of VT induction.5 6 7 9 Less information about the reproducibility of VT induction is available over the long term. Schoenfeld et al11 repeated EPSs a mean of 18 months apart in 17 patients with inducible VT in the absence of antiarrhythmic drug therapy. VT was initiated at both EPSs in 71% of patients and in all patients with coronary artery disease. However, these investigators included nonsustained VT as an end point. Reproducibility of the induction of sustained VT was only 60%. Miles et al12 performed serial noninvasive EPSs in 11 patients after implantation of a low-energy synchronized cardioverter. In 2 of these patients, VT could not be induced during several follow-up EPSs. In the present study, sustained VT was induced during 72% of follow-up visits over 16±13 months in patients in whom sustained VT was induced at baseline. Inability to induce sustained VT in the present study was noted in those with and without coronary artery disease and previous myocardial infarction. Although 58% of these patients were on chronic antiarrhythmic drug therapy during the follow-up studies, the inability to induce sustained VT was noted in patients receiving antiarrhythmic therapy as well as those not receiving antiarrhythmic therapy.
Predictors of Noninducibility of VT
We did not identify any clinical characteristics that predicted the probability that VT would be noninducible over time. Other investigators have suggested that the induction of VT is likely to be more reproducible in patients with coronary artery disease.5 11 However, Volgman et al15 recently reported that the reproducibility of inducibility of sustained VT is similar in patients with and without coronary artery disease. Similar results were found in the present study. The probability of inducing VT decreases over time after a myocardial infarction in experimental models as well as in humans.16 17 18 The probability of a recurrence of spontaneous VT also decreases over time after a myocardial infarction.19 Variability of VT induction or recurrence after myocardial infarction reflects changes in the electrophysiological substrate associated with healing and remodeling of the myocardium.17 In the present study, time of implantation of the ICD averaged 85±102 months after the index myocardial infarction. Thus, it is unlikely that ventricular remodeling contributed substantially to variability of VT induction. Furthermore, failure to induce VT at one follow-up study did not predict persistent noninducibility of VT during subsequent follow-up studies.
Serial EPSs were performed noninvasively, and impulses were delivered to the heart via epicardial or endocardial pacing leads. Maturation of the tissue-electrode interface over time might have contributed to changes in inducibility of VT.20 During the short term, we observed a loss of the ability to induce VT in patients in whom the electrode catheter is left in situ.6 Against this hypothesis, however, we did not observe significant changes in mean pacing thresholds in the study population, nor did we observe differences in ventricular pacing thresholds during visits when sustained VT was inducible and visits when sustained VT was not inducible. Moreover, pacing during programmed stimulation protocols was performed at 5.4 V and 1.0 ms, which was at least 5 times the pulse duration stimulation threshold that would be expected to overcome changes in the tissue-electrode interface.21 It is possible that the high stimulus current strength used for the EPS facilitated the induction of VT and resulted in the induction of nonclinical arrhythmias.21 Such high current strengths have also been reported to prevent the induction of VT in some patients.21 Other investigators have reported that nonreproducibility of VT induction is observed predominantly when three or four ventricular extrastimuli are required to induce VT at baseline.5 9 In the present study population, however, the number of extrastimuli used at baseline was not a significant predictor of noninducibility of VT over time. During the noninvasive EPS, ventricular stimulation could be performed from only one site. The site of ventricular stimulation varied among patients but was the same in a given patient over time. Thus, the ability to perform programmed stimulation at only one ventricular site might explain differences in reproducibility of inducibility of VT in the present study compared with studies in which programmed stimulation was performed at two ventricular sites.22 23
No significant variability was found in ventricular effective refractory periods, which might explain variability of inducibility of VT. Of course, the ventricular effective refractory period reflects the electrophysiology of tissue at the stimulation site, which might be quite distant from the reentrant circuit involved in VT. Therefore, changes in the electrophysiological properties of the distant reentrant circuit could explain variation in the induction of VT over time.16 17 24 25 26 The autonomic nervous system also influences arrhythmogenesis, and it is possible that changes in autonomic tone might have influenced the inducibility of VT.27 28 Measures of autonomic nervous system function were not evaluated in the present study. Finally, hemodynamic status might change over time and influence the arrhythmogenic substrate.29 30
Spontaneous Arrhythmia Events
We observed an association between inducibility of VT over time and the occurrence of spontaneous VT/VF. This association implies that the electrophysiological substrates for induced VT and spontaneous VT change in parallel. Patients with persistent inducibility of VT may have a robust arrhythmogenic substrate, whereas patients in whom VT sometimes cannot be induced may have an evanescent electrophysiological substrate that can be transiently primed by factors such as ischemia, neurohumoral substances, or hemodynamic alterations.16 17 24 25 26 27 28 29 30 Such a distinction in arrhythmogenic substrate may be important in developing preventive therapeutic strategies. Interestingly, the small subgroup of patients in whom a ventricular tachyarrhythmia could never be induced had a very low probability of experiencing spontaneous VT/VF. If these results can be confirmed in a larger patient population, this finding may identify a group of patients who are at extremely low risk of arrhythmic death and do not require ICD replacement when the device reaches its end-of-life indicators.
Our study population is heterogeneous, although the majority of patients had coronary artery disease. Previous studies assessing reproducibility of VT induction have been performed in the antiarrhythmic drug–free state.6 7 8 9 10 11 In the present study, some patients were on chronic antiarrhythmic drug therapy either for the purpose of reducing the frequency of spontaneous VT or to slow the VT rate and increase the efficacy of pacing therapies. However, the use of antiarrhythmic drug therapy did not predict the development of noninducibility in our study, nor does it predict occurrence of spontaneous events.31 Group 1 patients were also more likely to be receiving antiarrhythmic drug therapy, which may have made patients more susceptible to the induction of VT.32 This is improbable, since these patients were more likely to present with spontaneous VT and also were more likely to have VT induced at the invasive antiarrhythmic drug–free EPS than group 2 patients.
The EPS protocol was limited to the introduction of three ventricular extrastimuli, which was the maximum number that could be delivered by the ICD. It is possible that the incidence of noninducibility of VT would have been lower if four ventricular extrastimuli were introduced.9 Nevertheless, the number of extrastimuli required to induce VT at the baseline EPS did not predict the development of noninducibility.
The episodes of spontaneous VT were determined via ICD telemetry. Wherever possible, we confirmed that episodes were VT/VF via clinical correlation and ambulatory monitoring. However, stored electrograms were not available in most devices to confirm that the arrhythmias were ventricular in origin, and RR interval information was available only on the most recent episode of VT or VF. Furthermore, local electrogram characteristics may be similar in some supraventricular and ventricular arrhythmias, and an intraventricular conduction may develop during some episodes of supraventricular tachycardia.33 Thus, some spontaneous episodes classified as VT/VF may have been supraventricular.
The intermittent inability to induce sustained VT in patients in whom VT was induced at baseline was associated with a reduction in the probability of occurrence of spontaneous VT/VF compared with those with persistent inducibility. Persistent noninducibility was associated with a very low probability of occurrence of spontaneous VT/VF. These observations suggest that the electrophysiological substrates for induced and spontaneous VT change in parallel over time.
This study was supported by the Medical Research Council of Canada (PG-11188) and the Heart and Stroke Foundation of Ontario. Dr Gillis is a Scholar and Dr Duff is a Medical Scientist of the Alberta Heritage Foundation for Medical Research. Dr Klein is an Established Career Investigator of the Heart and Stroke Foundation of Ontario. We thank Marilyn Devlin for manuscript preparation, the electrophysiology staff at Foothills Hospital for help with data collection, and Margot McDonald, BN, for help with the data analysis.
- Received August 16, 1994.
- Revision received November 22, 1994.
- Accepted December 3, 1994.
- Copyright © 1995 by American Heart Association
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