Prognosis in Patients with Left Ventricular Dysfunction and Ventricular Tachycardia Following Programmed Ventricular Stimulation

We performed programmed ventricular stimulation on 69 patients with left ventricular ejection dysfunction (ejection fraction < 50%) and clinically recognized ventricular tachycardia including 28 patients with sustained ventricular tachycardia and 41 patients with nonsustained ventricular tachycardia. An inducible arrhythmia (> 6 beats ventricular tachycardia) was found in 74% of patients. Patients with clinically sustained arrhythmias were frequently inducible (89%) with a high incidence of inducible monomorphic ventricular tachycardia (82%). Patients with clinically nonsustained ventricular tachycardia had a lower rate of inducibility (63%) including a high incidence of inducible polymorphic ventricular tachycardia (27%). Inducible patients with left ventricular dysfunction and ventricular tachycardia had a low incidence of electrophysiologically demonstrated effective drug therapy (16%). However, if an effective drug was found, the prognosis was good. Empirical drug therapy was associated with a poor prognosis in inducible and noninducible patients. Finally, an unfavorable prognosis was associated with a clinically sustained arrhythmia, a lower ejection fraction, and the presence of a left ventricular aneurysm. An inducible arrhythmia did not predict an unfavorable course. Indeed, patients with noninducible ventricular tachycardia in this group of patients were still at risk for sudden cardiac death.     

Encainide for the Treatment of Refractory Ventricular Tachycardia in Patients Undergoing Programmed Electrical Stimulation

Encainide was evaluated in 26 patients undergoing programmed electrical stimulation (PES) for ventricular arrhythmias. These patients had inducible symptomatic ventricular tachyarrhythmias during baseline PES and had previously failed a mean of 3.2 antiarrhythmic agents. Encainide was discontinued in six patients prior to PES because of spontaneous ventricular tachycardia (VT) (five patients) and adverse effect (one patient). Encainide increased, the PR, QRS, QTc intervals, and right ventricular effective refractory period (RVERP) significantly from baseline (P < 0.05) in 16 patients who were extensive metabolizers. Encainide, at a mean dose of 110 ± 28 mg/day increased the ventricular tachycardia cycle length (VTCL) from 278 ± 77.1 msec to 334 ± 68.8 msec (P < 0.05). Encainide alone was effective (< 15 beats induced) or partially effective (converting inducible sustained VT to < 15 beats asymptomatic nonsustained VT or increasing the VTCL < 100 msec with no symptoms) in two and seven patients respectively. In seven patients, encainide was also reevaluated at a higher dose (mean dose 148 ± 22 mg/day), but this dose did not significantly alter the overall response or measured parameters. Seven patients were subsequently evaluated on combination of encainide and another antiarrhythmic agent. The combination was effective in three patients and partially effective in three patients. Serum concentrations were measured during each testing period; a moderate correlation was observed between the PR and RR intervals and total concentrations in patients who were extensive metabolizers. Eleven patients who were effective or partially effective during acute testing were placed on long-term encainide therapy (three patients alone and eight patients on combination therapy). In a mean follow-up of 8.9 months (1–25 months) encainide was discontinued in five patients (two patients due to nonsudden cardiac death, one patient due to recurrent nonfatal VT, and two patients due to side effects of combination therapy.) Conclusion: Encainide alone is minimally effective (7.7%) for preventing inducible ventricular tachycardia, but partially effective in 38.9%. Retesting at a higher dose does not offer any additional benefit. However, encainide in combination with another antiarrhythmic agent may improve the response in patients who remain inducible on encainide alone. Further studies are needed to verify this observation.     

Idiopathic Left Ventricular Aneurysm: An Unusual Substrate of Ventricular Fibrillation and Ventricular Tachycardia

Idiopathic left ventricular aneurysm (LVA) is a very rare clinical condition. This article describes a patient with idiopathic LVA associated with episodes of ventricular tachycardia and ventricular fibrillation. Clinical and instrumental examinations did not reveal the pathogenesis of the aneurysm. The malignant clinical course suggests that an aggressive antiarrhythmic treatment, including ICD implantation, may be warranted.     

Ultrarapid Train Stimulation Versus Conventional Programmed Electrical Stimulation for Induction of Ventricular Arrhythmias in Patients with Coronary Artery Disease

Conventional programmed electrical stimulation (PES) of the ventricle isuseful for establishing inducibility or noninducibility of clinicalventricular arrhythmias (VA) but is complex and time consuming. The presentstudy was designed to compare a standard PES protocol with an alternativemethod using ultrarapid train stimulation in patients with VA and coronaryartery disease (CAD). A prospective, randomized, crossover design was used.During each session in the electrophysiology laboratory, patients werestudied using both the trains and PES protocols in randomized order. In 82matched pairs of comparisons in 50 patients, results were concordant in85% (p < 0.0001). There were no differences related to type ofclinical arrhythmia or to the presence of antiarrhythmic drugs. There wereno significant differences in the induction of nonclinical arrhythmias withthe two methods (p < 0.0001 for concordance). There were no significantdifferences related to the cycle length of the trains (10, 20, or 30 ms,equivalent to 100, 50, or 33 Hz). The number of drive-extrastimuli sequencesand the time required to complete the trains protocol was significantlyshorter (p < 0.0001) using trains versus PES. Ultrarapid train stimulationprovides results in CAD patients that are comparable with those ofconventional PES protocols. There is a significant savings in time, addingpractical value to intrinsic electrophysiologic interest. Trains may beuseful when multiple inductions are desirable, for example, in the settingof antitachycardia pacing parameters in an implantable defibrillator (ICD),during ICD implantation, or in other circumstances where the main questionis inducibility of ventricular arrhythmias.     

Case Report: Adenosine Induced Ventricular Fibrillation in a Patient with Stable Ventricular Tachycardia

Adenosine is frequently used in emergency departments and intensive care units for the termination of narrow complex tachycardias. Recently its utility in terminating wide complex tachycardias has been reported in the literature. Adenosine is generally felt to be a safe medication even though its proarrhythmic effects in the setting of narrow complex or supraventricular tachycardias have been well documented. Herein, we describe the first case to our knowledge of adenosine inducing ventricular fibrillation in a patient with a stable wide complex tachycardia that was subsequently proven to be ventricular tachycardia at electrophysiologic study.     

Long-term Reproducibility of Response to Noninvasive Programmed Cardiac Stimulation in Spontaneous, Sustained Ventricular Tachycardia Treated with Amiodarone Therapy

A total of 73 noninvasive serial electrophysiological studies were carried out in 12 patients with spontaneous sustained ventricular tachycardia, inducible in spite of chronic treatment with amiodarone, in order to verify the effect of this drug on the long-term reproducibility of the test. A ventricular tachycardia was induced in 72 of 73 times; in 59% of cases, the clinical form was induced. In 8 of 12 patients, two or more types or morphologies of ventricular tachycardia could be induced. The induction modes (driving rate and number of extrastimuli) changed considerably in different studies. During a follow-up of 12 ± 6 months, 5 out of 12 patients had spontaneous relapses. We observed no differences between these patients and the others regarding inducibility, types and morphologies of the induced tachycardias, or induction modes. Therefore, when ventricular tachycardia is inducible in spite of chronic amiodarone therapy, it is always inducible during follow-up, even if a great intrapatient change of type and the morphology of induced tachycardias and induction modes is observed. However, since similar electrophysiological features are present in patients with and without spontaneous recurrence of ventricular tachycardia, serial electrophysiological studies are of little value in predicting the clinical outcome.     

Value of Programmed Ventricular Stimulation in Patients with Congenital Heart Disease

INTRODUCTION: The role of programmed ventricular stimulation (VSTIM) for risk stratification in congenital heart disease is unclear. We analyzed the results of VSTIM in selected congenital heart disease survivors at a single center to determine whether it improved the ability to predict a serious outcome. METHODS AND RESULTS: Between July 1985 and September 1996, 140 primary VSTIM studies were performed on 130 patients (median age 18.1 years, range 0 to 51). Tetralogy of Fallot (33 %), d-transposition of the great arteries (25 %), and left ventricular outflow tract obstruction (12%) accounted for the majority of patients. Indications included spontaneous ventricular tachycardia (VT) of > or = 3 beats (72%) and/or symptoms (68%). Sustained VT was induced in 25% of the studies, and nonsustained VT in 12%. Atrial flutter or other supraventricular tachycardia was documented in 32% and bradyarrhythmias in 26%. By univariate analysis, mortality was increased in patients with positive VSTIM versus negative VSTIM (18% vs 7%, P = 0.04). Using multivariate analysis, positive VSTIM was associated with a sixfold increased risk of decreased survival and a threefold increased risk of serious arrhythmic events, allowing up to 87% sensitivity in predicting mortality. However, 7 (33%) of 21 patients with documented clinical VT had false-negative studies. CONCLUSION: VSTIM in a large, selected group of congenital heart disease patients identified a subgroup with significantly increased mortality and sudden arrhythmic events. Failure to induce VT was a favorable prognostic sign, but the frequency of false-negative studies was high. Frequent supraventricular tachycardia further complicated risk stratification. Although VSTIM appears to be a reasonable tool for evaluation of this population, a larger, multicenter trial is recommended to clarify its utility.     

Prospective Clinical Evaluation of Programmed Atrial Stimulation Protocol for Induction of Sustained Atrial Fibrillation and Flutter

We sought to define a minimum standardized protocol for induction of atrial fibrillation [AF] and/or atrial flutter. In contrast to ventricular stimulation protocols, a stimulation protocol for induction of AF or atrial flutter has not been critically evaluated. Since suppression of inducible AF or atrial flutter is used as one of the endpoints of success of pharmacologic and ablation therapies, there is an obvious need to define minimally appropriate electrical stimulation protocol for induction of AF or atrial flutter. We prospectively evaluated 70 patients, 44 with spontaneous atrial flutter or AF and 26 controls without documented atrial arrhythmias. A standardized programmed stimulation protocol, which employed up to three atrial extrastimuli delivered at two atrial sites at two atrial drive pacing lengths, was used in attempt to reproduce sustained AF and atrial flutter. The study endpoint was induction of sustained (>30 s) AF or atrial flutter. Sustained AF or atrial flutter was induced in 39/44 (89%) patients and 2/26 (7%) of controls (p <0.01). The arrhythmia induced was atrial flutter in 19/21 (91%) of atrial flutter patients, AF in 17/18 (94%) AF patients, both atrial flutter and AF in 5 AF/atrial flutter patients (100%). Two patients with atrial flutter had both AF/atrial flutter and 1 patient with AF had atrial flutter induced. The arrhythmia was induced from first stimulation site in 37 patients (85%) using a single in 9 (20%) patients, double 18 (41%) patients and triple extrastimuli in 10 (23%) patients. Two patients (5%) required stimulation from second site with two and three extrastimuli, respectively. The overall sensitivity and specificity of this stimulation protocol were 89% and 92%, respectively with a positive predictive accuracy of 95%.Conclusions. 1. Up to three atrial extrastimuli and two atrial sites are needed to increase yield of AF/atrial flutter induction at electrophysiologic study. 2. Induction of either AF or atrial flutter correlates well with presence of a similar spontaneous arrhythmia. 3. A baseline determination of the induction mode may be desirable prior to evaluation of interventions directed at AF or atrial flutter.     

Electrocardiographic and Clinical Precursors of Ventricular Fibrillation: Chain of Events

Precursors of VF. Ventricular fibrillation is the final event in the majority of cases of sudden death. The ECG and clinical precursors of ventricular fibrillation are discussed in this article. Ventricular fibrillation usually appears as a consequence of a chain of events that leads to the appearance of this lethal arrhythmia. We review the markers of the vulnerable myocardium prone to ventricular fibrillation, the triggers and modulators that act on this vulnerable myocardium, and the event(s) that constitute the final step preceding this arrhythmia. The final step may be as unique as a sudden waterfall or present as a cascade of successive phenomena.     

Mapping and Ablating Ventricular Premature Contractions That Trigger Ventricular Fibrillation: Trigger Elimination and Substrate Modification

Ventricular fibrillation (VF) is a malignant arrhythmia, usually initiated by a ventricular premature contraction (VPC) during the vulnerable period of cardiac repolarization. Ablation therapy for VF has been described and increasingly reported. Targets for VF triggers are VPC preceded Purkinje potentials or the right ventricular outflow tract (RVOT) in structurally normal hearts, and VPC triggers preceded by Purkinje potentials in ischemic cardiomyopathy. The most important issue before the ablation session is the recording of the 12‐lead electrocardiogram (ECG) of the triggering event, which can prove invaluable in regionalizing the origin of the triggering VPC for more detailed mapping. In cases where the VPC is not spontaneous or inducible, ablation may be performed by pacemapping. During the session, mapping should be focused on the earliest activation and determining the earliest potential is the key to a successful ablation. However, a modification of the Purkinje network might be applied when the earliest site cannot be determined or is located close to the His‐bundle. Furthermore, the electrical isolation of the pulmonary artery (PA) can suppress RVOT type polymorphic ventricular tachycardia in some patients with rapid triggers from the PA. Suppression of VF can be achieved by not only the elimination of triggering VPCs, but also by substrate modification of possible reentry circuits in the Purkinje network, or between the PA and RVOT. Further studies are needed to evaluate the precise mechanisms of this arrhythmia.     

Divergence of Endocardial QT Interval Components during Programmed Electrical Stimulation Including Observations during Induction of Sustained Ventricular Tachyarrhythmias

Measurements were made in 12 normal subjects and during induction ofsustained ventricular tachyarrhythmias in 31 patients with remote myocardialinfarction. QT interval measurements were made semiautomatically withcomputer assistance and the total QT interval was divided into early (QT 1 )and late (QT 2 ) components. QT intervals and QT interval dispersion betweentwo right ventricular endocardial sites were plotted against the degree ofprematurity of the last extrastimulus (S 2 , S 3 , or S 4 ). In the controlgroup, total QT and QT 1 intervals shortened with increasing prematurity ofthe last extrastimulus (p , 0.001). Slopes (positive) were steeper withfaster pacing rates (600, 500, or 400 ms) and more extrastimuli (1 to 3).The relationship between QT 2 intervals and prematurity of the lastextrastimulus was flat, but the slope was slightly negative (p=0.05to,0.001) and did not vary with changes in pacing cycle length or number ofextrastimuli. QT interval dispersion in the control group was minor(95% CI 0-40 ms). During induction of sustained ventriculartachyarrhythmias, total QT and QT 1 intervals were longer (y intercepts)than in the control group (p , 0.05 at 400-ms pacing cycle length) and theirdispersion was increased (p , 0.05). Generally, QT 2 intervals were shorter(p , 0.05 at 600-ms pacing cycle length) during induction of ventriculararrhythmias in comparison with the control group but dispersion wasincreased (p , 0.05 at 400-ms pacing cycle length). QT intervals and QTinterval dispersion show an orderly and predictable relationship withprematurity of the last extrastimulus in normal subjects. These patternsdiffer during induction of sustained ventricular tachyarrhythmias. Suchdifferences may be exploited to derive clinically predictive and usefulmeasurements.     

Atrial Fibrillation/Flutter Induced by Implantable Ventricular Defibrillator Shocks:

Atrial Fibrillation/Flutter Induced by Defibrillator Shocks. Introduction : We evaluated the incidence and energy dependence of atrial fibrillation/flutter (AF) induced by implantable ventricular defibrillator shocks in 63 patients tested in the operating room or electrophysiology laboratory.
Methods and Results : Defibrillator shocks were epicardial monophasic in 32 patients, and through an Endotak® lead endocardial monophasic in 19 and biphasic in 12 patients. The epicardial and endocardial patient groups had similar clinical characteristics. A total of 517 defibrillator shocks were given. The epicardial group received 336 total defibrillator shocks and 10 ± 6 shocks (mean ± SD) per patient compared with the endocardial group, which received 181 total shocks and 6 ± 4 defibrillator shocks per patient (P = 0.004). In the epicardial group, AF occurred in 13 (41 %) patients and in 17 (5%) of the 336 shocks. No AF was induced with endocardial defibrillator shocks. The epicardial mean energy was 16 ± 9 J, lower than the endocardial mean energy of 20 ± 9 J (P < 0.004). In the epicardial monophasic group, energy correlated with AF induction. Each patient received 7 ± 6 defibrillator shocks < 15 J and 4 ± 2 shocks ≥ 15 J, yet AF occurred in only 2.3% versus 9.6% (P < 0.05) of defibrillator shocks < 15 J and ≥ 15 J, respectively. Of note, AF was not induced with energy < 4 J or > 31 J.
Conclusions : In the epicardial configuration, AF induction is energy dependent, with an apparent lower and upper limit of vulnerability. AF induction by defibrillator shocks delivered through an Endotak lead is very rare, possibly related to an apparent upper limit of vulnerability of less energy, avoidance of thoracotomy, or different energy field distribution.     

Idiopathic Ventricular Fibrillation

Idiopathic Ventricular Fibrillation. Idiopathic ventricular fibrillation is defined as cardiac arrest in the absence of structural heart disease and other identifiable causes of ventricular fibrillation. It occurs in 1% to 9% of survivors of out-of-hospital cardiac arrest. The mean age of these patients is 35 to 40 years, and 70% to 75% are male. The pathogenesis is unknown; psychosocial factors may play a role. Baseline clinical characteristics have not been found to identify the 20% to 30% of patients who will have recurrent cardiac arrest. At present, implantation of an automatic defibrillator is the treatment of choice. Two registries have been established to enhance our knowledge of this unusual catastrophic entity.     

Muscarinic Receptor Stimulation with Edrophonium Hydrochloride Does Not Elevate Ventricular Fibrillation Thresholds in Humans

INTRODUCTION: Although decreased vagal tone, as measured by heart rate variability is a risk factor for ventricular fibrillation (VF) and sudden cardiac death, it is unknown whether increasing vagal tone has an antiarrhythmic effect. The purpose of this study was to determine whether edrophonium hydrochloride (HCI), a vagomimetic agent, increases VF threshold. METHODS AND RESULTS: Twenty-eight consecutive patients with previously implanted defibrillators had two inductions of VF by monophasic direct-current shocks delivered at 10 to 30 msec after the T wave peak, escalating energies (0.4, 1, then 3 J) until VF was induced. If VF was not induced, this protocol was repeated at the T wave peak and then at 10 to 30 msec before the T wave until VF was induced. Patients were randomized to receive edrophonium HCl (12 to 18 mg) or no drug before repeating the protocol for the second VF induction. The mean sinus cycle length increased from 782 to 872 msec in the group receiving edrophonium HCI (P = 0.006 ). In the control group, the mean sinus cycle length remained unchanged (838 vs 858 msec). The mean energy to induce VF, coupling interval relative to the T wave, and the number of attempts to induce VF were not different between VF induction attempts 1 and 2, and they were not different between the group receiving edrophonium HCl and the control group. CONCLUSION: In a sedated patient population with implantable defibrillators, edrophonium HCI infusion prolongs sinus cycle length but does not change inducibility of VF using T wave shocks.     

Potassium and Magnesium Changes Associated with Programmed Electrical Stimulation

Serum potassium and magnesium concentrations decrease secondary to an increase in catecholamine concentrations. We hypothesized that during programmed electrical stimulation (PES), where stress of the procedure may elevate catecholamine levels, potassium and magnesium concentrations would decrease. To test this hypothesis, potassium and magnesium concentrations were measured at baseline, during, and after PES in 16 patients. Potassium concentrations (mean ± standard deviation) decreased from 4.5 ± 0.3 (mEq/L) at baseline to 3.9 ± 0.2 during PES (P < 0.05). At 2 hours post-PES, serum potassium concentrations returned to baseline values (mean 4.2 ± 0.5 mEq/L, P > 0.05 compared to baseline). Mean magnesium concentrations (mmol/L) decreased from 0.84 ± 0.07 at baseline to 0.81 ± 0.07 at the end of PES (P < 0.05) but did not decrease significantly during PES.
In conclusion, potassium concentrations decreased significantly during PES, whereas magnesium concentrations decreased slightly but significantly at the end of PES. These changes in electrolyte concentrations may be due to catecholamine influence secondary to the PES procedure. In light of these observations, serum concentrations of potassium and magnesium should be normalized prior to PES procedure in order to prevent hypokalemia and hypomagnesemia.     

Antiarrhythmic Efficacy of Oral Sotalol in Patients with Sustained Ventricular Tachycardia or Ventricular Fibrillation Postmyocardial Infarction

In order to assess the antiarrhythmic efficacy of oral sotalol we studied 46 patients with sustained monomorphic ventricular tachycardia (n = 40) or ventricular fibrillation (n = 6) by programmed ventricular stimulation. All patients had coronary artery disease with a history of myocardial infarction. Prior to sotalol, patients were treated with a mean of 3.4 ± 1.4 antiarrhythmic Class I drugs. None of these drugs prevented sustained monomorphic ventricular tachycardia or ventricular fibrillation. During control programmed ventricular stimulation (PVS 1) ventricular fibrillation was induced in 7 patients (15%), sustained monomorphic ventricular tachycardia in 30 patients (65%), and nonsustained ventricular tachycardia in 9 patients (20%). After loading with oral sotalol (320 mg/day) programmed ventricular stimulation (PVS 2) was repeated 4.2 ± 3.3 weeks after PVS 1. Ventricular fibrillation was not inducible in any of the patients; in 10 patients (22%) sustained monomorphic ventricular tachycardia was induced, and nonsustained ventricular tachycardia was induced in 10 patients (22%). In 26 patients (57%) either no response or a short ventricular response was inducible. Our data show that oral sotalol is an effective antiarrhythmic agent in patients with sustained monomorphic ventricular tachycardia or ventricular fibrillation following myocardial infarction.     

Unusual Overlapping Cardiac Sarcoidosis and Long-QT Type 3 Induced Ventricular Fibrillation

A 54-year-old woman had been resuscitated after ventricular fibrillation and her electrocardiogram showed a QT prolongation (QTc=510 ms), and genetic screening revealed a missense variant, R1644C, in the SCN5A gene. She was therefore diagnosed with congenital long-QT syndrome (LQTS) type 3. However, the patient had left ventricular dysfunction, and based on the findings of cardiac magnetic resonance imaging, positron emission tomography and pathological examinations, she was diagnosed with cardiac sarcoidosis. Although both are rare diseases, their overlapping presence in this case may have led to an increased cardiovascular risk compared with either alone. Thus, not only genetic but comprehensive clinical examinations are important for making a correct diagnosis.     

Pacing Threshold Testing Induced Ventricular Fibrillation Following Acute Rate Control of Atrial Fibrillation

Background: A properly placed stimulus on the T‐wave during ventricular repolarization can result in ventricular fibrillation (VF). Initiation of VF with pacing on T‐wave is a rare event with a few reported cases in the literature. We present a unique case of induced VF attributed to a pacing stimulus on T‐wave during ventricular pacing threshold testing of a permanent pacemaker. Case Report: A 64‐year‐old woman with persistent atrial fibrillation (AF) and a permanent pacemaker for tachycardia–bradycardia syndrome presented with symptomatic AF with rapid ventricular response. Acute rate control was achieved with intravenous diltiazem. During ventricular pacing threshold testing, noncapture occurred followed by a pacing spike on T‐wave initiating VF. Cardiopulmonary resuscitation and defibrillation converted the rhythm to rate‐controlled AF. An acute prolongation of the QT was noted and normalized within 12 hours. No antiarrhythmic medications were used. Postevent laboratory values were within normal limits. She was free of ischemia and an echocardiogram revealed normal left ventricular function. She recovered from the event and was discharged with rate‐controlled AF. No further pacing‐induced arrhythmias have occurred during follow‐up pacemaker interrogation and 12‐lead electrocardiograms continued to show normal QT intervals. Conclusion: Pacemaker‐induced VF is an extraordinarily rare complication of cardiac pacing. Alterations in ventricular repolarization with rapid slowing of the heart rate demonstrated by acute prolongation of QT intervals may play a role. This report should alert physicians to the possibility of QT prolongation and an increased risk of ventricular arrhythmias following acute rate control of AF.     

Idiopathic Ventricular Tachycardia and Fibrillation

Idiopathic Ventricular Tachycardia and Fibrillation. Important data have recently been added to our understanding of sustained ventricular tachyarrhythmias occurring in the absence of demonstrable heart disease. Idiopathic ventricular tachycardia (VT) is usually of monomorphic configuration and can be classified according to its site of origin as either right monomorphic (70% of all idiopathic VTs) or left monomorphic VT. Several physiopathological types of monomorphic VT can be presently individualized, according to their mode of presentation, their relationship to adrenergic stress, or their response to various drugs. The long-term prognosis is usually good. Idiopathic polymorphic VT is a much rarer type of arrhythmia with a less favorable prognosis. Idiopathic ventricular fibrillation may represent an underestimated cause of sudden cardiac death in ostensibly healthy patients. A high incidence of inducibility of sustained polymorphic VT with programmed ventricular stimulation has been found by our group, but not by others. Long-term prognosis on Class IA antiarrhythmic medications that are highly effective at electrophysiologic study appears excellentJfy Cardiovasc Electrophysiol, Vol. 4, pp. 356–368, June 1993 ).