Safety and Diagnostic Yield of Noninvasive Ventricular Stimulation Performed Via Tiered Therapy Implantable Defibrillators

Extensive electrophysiological testing is critical for the effective utilization of sophisticated tachycardia detection and termination algorithms available in tiered therapy ICDs. To evaluate the safety and diagnostic yield of electrophysiological testing via noninvasive ventricular stimulation, we performed 294 electrophysiological studies in 154 patients (age 65 ± 10; left ventricular ejection fraction 0.36 ± 0.15) with tiered therapy ICDs. Stimulation was performed under methohexital anesthesia. A total of 928 sustained ventricular tachyarrhythmias were induced (3.1 ± 2.5 per procedure); monomorphic VT, 550; ventricular flutter, 74; and VF, 246. The results of invasive and noninvasive programmed stimulation were compared for 79 patients wbo had both studies under similar treatment. Overall concordance iras 83%, and did not differ significantly between patients who bad the noninvasive stimulation via epicardial or endocardial pacing leads. VF could be induced in 206 of 257 studies (82%), and it was less likely to be induced in patients on amiodarone (74% vs 85%; P = 0.02), or beta blockers (55% vs 83%; P = 0.017). No patient presented a serious complication. Minor complications occurred during 39 studies; transient laryngospasm in 1, unintended delivery of an ICD sbock to a conscious patient in 4; induction of sustained atrial fibrillation in 8; need for external rescue defibrillation sbocks in 13; and delivery of inappropriate sbocks for supraventricular rhythms in 14 studies. Noninvasive ventricular stimulation performed under methobexital anestbesia is safe. Its diagnostic yield compares favorably with that of conventional electropbysiological studies. VF can be induced in a majority of patients. There is good correlation between invasive and noninvasive programmed stimulation for induction of VT. Noninvasive ventricular stimulation may emerge as standard procedure for the initial programming and follow-up of ICDs.     

Ventricular Fibrillation Induction Using Nonsynchronized Low Energy External Shock During Rapid Ventricular Pacing: Method of Induction When Fibrillation Mode of ICD Fails

Third-generation implantable cardioverter defibrillators (ICD) are frequently implanted with non-thoracotomy systems and provide noninvasive methods for electrical stimulation and ventricular fibrillation induction. These modalities facilitate postoperative testing of the ICD. Rapid right ventricular burst pacing via the defibrillator is commonly used for initiation of ventricular tachyarrhythmias. However, with the available third-generation devices, ventricular fibrillation (VF) induction may be impossible in up to 19% of the patients. In these cases, transvenous placement of a right ventricular catheter has been required to generate VF and appropriately evaluate the device. We report a new technique of noninvasive induction of VF using a low energy external nonsynchronized shock delivered during ICD fibrillation induction pacing. In three patients, after all efforts to induce VF by the Ventritex Cadence V-100 had failed, a 20 J nonsynchronized shock was delivered during rapid RV pacing. This resulted in VF on the first attempt in all patients. This noninvasive technique of VF initiation may provide a useful clinical approach to ICD testing that eliminates the costs and risks of an invasive procedure.     

Enhancement of myocardial vulnerability by atrial fibrillation

Certain groups are known to have an increased risk for sudden cardiac death. Epidemiologic studies have suggested that patients with atrial fibrillation may be at higher risk. The authors hypothesize that atrial fibrillation may increase myocardial vulnerability. To test this hypothesis, 37 dogs were studied using programmed electrical stimulation techniques to determine myocardial vulnerability as assessed by the ability to provoke ventricular tachycardia. Prior to atrial fibrillation, programmed electrical stimulation did not induce ventricular tachycardia. Aconitine was then topically applied to the right atrial appendage with care taken not to make contact with the ventricle. Application of aconitine caused atrial fibrillation with an increase in ventricular rate, but did not affect arterial blood pressure. Ventricular tachycardia was induced by programmed electrical stimulation studies in 25 of 26 dogs in atrial fibrillation. The enhanced vulnerability was noted following atrial fibrillation, not after aconitine application to the great veins, which did not cause atrial fibrillation. To further exclude the possibility that aconitine application may cause changes in ventricular threshold, atrial fibrillation was induced by pacing techniques in five dogs. Prior to atrial fibrillation induction, programmed electrical stimulation did not induce ventricular tachycardia. Following atrial fibrillation, ventricular tachycardia could be repeatedly induced. Mean heart rate following atrial fibrillation increased, while pacing animals at this increment in rate did not change the noninducibility of dogs in sinus rhythm. Six patients with a history of atrial fibrillation and ventricular tachycardia were studied to determine if AF lowered myocardial threshold to VT induction. Ventricular tachycardia could only be induced by PES techniques in four of five patients when the patients' rhythm was AF (P < 0.05). This study suggests that atrial fibrillation lowers myocardial threshold for ventricular tachycardia induction and thus enhances myocardial vulnerability. The association of AF with a higher incidence of sudden death may be due to an enhanced electrical instability.     

Inducibility of Sustained Ventricular Tachycardia in a Closed-Chest Ovine Model of Myocardial Infarction

The two goals of this study were (1) to develop a closed-chest animal model of monomorphic ventricular tachycardia; and (2) to investigate the effect of dual site pacing on inducibility of ventricular tachycardia. In the first part of the study, 10 of 14 sheep underwent successful induction of myocardial infarction by temporary balloon occlusion of the left anterior descending coronary artery. After a follow-up period of 21–43 days, sustained monomorphic ventricular tachycardia could be induced during programmed electrical stimulation using a "clinical" stimulation protocol in 8 of the 10 sheep. The number of ventricular tachycardia episodes per animal varied between 5 and 70. Ventricular fibrillation was never induced during programmed electrical stimulation. Ventricular tachycardia episodes lasted from 30 seconds up to 15 minutes and were terminated by antitachycardia pacing or DC cardioversion. In the second part of the study, the effect of dual site stimulation on ventricular tachycardia inducibility was investigated. High current stimuli from an area within the infarcted zone were given with the S1 programmed stimulation protocol. This dual site stimulation showed no effect on ventricular tachycardia induction during programmed electrical stimulation. This animal model shows a high induction rate of sustained monomorphic ventricular tachycardia in the chronic phase of myocardial infarction. The high incidence of ventricular tachycardia inducibility provides a reliable tool to study new techniques for the prevention of ventricular tachyarrhythmias.     

Ventricular Pacing Induced Ventricular Tachycardia in Patients with Implantable Cardioverter Defibrillators

Appropriately timed noncompetitive ventricular pacing potentially may initiate ventricular tachycardia in patients prone to these arrhythmias. The combination of bradycardia pacing and stored electrograms in a currently available cardioverter defibrillator provides an opportunity to evaluate the occurrence of such pacing induced ventricular tachycardia. During a surveillance period of 18.7 ± 11.4 months, stored electrograms documented 302 episodes of ventricular tachycardia in 77 patients. Five patients (6.5%) demonstrated 25 episodes (1–16 per patient) of ventricular tachycardia that were immediately preceded by an appropriately paced ventricular beat (8.3% of all episodes of ventricular tachycardia). All five patients had prior myocardial infarctions and a history of monomorphic ventricular tachycardia occurring both spontaneously and in response to programmed electrical stimulation. Antitachycardia pacing terminated pacing induced ventricular tachycardia in 22 episodes; in one episode antitachycardia pacing accelerated ventricular tachycardia. In two cases shock therapy was aborted for nonsustained ventricular tachycardia. We conclude that, in selected postinfarction patients with recurrent sustained monomorphic ventricular tachycardia treated with implantable cardioverter defibrillators, appropriately timed ventricular pacing may induce ventricular tachycardia.     

Direct Current Application: Easy Induction of Ventricular Fibrillation for the Determination of the Defibrillation Threshold in Patients with Implantable Cardioverter Defibrillators

For the determination of the defibrillation threshold, the induction of ventricular fibrillation is mandatory. However, in severely damaged hearts it is sometimes difficult to induce ventricular fibrillation by rapid stimulation or alternating current. Only rapid nonclinical ventricular tachycardias may result, and their cardioversion threshold may be different from the defibrillation threshold. Therefore, it was the purpose of this study to test the potential of direct current (DC) application to rapidly induce ventricular fibrillation in patients with an implanted cardioverter defibrillator. The defibrillation threshold had to be determined in 13 patients (9 with coronary heart disease, 4 with dilative cardiomyopathy, ejection fraction 35%) during and 2 weeks after the implantation of a cardioverter defibrillator. DC was applied 37 times by a commercially available 9-V DC battery via a bipolar catheter for about 3 seconds. Ventricular fibrillation was induced 23 times (62%) and rapid nonclinical ventricular tachycardias were induced six times (16%). In one patient clinical ventricular tachycardia was observed. In seven instances (19%) sinus rhythm remained. In 12 of the 13 patients, ventricular fibrillation could be induced by DC. Thus, the induction of ventricular fibrillation by DC application may serve as an additional tool to induce ventricular fibrillation, determining the defibrillation threshold in implantable cardioverter defibrillator patients.     

Promotion of Ventricular Tachycardia Induction by Procainamide in Dogs with Inducible Ventricular Fibrillation Late After Myocardial Infarction

The influence of procainamide on inducible ventricular tachyarrhythmias was evaluated in 35 dogs with experimental myocardial infarction, and 9 normal dogs. Programmed stimulation was performed from the right ventricular apex via a percutaneously positioned electrode catheter, using up to five extrastimuli before and after intravenous administration of procainamide (15 mg/kg). Procainamide levels in postinfarct dogs were 8.5 +/- 0.7 micrograms/mL (range 5.3-13.6 micrograms/mL). Procainamide exerted its greatest effect in postinfarct dogs with reproducible baseline ventricular fibrillation. Six of nine dogs (P less than 0.05) with ventricular fibrillation had sustained monomorphic ventricular tachycardia (cycle length: 147 +/- 4 msec) induced after procainamide administration. This ventricular tachycardia required significantly more extrastimuli than baseline ventricular fibrillation (3 +/- 0.3 extrastimuli before vs 4 +/- 0.3 extrastimuli after procainamide). Procainamide never converted ventricular fibrillation to ventricular tachycardia in normal dogs. Procainamide had minimal effect on inducible ventricular tachycardia after myocardial infarction. Ventricular tachycardia induction was abolished in only 2 of 17 dogs despite significant prolongation of electrophysiological parameters. Ventricular tachycardia cycle length, and the number of extrastimuli required were unchanged by procainamide in this subgroup. Conclusion: Ventricular tachycardia is insensitive to the antiarrhythmic properties of procainamide in this model. In contrast, procainamide is able to convert postinfarction ventricular fibrillation to ventricular tachycardia, presumably by promoting sustained, organized reentry. This previously undescribed action is an unusual form of proarrhythmic effect, and suggests that this drug should be used cautiously in patients after myocardial infarction.     

Clinical intracardiac electrophysiologic testing: technique, diagnostic indications, and therapeutic uses

Clinical cardiac electrophysiologic testing has evolved rapidly since 1968, when the technique was first described. In an electrophysiologic study, electrode catheters are positioned within the heart to record electrical activity from the atrium, atrioventricular conduction tissue, and ventricle. Programmed stimulation is then performed, which involves pacing of the atrium or ventricle and introducing critically timed premature stimuli during sinus rhythm or paced rhythm. The use of programmed stimulation in conjunction with intracardiac recordings in electrophysiologic studies has facilitated the diagnosis of mechanisms of arrhythmias and the assessment of therapy. Electrophysiologic testing is useful in selected patients with sinus node dysfunction, conduction system disorders, supraventricular tachycardia, ventricular tachycardia, or ventricular fibrillation and in survivors of out-of-hospital cardiac arrest and patients with symptomatic but unsubstantiated rhythm disturbances. Therapeutic approaches that can be assessed by electrophysiologic testing include serial drug testing to determine the effectiveness of antiarrhythmic agents, antitachycardia pacing, the implantable defibrillator, transcatheter ablation, and electrophysiologically guided surgical procedures. In this review, we discuss the methods of electrophysiologic testing, its clinical applications in diagnosing the various cardiac rhythm disturbances, and its use in assessing various therapeutic modalities.     

Idiopathic Ventricular Fibrillation in Out-of-Hospital Cardiac Arrest Survivors

This study examined diagnostic and therapeutic roles of electrophysiological testing and long-term clinical outcome after out-of-hospital cardiac arrest due to idiopathic ventricular fibrillation. This is defined as ventricular fibrillation occurring in the absence of detectable underlying heart disease or metabolic or electrolyte disturbance. Out-of-hospital cardiac arrest resulting from idiopathic ventricular fibrillation is uncommon. Records of all patients who underwent electrophysiological testing between June 1979 and June 1992 were reviewed. Patients with out-of-hospital cardiac arrest due to idiopathic ventricular fibrillation were identified. Follow-up information was obtained by telephone interview in June 1992. Of 194 patients who underwent electrophysiological study after out-of-hospital cardiac arrest not associated with acute myocardial infarction, only six (4 male and 2 female) had idiopathic ventricular fibrillation. It was induced in only two patients by programmed ventricular stimulation. No sustained ventricular arrhythmias were induced in the remaining four patients. Four patients received implantable cardioverter defibrillators, one was treated with a β-adrenergic blocker, and one received no treatment. All patients were alive at a mean follow-up of 50 months. Two of the four patients without inducible sustained ventricular arrhythmias had events during follow-up. Of the two patients with inducible ventricular fibrillation, one experienced a cardiac arrest and documented ventricular fibrillation at 41 months after the index event and the other had had no recurrence at 15-month follow-up. All four patients with implantable cardioverter defibrillators were alive at last follow-up, and two had device discharges. In survivors of out-of-hospital cardiac arrest due to idiopathic ventricular fibrillation: (1) programmed electrical stimulation is of limited value for evaluating cause and guiding therapy; (2) a high rate of recurrent events is observed (50%); and (3) an implantable cardioverter defibrillator is effective for preventing a fatal outcome.     

Transcutaneous T Wave Shock: A Universal Method for Ventricular Fibrillation Induction

Our objective was to develop a universal noninvasive method for VF induction. ICD implantation requires VF induction. Conventional rapid ventricular stimulation may fail to induce VF. Some ICDs can deliver low energy shocks on the T wave to induce VF. We hypothesized that an external dual chamber pacemaker and an external defibrillator could be configured to allow reliable VF induction with any ICD system. A surface ECC signal was delivered to the atrial channel of an external dual chamber DDD pacemaker. The 'AV' delay was adjusted so that the ventricular output of the pacemaker was delivered to an external defibrillator synchronized to deliver 5–50 J. Twenty-six patients at ICD implant or follow-up had VF induced in native rhythm (sinus rhythm or atrial fibrillation), or during a ventricular pacing train (3–8 beats at cycle length 500–880 ms). VF was successfully induced in 14 of 25 (56%) patients in native rhythm; and in 16 of 17 (94%) patients during pacing (P = 0.013). VF induction success rate was 36% in native rhythm (31/86 attempts) and 88% during pacing (69/78 attempts) (P < 0.001). The 'R' to shock interval was 269 ± 31 ms in native rhythm and 257 ± 48 ms during pacing. Energy delivered from the external defibrillator was 19 ± 3 J in native rhythm and 21 ± 6 J during pacing. We concluded that VF induction by synchronizing a small external shock to the T wave is a fast, effective way to reliably ensure arrhythmia induction with any ICD at implant or follow-up. This method is more successful during pacing than in sinus rhythm.     

Termination Of Sustained Tachycardia By External Noninvasive Pacing

Invasive cardiac pacing has proved useful in the induction and termination of reentrant sustained tachycardias. In one of our two cases, programmed ventricular extra-stimulation was used to induce sustained ventricular tachycardia from the endocardial surface of the right ventricle. Induced ventricular tachycardia was terminated by burst ventricular pacing with an external cardiac pacemaker. In our second patient, external pacing was effective at inducing and terminating sustained supraventricular tachycardia. These patients illustrate that the principles of terminating sustained reentrant tachycardia with invasive pacing may also apply to noninvasive external pacing. The usefulness of this approach in treating reentrant tachycardias needs further evaluation.     

A gastroesophageal electrode for electrophysiological studies

A novel gastroesophageal electrode has been developed capable of atrial and ventricular pacing. We performed electrophysiological studies using the gastroesophageal electrode (Esothoracic) and compared the results with the standard endocardial approach. The flexible polythene gastroesophageal electrode was passed into the stomach under light sedation. Five ring electrodes, now positioned in the lower esophagus were used for bipolar atrial pacing and recording. Ventricular pacing was performed using a cathodic point source on the gastroesophageal electrode tip; the indifferent electrode (anode) was a high impedance chest pad. Parameters of sinus and AV nodal function were obtained by atrial pacing. Programmed ventricular stimulation was performed using a standard protocol. These electrophysiological parameters were subsequently determined using the endocardial approach. There was close correlation between measurements of sinus and AV node function using the two approaches in 48 subjects: sinus node recovery time (SNRT) r2 = 0.70, corrected sinus node recovery time (CSNRT) r2 = 0.87, AV Wenckebach cycle length (AVWCL) r2 = 0.97. The degree of agreement between the two approaches was estimated by the mean difference delta and standard deviation of the difference sigma (SNRT delta = 40 ms, sigma = 257 ms; CSNRT sigma = 14 ms, delta = 164 ms; AVWCL sigma = 7 ms, delta = 16 ms). Programmed ventricular stimulation was performed in 15 of 48 subjects with known or suspected ventricular tachyarrhythmias. Seven had ventricular tachycardia induced using both esothoracic and endocardial programmed ventricular stimulation. One subject was noninducible using esothoracic programmed ventricular stimulation, but inducible at endocardial electrophysiological studies. Another subject was inducible at esothoracic electrophysiological studies, but noninducible using endocardial programmed ventricular stimulation. Six subjects were noninducible using both endocardial and esothoracic programmed ventricular stimulation. The gastroesophageal electrode permits reliable atrial and ventricular pacing without transvenous catheterization or fluoroscopy. Electrophysiological parameters determined using this electrode are similar to those obtained using endocardial stimulation.     

Comparative Effectiveness of Pacing Techniques for Termination of Well-Tolerated Sustained Ventricular Tachycardia

Ventricular tachycardias can be terminated by a variety of pacemaker techniques, including rapid and slow stimulation. Fast tachycardias are typically poorly tolerated, and require prompt intervention, usually with rapid pacing. Termination of ventricular tachycardia by slow or single capture pacemaker stimulation techniques is attractive, because of its presumed safety and the possibility of using simple implantable pacers. To identify factors favoring termination, single capture stimulation was used in 390 episodes of ventricular tachycardia in 21 patients, 16 with coronary artery disease, able to tolerate ventricular tachycardia forseveral minutes. Single capture stimulation terminated 223 episodes (57%) in 18 patients, and two were accelerated. Of 157 episodes exposed to 2–3 programmed extrastimuli or rapid pacing 149 (94%) were terminated and 7 were accelerated. Direct current cardioversion was needed in 12 episodes. Without medications, only two patients tolerated VT. Only one patient had reliable termination with single capture stimulation over several days. Systolic blood pressure was similar in episodes terminated and not terminated by single capture stimulation, but the ventricular rate was significantly lower in episodes terminated, 116 ± 19 vs. 133 ±24 (p<0.001). Termination of ventricular tachycardia was not affected by QRS morphology. Single capture termination of ventricular tachycardia is largely unpredictable, with limited reproducibility over a period of time. Although comparatively safe, single capture techniques are not likely toprove useful in the long-term treatment of many patients with recurrent ventricular tachycardia.     

A prospective randomized-controlled trial of ventricular fibrillation detection time in a DDDR ventricular defibrillator. Ventak AV II DR Study Investigators

Implantable cardioverter defibrillators (ICDs) with dual chamber and dual chamber rate responsive pacing may offer hemodynamic advantages for some ICD patients. Separate ICDs and DDDR pacemakers can result in device to device interactions, inappropriate shocks, and underdetection of ventricular fibrillation (VF). The objectives of this study were to compare the VF detection times between the Ventak AV II DR and the Ventak AV during high rate DDDR and DDD pacing and to test the safety of dynamic ventricular refractory period shortening. Patients receiving an ICD were randomized in a paired comparison to pacing at 150 beats/min (DDD pacing) or 175 beats/min (DDDR pacing) during ICD threshold testing to create a "worst case scenario" for VF detection. The VF detection rate was set to 180 beats/min, and VF was induced during high rate pacing with alternating current. The device was then allowed to detect and treat VF. The induction was repeated for each patient at each programmed setting so that all patients were tested at both programmed settings. Paired analysis was performed. Patient characteristics were a mean age of 69 +/- 11 years, 78% were men, coronary artery disease was present in 85%, and a mean left ventricular ejection fraction of 0.34 +/- 0.11. Fifty-two episodes of VF were induced in 26 patients. Despite the high pacing rate, all VF episodes were appropriately detected. The mean VF detection time was 2.4 +/- 1.0 seconds during DDD pacing and 2.9 +/- 1.9 seconds during DDDR pacing (P = NS). DDD and DDDR programming resulted in appropriate detection of all episodes of VF with similar detection times despite the "worst case scenario" tested. Delays in detection may be seen with long programmed ventricular refractory periods which shorten the VF sensing window and may be avoided with dynamic ventricular refractory period shortening.     

Inadvertent Catheter-Induced Right Bundle Branch Block in a Patient with Preexistent Left Bundle Branch Block and Recurrent Macroreentrant Ventricular Tachycardia

This article describes the inadvertent, catheter-induced induction of right bundle branch block resulting not only in transient complete infra-His heart block but also in temporary interruption of the macroreentry circuit of ventricular tachycardia. A patient with preexistent left bundle branch block and spontaneous ventricular tachycardia based upon the bundle branch reentry mechanism underwent electrophysiological testing for the evaluation of sotalol drug efficacy. In search of an optimal His-bundle recording, the manipulation of a 6 Fr quadripolar catheter caused a right bundle branch block, thus advancing the preexistent left bundle branch block to complete heart block. Retrograde ventriculoatrial conduction remained unaffected. The macroreentrant tachycardia with left bundle branch block configuration was no longer inducible. While the patient continued on unchanged sotalol medication (320 mg/d) he required temporary pacing for 16 hours until the block subsided. A subsequent induction attempt demonstrated initiation of the tachycardia. Finally, guided by invasive testing, the patient successfully received amiodarone therapy (300 mg/d). The patient completed an uneventful follow up of 27 months. No progression of conduction delay was observed. This case suggests that the inadvertent induction of right bundle branch block prevents the initiation of ventricular tachycardias relying on bundle branch reentry. Therefore, missed diagnosis or misinterpretation of antiarrhythmic drug efficacy might occur if there is no electrophysiological reevaluation after right bundle branch recovery.     

The Response of Regular Re-entrant Supraventricular Tachycardia to Right Heart Stimulation

The study was designed to assess the effect of various forms of right atrial or ventricular stimulation on the termination of re-entrant "supraventricular" tachycardias. Standard electrophysiological techniques were used in 81 patients to study 86 stable tachycardias. All tachycardias were initiated by single or double atrial or ventricular premature stimuli or incremental atrial pacing. Eight groups of tachycardia circuit were defined in terms of the anterograde and retrograde pathways. Termination of each tachycardia was studied by atrial underdrive, ventricular underdrive, rapid atrial stimulation and single or double atrial and ventricular premature extrastimuli. Intranodal re-entrant tachycardias formed 33% of the total and WPW tachycardias as a whole formed 55% of the total number of arrhythmias. The remainder were comprised of atrial tachycardia (5%), tachycardias in association with a partial AV nodal bypass (3%) and pre-excited tachycardias (5%). A single atrial extrastimulus was most effective where the circuit involved the right atrium. Atrial underdrive was consistently less successful than a single atrial extrastimulus in all groups. Rapid atrial pacing was effective in all groups, but caused transient atrial flutter or fibrillation in a proportion of each group except one. Ventricular underdrive stimulation was most effective in those groups where the right ventricle was involved in the circuit, but tended to be less effective than programmed single or double ventricular extrastimuli. Pacemakers designed to deliver appropriately timed single or double extrastimuli may offer an important alternative to other pacing modalities.     

Effects of Coronary Artery Bypass Grafting on Ventricular Arrhythmias: Results with Electrophysiological Testing and Long-Term Follow-Up

Myocardial revascularization was performed in 56 patients with coronary artery disease who presented with ventricular tachycardia (VT) (n = 39) or ventricular fibrillation (n = 17). There were 46 men and 10 women, aged 65 ± 10 years. Three vessel (n = 42) or left main disease (n = 4) was present in 82%. Left ventricular ejection fraction averaged 36%± 11%. Electrophysioiogical studies were performed preoperatively in all patients; 50 (89%) had inducible ventricular arrhythmias. Sustained monomorphic VT was induced in 40 patients (cycle length 284 ± 61 msec). Reproducible symptomatic nonsustained VT was induced in four patients and ventricular fibrillation in six patients, while six patients had no inducible arrhythmia. Preoperatively the patients with inducible VT failed 3.3 ± 1.2 drug trials during electrophysiological studies. In addition to coronary bypass, 22 patients also received an automatic implantable cardioverter defibrillator (ICD), 26 patients received prophylactic ICD patches, and 1 patient had resection of a false aneurysm. There were no perioperative deaths. Postoperative electrophysiological studies were performed in all 56 surgical survivors. Ventricular tachyarrhythmia could not be induced in the six patients who had no inducible VT preoperatively and in 13 of 40 (33%) with preoperatively inducible sustained VT or in 19 of 50 (38%) patients with any previously inducible ventricular arrhythmia, thus a totaJ of 25 patients (45%) had no inducible VT postoperatively. Of the remaining, 11 patients were treated with antiarrhythmic drugs alone, 11 had already received an ICD (combined with drugs in 7), and another 9 received the ICD postoperatively (combined with drugs in 4). At a mean foJJow-up of 28 ± 21 months there were 11 deaths (20%): 2 sudden, 5 nonsudden cardiac, and 4 noncardiac deaths. There were 16 nonfatal VT recurrences (29%): 14 among patients with persistently inducible arrhythmias, and onJy 2 among those with no inducible arrhythmia postoperatively (P = 0.004); 13 occurred in patients with an ICD (P = 0.01). Thus among these patients with malignant ventricular arrhythmias who underwent revascuJarization, 45% had no inducible arrhythmia postoperatively with 33% of those with preoperatively inducible sustained VT apparently rendered noninducible by revascularization, while the majority (70%) remained free of major arrhythmic events during long-term follow-up. We conclude that myocardial revascularization alone can result in no ventricular arrhythmia induction in selected patients with VT inducible prior to surgery. Long-term follow-up of such patients indicates a low sudden death and arrhythmia recurrence rate. Furthermore, in patients with persistently inducible ventricular tachyarrhythmias after coronary revascuJarization, the sudden death rate is low despite a high frequency of nonfatal arrhythmia recurrence when antiarrhythmic medications are guided by programmed stimulation or an ICD is used.     

The Impact of Antitachycardia Pacing with Defibrillation

Chronic recurrent ventricular tachycardia (VT) can be reproducibly terminated by programmed endocardiaJ right ventricular stimulation. However, antitachycardia pacing can be associated with possible acceleration of VT, while frequent episodes of VT and patient discomfort can limit treatment by an implantable cardioverter defibrillator (ICD). The combined use of antitachycardia pacing and the AICD (automatic implantable cardioverier defibrillator) was evaluated in 6 out of 51 patients (age 57 ± 11 years) in whom the AICD had been implanted because of recurrent VT. In each instance VT could be terminated by temporary overdrive pacing. The interactive mode of VT termination by a pacemaker (Tachylog) as well as by the AICD was assessed after implantation. In the automatic mode, the Tachylog functioned as a bipolar, ventricular inhibited (VVI) device with antitachycardia burst stimulation capability, allowing two to five stimuli at intervals of 260–300 ms and one or two interventions. During follow-up of 47 ± 24 months, the Tachylog terminated VT reliably 50–505 times per patient. When burst stimulation accelerated VT, termination was achieved by AICD discharge. Thus, drug resistant VT can be terminated by antitachycardia pacing to avoid patient discomfort. In the event of tachycardia acceleration, VT was terminated by the AICD. A universal pacemaker-defibrillafor should combine antibradycardia and antitachycardia pacing with back-up cardioversion defibrillation.     

Comparison of Epicardial and Endocardial Programmed Stimulation in Patients at Risk for Ventricular Arrhythmias After Cardiac Surgery

Programmed ventricular stimulation was performed on 36 patients after recent cardiac surgery using implanted right ventricular epicardial temporary wires and with catheters positioned percutaneously at two right ventricular endocardial sites. Patients were followed for a mean of 18.5 months (range 3 to 36 months). Epicardial wires were nonfunctional in 10 patients (28%) due to excessively high pacing thresholds. Overall, 22 patients (61%) had inducible sustained ventricular tachycardia; epicardial wires were functional in 15 (68%) of these patients. Six patients without inducible ventricular tachycardia with epicardial stimulation were inducible using endocardial stimulation. Of the 24 patients in whom epicardial and endocardial ventricular stimulation could be performed, concordant results were obtained in only 17 (71%), despite similar epicardial and endocardial ventricular effective and functional refractory periods. A total of 14 arrhythmic events occurred during the follow-up period. Of the 22 patients with an inducible sustained ventricular tachycardia, 12 (64%) had subsequent arrhythmic events. Only 2 of the 14 noninducible patients had follow-up arrhythmic events, one of which was caused by medication proarrhythmia. Endocardial ventricular stimulation had a superior sensitivity (83% versus 30%, P < 0.0001) and an improved negative predictive value (86% versus 61%, P < 0.05) compared with epicardial ventricular stimulation. These results indicate that noninducibility using epicardial programmed ventricular stimulation does not reliably portend a low risk for recurrent ventricular tachyarrhythmias. Epicardial programmed stimulation, used alone, may be inadequate for postoperative electrophysiological evaluation of patients at risk for ventricular arrhythmias.     

A Comparison of Ventricular Arrhythmias Induced with Programmed Stimulation Versus Alternating Current

In patients undergoing implantation and testing of the implantable cardio-verter defibrillator (ICD), alternating current (AC) may be used to induce ventricular tachyarrhythmias in a prompt, safe, and efficient manner. These arrhythmias have been previously reported to be similar to those induced during programmed electrical stimulation (PES). We compared the ventricular tachyarrhythmias induced by both methods in 14 patients: 8 male, 6 female; mean age 61 years; coronary disease in 10, cardiomyopathy in 4; mean ejection fraction 31%. The presenting arrhythmia was nonsustained ventricuiar tachycardia (VT) in four, sustained monomorphic ventricular tachycardia (SMVT) in five, ventricular fibrillation (VF) in four, and unknown in one patient with syncope. PES (single, double, triple extrastimuli; burst pacing) and AC (1–2 sec application) stimulation via right ventricular endocardial electrode catheter was performed off antiarrhythmic drugs in the nonsedated state. PES induced SMVT in nine, polymorphic VT in two, and VF in three. AC induced VF in all patients. Although AC can reliably induce ventricular tachyarrhythmias during de/ibrillation threshold and ICD testing, there is poor correlation to PES induced tachyarrhythmias.