Reproducibility of Electrophysiological Testing During Antiarrhythmic Therapy for Ventricular Arrhythmias Unrelated to Coronary Artery Disease

Although electrophysiological studies are commonly used in the management of patients with ventricular tachycardia (VT), the reproducibility of these studies during therapy has not been established in patients in whom VT is associated with conditions other than coronary artery disease. Therefore, we performed confirmation studies during drug therapy in 60 patients (mean age 48 ± 18 years; 41 male) with sustained ventricular arrhythmias induced during initial study to assess the reproducibility of drug effect. The stimulation protocol used included the serial introduction of up to three premature ventricular stimuli during sinus rhythm and with ventricular pacing at two pacing rates. Rapid ventricular pacing techniques were also used. Antiarrhythmic drug efficacy was confirmed in 78% of patients. Sustained VT was induced at repeat electrophysiological study in 18% of patients daring antiarrhythmic therapy that had been felt to be effective on the basis of a single drug study. We conclude that electrophysiological study results during antiarrhythmic therapy exhibit significant day-to-day variability. Sustained VT can be induced during antiarrhythmic therapy previously determined to be effective by electrophysiological techniques in many patients.     

Value of Serial Electropharmacological Testing in Managing Patients Resuscitated from Cardiac Arrest

Electrophysiologic studies were performed in 11 patients (9 men, 2 women; mean age: 59.9 yrs) who had survived an episode of cardiac arrest due to ventricular tachycardia (VT) or ventricular fibrillation. The purpose of the studies was to evaluate the usefulness of serial acute drug testing in selecting an effective chronic antiarrhythmic regimen. Ten of the patients were suffering from chronic ischemic heart disease with one or more previous myocardial infarctions while one had no evidence of structural heart disease. A ventricular aneurysm was present in four of them. During control electrophysiologic study, a sustained VT was induced by ventricular stimulation (single and double extrastimuli at various paced ventricular cycle lengths plus bursts of rapid ventricular pacing) in nine of the ten patients (90%) who were studied while not receiving antiarrhythmic drugs; a non-sustained VT was induced in one of them (10%). In three patients (30%) VT could be initiated only by right ventricular stimulation at a side different from the apex (outflow tract). No arrhythmia was observed in the only patient who was studied while taking amiodarone orally (400 mg/day for more than three months). During serial acute drug testing a totally effective drug regimen (successful in preventing the induction of any ventricular arrhythmia) was found in seven of the ten patients (70%) who underwent this procedure and a partially effective drug regimen (a sustained VT was no longer inducible; it was easier to interrupt and it was considerably slower) was found in two patients (20%). None of the nine patients who received chronic antiarrhythmic therapy based on the results of serial acute drug testing died suddenly during a mean follow-up of 14 months (range: 3-28) and only one had a recurrence of cardiac arrest. The latter, however, was taking antiarrhythmic drugs at a dosage less than that proved to be effective during electropharmacological testing. The only patient who refused serial acute drug testing and received an empiric antiarrhythmic therapy died suddenly at the 21st month of follow-up. These results indicate that serial electropharmacological testing is useful in selecting an effective long-term drug regimen in survivors of cardiac arrest.     

Is programmed ventricular stimulation still up to date in the medicinal evaluation of ventricular tachycardia?

Despite considerable advances in the understanding of cardiac arrhythmia mechanisms, death in relation to ventricular tachyarrhythmias remains an important public health problem, and management of ventricular arrhythmias remains a perpetual challenge in clinical cardiology. In the last decade, the development and refinement of implantable cardioverter defibrillators and the progress in techniques of radiofrequency electrode catheter ablation and antiarrhythmic surgery have been revolutionary in the management of ventricular tachycardia. On the other hand, there have been major changes in the use of drug therapy since the publication of the results of the CAST study. Inclusion of mortality as an endpoint in clinical trials highlights the fact that some antiarrhythmic drugs may have the proclivity to exert fatal proarrhythmic reactions while also having the potential to control recurrences of ventricular tachycardia. All these changes that now need to be integrated into global approaches for ventricular arrhythmia control led us to wonder whether serial testing is still up to date in the management of ventricular tachycardia. After more than 20 years of clinical use, there is much concern about the use of serial drug testing to guide antiarrhythmic drug therapy for the management of life-threatening sustained ventricular tachyarrhythmias in light of recent advances in the management of cardiac arrhythmias. The purpose of this article is to discuss, within a relatively brief compass, the cumulative data from different lines of investigations, results of randomized clinical trials, recently acquired beliefs and meta-analytic findings concerning the present place of serial electrophysiologic drug testing in the management of ventricular tachycardia.     

Sustained ventricular tachycardia in the emergency department.

The aim of the study was to evaluate the demographics, haemodynamics, ECG characteristics, underlying disease, tachycardia termination and outcome of patients with sustained ventricular tachycardia (VT). We registered 75 patients presenting with VT (51 male, median age 63) from December 1993 to August 1998 in our emergency department (ED). Seventeen of these patients were haemodynamically unstable (23%), and 58 patients were stable (77%); there was no difference in the tachycardia cycle length (median 320 ms) and QRS width (median 140ms) between the two groups; however, five of the seven patients with polymorphic VT pattern were in the unstable group. Ischaemic heart disease was the underlying disorder in 57 patients (76%). Acute myocardial infarction (AMI) was present in 12 of the 58 stable (21%) compared to 11 of the 17 unstable (65%) patients. In three patients (4%) VT terminated spontaneously, in 34 patients (45%) VT was terminated by first-line intravenous drug therapy, and in 38 patients (51%) including all 17 unstable and 22 stable who failed to respond to the intravenous antiarrhythmic therapy challenge out of 55 patients, VT was terminated by electrical therapy. Within 2 days, 48 patients (64%) were transferred to an open ward, 13 (17%) still needed intensive care, nine (12%) were discharged to home and five (7%) died. Death occurred due to cardiac failure from AMI with extensive anterior wall infarction in three patients, and due to constrictive pericarditis and reocclusion of stented LAD each in one patient. At presentation in the emergency department, the majority of the patients with VT were haemodynamically stable, thus allowing first-line antiarrhythmic drug administration. However, in the course of the disease, half needed electrical therapy for definitive termination of the tachycardia. Therefore, direct current cardioversion must be available in the emergency department. Haemodynamic instability and death occurs significantly more often if VT occurs during the course of AMI.     

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.     

Long-Term Outcome Following Programmed Electrical Stimulation in Patients with High-Grade Ventricular Ectopy

To determine if programmed electrical stimulation (PES) could be utilized to identify patients with high-grade ventricular ectopy at low- or high-risk for sudden cardiac death, we performed PES in 40 patients with high-grade ventricular ectopy refractory to conventional antiarrhythmic agents. Twenty-one patients had a previous myocardial infarction, five had cardiomyopathy, six had hypertension, three had valvular heart disease and five had no known structural heart disease. The mean age was 50 years (range, 18 to 76). During programmed ventricular stimulation, eight patients had inducible sustained (more than 30 seconds) monomorphic ventricular tachycardia (Group I) but in 32 patients sustained ventricular tachycardia was not inducible (Group II). None of the five patients without structural heart disease were inducible while seven out of 21 (33%) patients with previous myocardial infarction had inducible ventricular tachycardia (VT). Antiarrhythmic therapy was instituted in patients with inducible VT; patients without inducible VT did not receive antiarrhythmic agents. In Group I, seven of the eight patients are alive (mean follow-up, 16 months) and in Group II, 28 of the 32 patients are alive (mean follow-up, 17 months). None of the five deaths were sudden. We conclude that in the absence of antiarrhythmic therapy, the incidence of sudden cardiac death is very low in patients with high-grade ventricular ectopy who do not have inducible monomorphic ventricular tachycardia during programmed ventricular stimulation.     

Predictors of Ventricular Tachvcardia Inducibility in Programmed Electrical Stimulation and the Effectiveness of Serial Drug Testing: Polish Multicenter Study

WNUK-WOJNAR, A.M., ET AL.: Predictors of Ventricular Tachycardia Inducibility in Programmed Electrical Stimulation and Effectiveness of Serial Drug Testing: Polish Multicenter Study. In 100 patients with IHD and complex ventricular arrhythmias, programmed electrical stimulation was performed using up to three extrastimuli at sinus rhythm, and paced 100, 120, and 140 beats/min delivered from the RV apex, outflow tract or the LV with ventricular mapping to evaluate late potentials (LP) in 41 patients. Sustained monomorphic VT (SMVT) was provoked in 91% of 42 patients with a history of VT/VF, p < 0.001, all five patients had SMVT in 24-hour ECG, p < 0.005, and 91% of 21 patients with LV dyskinesis, p < 0.01. After depolarizations were found in 62% of 21 patients with a history of VT, in 58% of 31 patients with inducible VT, p < 0.01 and in five of six patients with LV dyskinesis. In patients with inducible VT, LP had a higher amplitude (105 ± 35 vs 60 ± 47 µV) and were more delayed (202 ± 96 vs 133 ± 75 msec) than in noninducible patients. In 17 patients, serial drug testing was performed after oral administration using mexilitene, disopyramide, chinidine, propafenone, sotalol, and amiodarone. If one drug was tested, the therapy efficacy was 25% if two drugs-60%, and if three drugs-75%. In eight patients, VT was inducible in all tests, but in only one of these patients chronic antiarrhythmic therapy was not effective. We conclude that the most important predictors of VT inducibility are a history of VT or 24-hour ECG, and LV dyskinesis. Serial drug testing is efficient only when many drugs are tested, but even if VT is inducible, it does not exclude the possibility of a good clinical outcome in chronic therapy.     

Induced Sustained Ventricular Tachycardia in Nonischemic Dilated Cardiomyopathy: Dependence on Clinical Presentation and Response to Antiarrhythmic Agents

Thirty-one patients with nonischemic dilated cardiomyopathy either idiopathic or due to regurgitant valvular disease were studied in the cardiac electrophysiology lab. The indications for study were sustained ventricular tachycardia (VT) in 26, ventricular fibrillation (VF) in 11, and syncope of unknown etiology in 4. Sustained VT was reproducibly induced in 17 patients, including 12 with a history of sustained VT, 2 with VF and 3 with syncope. Of 15 patients undergoing serial antiarrhythmic drug studies, sustained VT was rendered noninducible or nonsustained in 23. Three had recurrent arrhythmic events while on therapy predicted to be effective. One of 2 patients discharged on a regimen predicted to be ineffective had a recurrence of sustained VT that resulted in cardiac arrest. Of 14 patients in whom sustained VT could not he reproducibly induced, 2 subsequently had spontaneous occurrences of sustained VT, and 2 experienced aborted sudden death. These results suggest the following; (1) the induction of sustained VT in the setting of nonischemic dilated cardiomyopathy is dependent on the clinical presentation; (2) antiarrhythmic drugs frequently render sustained VT noninducible or nonsustained; (3) antiarrhythmic drug suppression of inducible sustained VT predicts long-term prevention of spontaneous recurrences; and (4) noninducibility of sustained VT in the baseline state does not predict freedom from subsequent episodes of VT or sudden death.     

Therapy Assessment for Sustained Ventricular Tachyarrhythmias: How Many Electropharmacological Tests are Appropriate?

Surgery, implantable devices or catheter ablations offer therapeutic choices for the treatment of malignant ventricular tachyarrhythmias (VT) resistant to antiarrhythmic drugs. The number of electropharmacological (EP) tests that should precede consideration of a nonpharmacological therapy has not been defined. We performed serial EP tests in 94 patients with inducible sustained VT until an effective drug was identified or all available drugs had failed to suppress VT induction. With up to 11 tests in individual patients, suppression of VT inducibility was finally achieved in 66 patients (70%). In 47 of these 66 patients (70%), only one or two tests were necessary to identify an effective regimen. However, in 40%, 28%, 18%, and 9% of the patients still inducible after 2, 3, 4, and 5 drug tests, respectively, an effective agent could be identified during subsequent tests. No critical number of unsuccessful EP tests clearly separated responders and nonresponders to medical therapy. During follow-up (34 +/- 11 months), 14 patients placed on antiarrhythmic drugs predicted to be effective had symptomatic VT recurrence. VT recurrence was unrelated to the type or the number of unsuccessful EP tests preceding identification of the prescribed drug. Extensive EP testing with all available agents might therefore be worthwhile in selected patients. An "appropriate" number of EP studies has to be determined individually for each patient, based on the chance of finding an effective drug during subsequent studies and the risk and benefit of the therapeutic choices.     

Hybrid Therapies for Ventricular Arrhythmias

In recent years several trials demonstrated the efficacy of implantable cardioverter-defibrillation (ICD) therapy in reducing cardiac and total mortality in patients affected by rapid ventricular tachycardia (VT) and/or ventricular fibrillation. Nevertheless, ICD do not prevent arrhythmia recurrences, thus being a palliative and not a curative treatment modality. The tolerance to ICD therapy varies greatly, and within individuals, this leading to a nonuniform acceptance of this form of therapy. The very frequent occurrence of VT, defined as an arrhythmic storm, may be a life threatening condition. The majority of ICD patients is under antiarrhythmic drug therapy, to reduce episodes of VT or to make antitachycardia pacing more effective by slowing the tachycardia rate. Drug therapy, however, may cause additional problems, and does not represent the optimal solution. The prevention of VT and/or ventricular fibrillation episodes and excessive ICD therapy, remains a worthwhile goal. Radiofrequency catheter ablation (RFCA) is a curative approach, and can be expected to reduce the frequency of recurrent VT episodes in the majority of patients. The combination of these treatment modalities (ICD and RFCA) is often described as hybrid therapy, implying that the two treatments act providing some form of synergism. In experienced centers, RFCA is now performed, regardless of whether the VT rate is rapid and/or is hemodynamically unstable. Newer mapping and ablation techniques are now available, enhancing the acute success rate of the procedure. In this review the most recent application of VT catheter ablation and the use of advanced mapping and ablation techniques will be discussed.     

Drug Therapy for Survivors of Sudden Cardiac Death

The proliferation of standard as well as novel community based systems for resuscitation of victims of out-of-hospital cardiac arrest has provided a large group of sudden cardiac death survivors who present a therapeutic challenge. The nature and severity of the underlying heart disease must be delineated. Particularly, myocardial ischemia and congestive heart failure must be controlled. Prior to considering device therapy of surgical intervention, pharmacologic therapy should be evaluated. Baseline electrophysiological studies determine the applicability of serial pharmacologic testing. In patients with inducible VT/VF, serial electrophysiological testing can identify drug regimens that prevent the arrhythmia in approximately 40% of patients. In an additional 20% of patients, regimens which slow the ventricular tachycardia and significantly reduce the arrhythmia related mortality can be identified. Three to 5-year follow-up has shown such an approach can reduce the sudden death mortality in these patients to less than 3% per year. It has been suggested that certain medication, most notably amiodarone, electrophysiological testing has not been useful in assessing efficacy. Several recent studies, however, have shown that electrophysiological testing is indeed useful even in evaluating the efficacy of amiodarone. In patients in whom ventricular tachycardia/ventricular fibrillation cannot be prevented or significantly slowed, medical therapy is generally ineffective and the sudden death mortality is 20% to 40% per year. In such patients, other therapeutic modalities should be considered.     

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.     

Efficiency of antiarrhythmic therapy and resistance to it in patients with malignant ventricular tachyarrhythmias: formulation of prognosis]

AIM: To study feasibility of predicting results of drug antiarrhythmic therapy in patients with malignant ventricular arrhythmias (MVA) basing on the results of clinical and device examinations. MATERIALS AND METHODS: 136 patients with documented MVA entered the study. 100 patients were in the retrospective analysis group, 36 patients comprised the study group. All the patients underwent physical examination, resting ECG, chest x-ray, radionuclide ventriculography. Intracardiac electrophysiological examination, Holter 24-h ECG monitoring and bicycle exercise provided data for diagnosis of MVA and control over effects of antiarrhythmic drugs. The mathematical model was derived using discriminant analysis. RESULTS: Significant differences were obtained in patients with positive and negative results of drug testing by the number and recurrence time of ventricular tachycardia (VT) for 3 years, survival, cardiac and sudden death, some other parameters. A mathematic model has been designed which allows prognosis of the results of antiarrhythmic therapy (AAT) in patients with MVA. 7 independent predictors of AAT efficiency are shown: left ventricular ejection fraction, duration of P-Q interval, cardiac failure, left ventricular aneurysm, age, number of VT morphologies, insufficiency of aortic valve. Verification of the model on the study group patients showed that prognostic accuracy of the model was 82%. CONCLUSION: The results of the drug tests predict life span of MVA patients. The developed mathematical model allows prediction of AAT results in such patients before the pharmacological test with accuracy 82-87%. The model can help objectivize indications to use of non-pharmacological methods for each patient basing on prognosis of resistance to drug AAT.     

Effect of Antiarrhythmic Drug Therapy on the Incidence of Shocks in Patients who Receive an Implantable Cardioverter Defibrillator after a Single Episode of Sustained Ventricular Tachycardia/Fibrillation

Seventy-four patients (16 women, 58 men, age 58 ± 21 years, mean ± standard deviation) who received an implantable Cardioverter de/ibrillator (ICD) after experiencing a single episode of ventricular tachycardia or ventricular fibrillation were followed to determine if antiarrhythmic drug therapy affects the incidence of ICD discharges. Thirty-three patients (group A) were treated with an antiarrhythmic drug that was either untested or previously demonstrated during electropharmacological testing to be ineffective in suppressing the induction of ventricular tachycardia. Forty-one patients (group B) were not treated with an antiarrhythmic drug. There were no significant differences between the two groups in regards to age, sex, incidence of coronary artery disease, left ventricular function or the type of ICD pulse generator used. During a mean follow-up of 14 months for the entire cohort, 15 patients (46%) in group A and 18 patients (44%) in group B experienced at least one ICD shock. The time to the first appropriate shock (5 ± 5 months in both groups) and the frequency of ICD shocks (0.3 ± 0.2/month in group A vs 0.4 ± 0.5/month in group B) were similar in both groups. The incidence of syncope at the time of ICD discharge was higher in group A than group B patients (31% vs 5%, P < 0.05). In conclusion, antiarrhythmic drugs that are untested or have failed electropharmacological testing do not appear to reduce the probability of ICD discharge over a short-term (mean 14 months) follow-up in patients who have had only one clinical episode of VT/VF and may increase the risk of syncope during ICD discharge. Studies with a larger sample size and longer follow-up period will be needed to confirm these findings.     

Mexiletine-quinidine combination: enhanced antiarrhythmic and electrophysiologic activity in the dog

Combination treatment with mexiletine and quinidine has been shown to be more effective than either monotherapy in the treatment of ventricular tachycardia in humans. The purpose of this study was to assess the electrophysiologic changes which correlated with enhanced antiarrhythmic activity during treatment with the monotherapies and this combination. Twenty-seven dogs with inducible sustained ventricular tachyarrhythmias (VT) late after ischemic injury were treated with mexiletine and quinidine, alone and in combination. Conscious but sedated animals were assigned randomly to receive serial drug treatments. Sustained VT was consistently inducible during serial placebo studies. In 13 dogs who received all four drug treatments (mexiletine, quinidine, combination and placebo) significantly greater antiarrhythmic efficacy was seen with combination therapy (8 of 13) than was seen with mexiletine alone (1 of 13), quinidine alone (3 of 13) and saline (0 of 13) (P less than .005). This enhanced antiarrhythmic activity was paralleled by greater prolongation of intraventricular conduction to the border zone and increase in excitability threshold at the border zone and increase in ventricular effective refractory period in the infarct zone. Serum concentrations of quinidine were 19 +/- 5 microM when given alone and 15 +/- 5 microM when given in combination. Mexiletine concentrations were 3.6 microM when given alone and 4.2 microM when given in combination. In conclusion, mexiletine and quinidine in combination produced enhanced antiarrhythmic activity which was paralleled by electrophysiologic changes occurring in the perinfarct zone. These electrophysiologic changes appear to be correlates of enhanced antiarrhythmic activity.     

Heart failure

Survival of patients with heart failure has improved over the past decade due to advances in medical therapy. However, sudden cardiac death continues to cause 35 to 65% of death. Ventricular arrhythmias are important causes of sudden cardiac death in patients with heart failure. The risks of antiarrhythmic drugs are increased in patients with heart failure. Therefore, in the absence of a clear indication, antiarrhythmic drug therapy should be avoided. A number of recent randomized trials have provided evidence that beta-adrenergic blockers, angiotensin-converting enzyme(ACE) inhibitors and angiotensin II receptor blockers(ARB) significantly reduces the risk of sudden death in patients with chronic congestive heart failure. For patients who have a history of sustained ventricular tachycardia(VT) or ventricular fibrillation(VF) amiodarone or an implantable cardioverter defibrillator(ICD) should be considered, and these therapy may benefit some high risk patients who have nonsustained VT.     

The Role of Combination Therapy with Mexiletine and Procainamide in Patients with Inducible Sustained Ventricular Tachycardia Refractory to Intravenous Procainamide

This study evaluated the role of serial electropharmacological testing on combination therapy with mexiletine and procainamide in 20 patients with inducible sustained ventricular tachycardia (VT) refractory to intravenous procainamide. The clinical arrhythmias were cardiac arrest in five patients, sustained VT in 11 patients, and recurrent syncope of presumably arrhythmic origin in four patients. The mean left ventricular ejection fraction (LVEF) was 0.40 +/- 0.12 (mean +/- SD). All patients had inducible sustained VT at baseline and after administration of intravenous procainamide. All 20 patients underwent electropharmacological testing on combination therapy with mexiletine and procainamide. The mean cycle length of inducible sustained VT was 251 +/- 48 ms at baseline, 324 +/- 81 ms on intravenous procainamide (P less than 0.014 vs baseline), and 365 +/- 82 ms on combination therapy (P less than 0.0001 vs baseline, P = NS vs intravenous procainamide). Combination therapy did not suppress VT inducibility, nor did it make VT more difficult to induce in 19 of 20 patients. The remaining one patient had a partial response (runs of nonsustained VT, longest 10 seconds). Furthermore, combination therapy did not significantly prolong the VT cycle length over and above that observed during testing with intravenous procainamide. Therefore, in patients with inducible sustained VT refractory to procainamide during initial electropharmacological testing, mexiletine in combination with procainamide appears to be of little or no value and serial electropharmacological testing on these drugs is of limited usefulness. Early initiation of alternative therapy may be the preferred clinical option.     

Identification of Ventricular Tachycardia Using Intracavitary Ventricular Electrograms: Analysis of Time and Frequency Domain Patterns

Tachycardia detection by implantable antitachycardia devices using rate alone has major limitations. Several alternative methods have been proposed to distinguish ventricular tachycardia or ventricular fibrillation from normal sinus rhythm using intracardiac electrograms. These methods have not been tested, however, for recognition of ventricular tachycardia in patients with abnormal surface QRS conduction during sinus rhythm or with antiarrhythmic drug therapy. In this study, three techniques for the indentification of ventricular tachycardia from intracavitary bipolar ventricular electrograms were examined and compared: correlation waveform analysis, amplitude distribution analysis, and spectral analysis using Fast Fourier transformation. Thirty episodes of induced monomorphic ventricular tachycardia were analyzed and compared sinus rhythm in four groups of patients with: I. Normal surface QRS conduction during sinus rhythm without antiarrhythmic drug therapy (five episodes); II. Intraventricular conduction delay or bundle branch block during sinus rhythm without antiarrhythmic drug therapy (nine episodes); III. Normal surface QRS conduction during sinus rhythm with antiarrhythmic therapy (six episodes); and IV. Intraventricular conduction delay or bundle branch block during sinus rhythm with antiarrhythmic drug therapy (ten episodes). Correlation waveform analysis had 100% sensitivity and specificity in distinguishing ventricular tachycardia from sinus rhythm, even in the presence of an intraventricular conduction delay, bundle branch block, and antiarrhythmic drug therapy. In contrast, amplitude distribution analysis differentiated 15/30 episodes (50.0%) of ventricular tachycardia from sinus rhythm, and a maximum of 18/30 episodes (60.0%) of ventricular tachycardia were identified by specal analysis using Fast Fourier transformation. Correlation waveform analysis appears to be a reliable technique to discriminate ventricular tachycardia from sinus rhythm using intracavitary ventricular electrograms. Its computational demands are modest, making it suitable for consideration in an implantable antitachycardia device.     

Bilateral sympathectomy for treatment of refractory ventricular tachycardia

Ventricular tachycardia (VT) commonly occurs in patients with ischemic or nonischemic cardiomyopathy and requires antiarrhythmic drugs, ablation, or advanced circulatory support. However, life‐threatening VT may be refractory to these therapies, and may cause frequent implantable cardioverter defibrillator (ICD) discharges. Left cardiac sympathetic denervation reduces the occurrence of these fatal arrhythmias by inhibiting the sympathetic outflow to the cardiac tissue. We present a 69‐year‐old man with nonischemic cardiomyopathy, life‐threatening VT, and hemodynamic instability with numerous ICD discharges, who remained refractory to antiarrhythmic drug therapy and ablation attempts. He was effectively treated with bilateral cardiac sympathectomy. Six months later, he remained free of VT with no ICD discharges.     

The Use of the Block Cycle Length as a Safe and Efficient Means of Interrupting Sustained Ventricular Tachycardia and Its Pharmacological Modification

In nine patients who had inducible monomorphic sustained ventricular tachycardia (VT), rapid pacing was performed in 11 episodes of morphologically distinct VT at progressively shorter cycle lengths and VT was interrupted at a critical cycle length. The VT interrupting critical cycle length was defined as the block cycle length (BCL) and the effect of Class I antiarrhythmic drugs were examined. Both the VT cycle length (VTCL) and the BCL were prolonged after administration of either drug. The overall mean ratio of the BCL to the VTCL was unchanged after procainamide administration, but increased after the use of mexiletine. The ratio, however, varied in individual VTs and the BCL after treatment with Class I antiarrhythmic drugs could not be predicted from the ratio baseline value, although the ratio was always > 60% and the hazard of VT acceleration might be avoided if the BCL is used.