Epidemiology of ventricular arrhytmias and sudden death

Patients who present with ventricular tachyarrhythmias constitute a diverse group in which a variety of factors may combine to cause ventricular tachycardia or fibrillation. For this reason, we believe that each patient should undergo a comprehensive medical evaluation directed at identifying and treating such factors as ischemia, congestive heart failure, valvular heart disease, sensitivity to cardioactive drugs, and metabolic derangements. Antiarrhythmic treatment is not necessary for many patients with simple VPBs. However, certain patients who have already suffered a life-threatening arrhythmia or who are at high risk for such arrhythmias should be vigorously treated with specific antiarrhythmic therapy. Such therapy must be carefully selected for each individual. The efficacy of any antiarrhythmic treatment should be assessed by ECG monitoring, exercise testing, or electrophysiologic study.In studies reported to date, antiarrhythmic therapy guided by these methods greatly reduced the risk of recurrent arrhythmias. It is too early to assess the impact of these techniques on overall long-term survival in the various patient populations studied.     

Long-term reproducibility of responses to programmed cardiac stimulation in spontaneous ventricular tachyarrhythmias

Programmed electrical stimulation (PES) of the heart has been used to initiate and terminate ventricular tachyarrhythmias under controlled conditions in patients in whom these arrhythmias have occurred spontaneously. The long-term reproducibility of the response to programmed cardiac stimulation in patients with ventricular arrhythmias is unknown. Seventeen patients with previously documented spontaneously occurring ventricular tachyarrhythmias were evaluated: 5 with nonsustained ventricular tachycardia (VT), 10 with sustained VT and 2 with ventricular fibrillation. The underlying cardiac diagnosis was atherosclerotic coronary heart disease (CAD) in 11 patients, dilated cardiomyopathy in 2 patients, congenital heart disease in 1 patient and no structural heart disease in 3. All patients underwent PES in the absence of antiarrhythmic drug treatment, and patients with inducible VT underwent serial electrophysiologic-pharmacologic testing in an attempt to suppress the arrhythmia. All 17 patients were reexamined with PES at a mean of 18 months (range 2 to 42) after their initial electrophysiologic study, during which time none had a myocardial infarction or intervening cardiac surgery. Repeat electrophysiologic studies, performed in the absence of antiarrhythmic agents, were undertaken because of drug intolerance, availability of new drugs, recurrent arrhythmia or preoperative reevaluation. All 11 patients with CAD had inducible VT on both the first and second electrophysiologic evaluation. Of the 6 patients with no CAD, only 1 had inducible VT on both occasions. Thus, long-term reproducibility of PES-induced VT in patients with stable CAD appears to be high.     

Symptomatic ventricular tachycardia

Opinion statement The approach to patients with symptomatic ventricular tachycardia (VT) depends on the presence and type of structural heart disease. In patients with underlying heart disease and ventricular fibrillation or sustained symptomatic VT with hemodynamic compromise, the implantable cardioverter-defibrillator (ICD) is superior to antiarrhythmic drugs for the improvement of overall survival. These patients should receive an ICD unless contraindications are present. For patient with sustained VT and a structurally normal heart (idiopathic VT), radiofrequency catheter ablation is a reasonable option. If patients are symptomatic, nonsustained VT should be treated with beta-adrenergic blocking agents or antiarrhythmic drugs, which should be selected on the basis of the underlying cardiovascular substrate. In patients with coronary artery disease, depressed left ventricular function, and nonsustained VT, we recommend the use of programmed electrical stimulation for additional risk stratification. If a sustained ventricular arrhythmia is induced, an ICD should be implanted.     

Spontaneous sustained ventricular tachyarrhythmias during treatment with type IA antiarrhythmic agents

Twenty-six patients who developed their first clinical episode of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) while taking type IA antiarrhythmic agents for more benign rhythm disturbances were rechallenged with the identical drug during electrophysiologic testing. Patients with these new drug-associated spontaneous ventricular arrhythmias often manifested a preexisting substrate for such arrhythmias: sustained VT or VF was induced in 65% of patients at baseline, and in 58% of patients when tested with their previously taken antiarrhythmic drug. Among those without inducible sustained ventricular arrhythmias in the drug-free state, 78% remained free of inducible sustained arrhythmias when tested with the same drug they had been taking at the time of the clinical arrhythmia. Even patients without a definable electrophysiologic substrate for sustained VT or VF remained at risk for arrhythmia recurrence if treated with alternative antiarrhythmic medications: 40% of such patients who continued to receive an antiarrhythmic agent different from that being administered when their clinical VT or VF occurred had recurrent spontaneous ventricular tachyarrhythmias during follow-up. Thus, patients with drug-associated clinical sustained ventricular tachycardias form a heterogenous group that should be evaluated individually and not empirically managed for a "proarrhythmic effect" simply by antiarrhythmic drug withdrawal or drug substitution.     

Sustained ventricular tachycardia in patients with idiopathic dilated cardiomyopathy: electrophysiologic testing and lack of response to antiarrhythmic drug therapy

Eleven consecutive patients with idiopathic dilated cardiomyopathy and spontaneous, sustained ventricular tachycardia (VT) of uniform morphology underwent programmed ventricular stimulation and serial antiarrhythmic drug testing. The mean ejection fraction was 30 +/- 6.4%. Sustained VT was induced by programmed electrical stimulation in all 11 patients. A mean of 3.7 +/- 2.4 antiarrhythmic drugs were evaluated by programmed stimulation, including at least one experimental agent in eight patients. In nine of 11 patients VT remained inducible on all drug therapy. During a mean follow-up period of 21 +/- 14 months there were four sudden deaths and two patients with recurrences of VT. In all six patients with sudden death or recurrence of VT, the arrhythmia remained inducible on drug therapy. Three patients who died suddenly had a hemodynamically stable, induced tachycardia on antiarrhythmic therapy. Of eight patients treated with amiodarone, only two were successfully treated. We conclude that in patients with sustained VT and idiopathic dilated cardiomyopathy, VT can be induced by programmed electrical stimulation. VT will usually remain inducible on antiarrhythmic therapy, and sudden death can occur despite slowing and improved tolerance of the induced arrhythmia. Amiodarone may have limited efficacy, and more aggressive therapy, such as surgery or implantation of an automatic internal defibrillator, should be considered in this patient population.     

Heart transplantation in therapy-resistant, recurrent ventricular tachycardias and ventricular fibrillation

In life-threatening, drug resistant ventricular tachycardia (VT) or ventricular fibrillation (VF), orthotopic heart transplantation should be considered as an alternative to a directed surgical approach or to the implantation of an automatic defibrillator. We report on nine patients with primary VT or VF who underwent transplantation. These comprised eight men and one woman with a mean age of 35 years (range, 19-51 years); dilative cardiomyopathy was present in seven and coronary artery disease in two. Left ventricular ejection fraction was 19% (11-26%), arrhythmia was recurrent VF in five cases, recurrent VT in two, and recurrent VT/VF in two. Two patients died, one due to acute rejection, and the other 8 months postoperatively due to chronic rejection. The seven other patients are all asymptomatic and leading normal lives without arrhythmias or antiarrhythmic drug therapy. Based on our preliminary experience, some advantages and disadvantages of heart transplantation are discussed in comparison with other treatment modalities. Despite limited indications for orthotopic heart transplantation we feel that it should become the therapy of first choice in young patients with progressive, surgically incorrectable cardiac disease complicated by drug resistant VT or VF.     

Arrhythmogenic Right Ventricular Cardiomyopathy

Abstract Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a major cause of sudden cardiac death and ventricular tachyarrhythmias in young, apparently healthy individuals and athletes. Myocardial atrophy with subsequent fibrofatty replacement predominantly affects right ventricular myocardium and results in global and regional dysfunction as well as areas of slow conduction and dispersion of refractoriness which are prerequisites for reentrant ventricular tachyarrhythmias.Patients affected with ARVC should be excluded from competitive sports and vigorous training. To provide optimal treatment, a detailed diagnostic evaluation and risk stratification are mandatory. Tailored treatment strategies aim at the suppression or effective termination of recurrent ventricular tachyarrhythmias and prevention of sudden death by antiarrhythmic drug therapy, catheter ablation, or implantation of a cardioverter defibrillator (ICD).Antiarrhythmic drugs may be used as a stand-alone treatment to suppress ventricular tachycardia (VT) recurrences in patients with ARVC and low risk of sudden death. Sotalol (preferred) or amiodarone in combination with -blockers showed the highest efficacy rates. In patients at higher risk, an ICD should be implanted and antiarrhythmic drugs be used only as an adjunct to prevent or suppress frequent VT recurrences and ICD discharges.Catheter ablation using conventional or electroanatomic mapping techniques yields good acute results for eliminating the targeted arrhythmia substrate. However, during the progressive long-term course of ARVC, VT recurrences from new arrhythmia foci are frequent and therefore limit the curative value of catheter ablation. In patients with frequent VT recurrences and ICD discharges, however, catheter ablation plays an important role as a palliative and adjunctive treatment option for arrhythmia suppression.ICD therapy has been increasingly used for secondary and also primary prevention of sudden death in patients with ARVC. In secondary prevention, the ICD has shown to improve the long-term prognosis of patients at high risk of sudden death by effective termination of life-threatening recurrences of ventricular tachyarrhythmias. However, adequate lead placement may be difficult and lead-related complications during long-term follow-up must be taken into account. The role of ICD therapy for primary prevention of sudden death in ARVC is not yet adequately defined.Ongoing international registries will provide important additional data to improve risk stratification and refine treatment algorithms in order to select the best individual treatment for arrhythmia suppression and prevention of sudden death in patients with ARVC.     

Limited clinical utility of endomyocardial biopsy in patients presenting with ventricular tachycardia without apparent structural heart disease.

To determine the cardiac pathology underlying ventricular tachyarrhythmias, endomyocardial biopsy was performed in 14 patients, 10 men and 4 women, with a mean age of 40 years (range 17-63) and no apparent structural heart disease, presenting with high-density symptomatic nonsustained ventricular tachycardia (VT) (n = 4), sustained VT (n = 6), and ventricular fibrillation (n = 4). The absence of coronary or valvular heart disease was documented by cardiac catheterization. The mean left ventricular ejection fraction was 56 +/- 10%. Noninvasive assessment of the ventricular arrhythmia was made in all patients with Holter monitoring and/or exercise testing, while invasive evaluation with programmed electrical stimulation was performed in 13 patients. Biopsy findings included subendocardial and interstitial fibrosis in 7 patients, and monocytes containing periodic acid Schiff (PAS) positive vacuoles in 1 patient; biopsy was normal in 6 patients. There was no relationship between the presence or absence of pathologic abnormalities on biopsy and left ventricular ejection fraction, presenting or induced arrhythmias, or prognosis. Pathologic evidence supporting a specific treatable diagnosis was not present in any biopsy. Drugs to suppress spontaneous (3 patients) or induced (8 patients) VT were instituted, while 2 patients were not treated. In 1 patient who was resuscitated from out-of-hospital cardiac arrest an automatic defibrillator was implanted. In 24.6 months of mean follow-up there was 1 nonfatal arrhythmia recurrence, 1 noncardiac death, and 1 sudden death in a patient with fibrosis on biopsy, an ejection fraction of 45%, and both inducible and spontaneous sustained VT suppressed with an antiarrhythmic agent.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventricular tachycardia late after repair of congenital heart disease: efficacy of combination therapy with radiofrequency catheter ablation and class III antiarrhythmic agents and long-term outcome

OBJECTIVE: This study investigated the treatment of ventricular tachycardia (VT) after repair of tetralogy of Fallot or double outlet of the right ventricle. BACKGROUND: The ideal antiarrhythmic therapy for VT in patients after repair of congenital heart disease, especially without left ventricular dysfunction, has not yet been established. METHODS: Seven consecutive patients (2 women and 5 men) with stable monomorphic sustained VT were investigated. The mean age was 25 +/- 7 years (range, 16-35 years). Four patients had undergone surgical repair of tetralogy of Fallot, and 3 had surgical correction of double outlet of the right ventricle at the mean age of 18 +/- 7 years (range, 9-27 years) before documentation of the arrhythmia. RESULTS: The mean ejection fraction of the left ventricle was 60% +/- 8% (range, 50-72). Fourteen sustained monomorphic VTs were induced in 7 patients using programmed electrical stimulation. The mean cycle length of tachycardia was 346 +/- 77 milliseconds (range, 260-480 seconds). The site of the surgical correction of the right ventricle was associated with the origin of VT in all patients. Radiofrequency catheter ablation was attempted in 8 VTs in 7 patients: 7 clinical and 1 nonclinical VTs. In 6 patients, class III antarrhythmic agents were added because VT remained inducible after ablation. During a follow-up of 61 +/- 29 months (range, 15-110 months), there were no recurrences of VT. CONCLUSION: In patients with drug-refractory VT originating from the right ventricle late after congenital heart disease, and when their left ventricular function do not deteriorate, combined therapy for radiofrequency catheter ablation with class III antiarrhythmic agents might effective and should be considered as a therapeutic option.     

Häufige ventrikuläre Tachykardie: Antiarrhythmika oder Ablation?

Antiarrhythmic drugs are used in at least 50% of patients who received an implantable cardioverter defibrillator (ICD). The potential indications for antiarrhythmic drug treatments in patients with an ICD are generally the following: reduction of the number of ventricular tachycardias (VTs) or episodes of ventricular fibrillation and therefore reduction of the number of ICD therapies, most importantly, the number of disabling ICD shocks. Accordingly, the quality of life should be improved and the battery life of the ICD extended. Moreover, antiarrhythmic drugs have the potential to increase the tachycardia cycle length to allow termination of VTs by antitachycardia pacing and reduction of the number of syncopes. In addition, supraventricular arrhythmias can be prevented or their rate controlled. Recently published or reported trials have shown the efficacy of amiodarone, sotalol and azimilide to significantly reduce the number of appropriate and inappropriate ICD shocks in patients with structural heart disease. However, the use of antiarrhythmic drugs may also have adverse effects: an increase in the defibrillation threshold, an excessive increase in the VT cycle length leading to detection failure. In this situation and when antiarrhythmic drugs are ineffective or have to be stopped because of serious side effects, catheter ablation of both monomorphic stable and pleomorphic and/or unstable VTs using modern electroanatomic mapping systems should be considered. The choice of antiarrhythmic drug treatment and the need for catheter ablation in ICD patients with frequent VTs should be individually tailored to specific clinical and electrophysiological features including the frequency, the rate, and the clinical presentation of the ventricular arrhythmia. Although VT mapping and ablation is becoming increasingly practical and efficacious, ablation of VT is mostly done as an adjunctive therapy in patients with structural heart disease and ICD experiencing multiple shocks, because the recurrence and especially the occurrence of "new" VTs after primarily successful ablation with time and disease progression have precluded a widespread use of catheter ablation as primary treatment.     

Programmed electrical stimulation to determine the need for antiarrhythmic therapy in patients with complex ventricular ectopic activity

Patients with complex ventricular ectopy (greater than or equal to Lown grade III) and organic heart disease (OHD) are at increased risk for sudden cardiac death. Despite this fact, many such patients will remain free of symptomatic ventricular arrhythmia and thus are unnecessarily exposed to antiarrhythmic drug toxicity and arrhythmic potentiation. Programmed stimulation (PS) was used to direct therapy in 88 patients with asymptomatic ventricular ectopy complicating OHD. Thirty-three had inducible ventricular tachycardia (VT) and underwent treatment. The 55 patients without inducible VT (less than or equal to 6 repetitive ventricular responses) are the focus of this study. Three patients required treatment for persistent cardiac awareness. The remaining 52 have been followed for 22 months off antiarrhythmic drugs and all have remained free of subsequent major arrhythmic events. Therefore, in patients with complex ventricular ectopy, OHD, and absence of prior symptomatic ventricular arrhythmia, PS identifies patients at low risk for future disabling or life-threatening arrhythmic episodes and patients with absence of inducible VT can usually be managed without antiarrhythmic drugs.     

Efficacy and safety of class IC antiarrhythmic agents for the treatment of coexisting supraventricular and ventricular tachycardia

Thirty-three patients with concurrent supraventricular (SVT) and ventricular tachycardia (VT) were treated with class IC antiarrhythmic agents. Twenty-two patients had atrial fibrillation (17 with paroxysmal and 5 with chronic fibrillation), 1 patient had ectopic atrial tachycardia and 11 patients had reentrant paroxysmal SVT (8 with atrioventricular node reentrant tachycardia, 3 with atrioventricular reentrant tachycardia). Of 5 patients with Wolff-Parkinson-White syndrome, 2 had only atrial fibrillation. Six patients had sustained VT and 27 had nonsustained VT. Twenty-nine patients had organic heart disease (16 with coronary artery disease, 8 with cardiomyopathy and 5 with valvular heart disease) and 4 had primary electrical disease. The mean ejection fraction was 40 +/- 14% (range 15 to 66%). The study population's arrhythmias were not controlled despite having received 2 to 5 (mean 3.1) previous drug trials. Eighteen patients were referred for treatment of SVT and 15 were referred for treatment of VT (mean symptom duration 107 months). Efficacy was determined in 13 of 33 patients with sustained SVT or VT by programmed electrical stimulation and in 20 of 33 by telemetry and 24-hour Holter response. Twenty-two flecainide and 15 encainide trials were conducted in the 33 patients. Four patients underwent trials with both drugs. Of 33 patients with coexisting SVT and VT, 15 (45%) were controlled with an IC agent alone and 3 continued therapy with an IC agent plus additional therapy (2 drugs, 1 antitachycardia pacing). During the follow-up period (mean 10.4 months), flecainide produced a complete response in 9 patients and encainide in 9 patients. SVT was not controlled in 7 patients and VT was not controlled in 7 patients. One patient had neither arrhythmia controlled. Atrial or ventricular proarrhythmia was seen in 9 of 33 patients (27%) (5 with ventricular and 4 with atrial arrhythmia). Noncardiac side effects were uncommon. Oral class IC agents may be effective therapy for some patients with coexisting VT and SVT of different mechanisms. Patients with such complex arrhythmias should be evaluated carefully because there is a potential for both atrial and ventricular proarrhythmia.     

Malignant ventricular tachyarrhythmias associated with the use of encainide

In patients treated with the antiarrhythmic drug, encainide, the agent appeared to cause or exacerbate malignant ventricular tachyarrhythmias in 11 cases. The most common type of arrhythmia associated with encainide toxicity was polymorphic ventricular tachycardia (VT) resulting in cardiac arrest. In contrast to drug-induced arrhythmias commonly encountered with quinidine and other type I antiarrhythmic drugs, encainide-induced rhythm was not associated with marked QT prolongation, was not necessarlly initiated by R-on-T premature ventricular beats, and usually did not self-terminate. Two patients could not be resuscitated from the rhythm, and several others required prolonged or multiple resuscitations. The risk of encainide-induced ventricular tachyarrhythmias was 11% in 90 patients receiving the drug for recurrent sustained VT and/or fibrillation (VF), 2.2% in 47 patients receiving the drug for chronic complex ventricular ectopic activity. Encainide-induced arrhythmias occurred 29.8 ± 11.3 hours (range 17 to 48 hours) after starting chronic oral maintenance doses or after dose increases, or 1 to 2 hours after single large doses. Patients experiencing this adverse effect could not be distinguished from those who did not on the basis of encainide dose, degree of QRS widening, or clinical status. We recommend that patients with history of sustained VT or VF have encainide therapy started only in a hospital setting with continuous ECG monitoring and capabilities for cardiopulmonary resuscitation. Dose changes should not be made more frequently than every 48 hours, and patients should not be discharged from the hospital until they have been on a stable dose of encainide for a minimum of 48 hours.     

Usefulness of programmed stimulation in idiopathic dilated cardiomyopathy

The response to programmed electrical stimulation and the clinical outcome was determined in 47 patients with nonischemic dilated cardiomyopathy (DC). Thirteen patients (group 1) presented with sustained uniform ventricular tachycardia (VT), 14 (group 2) presented with cardiac arrest and 20 (group 3) presented with nonsustained VT. The mean ejection fraction of the study population was 28 +/- 9%. The response to programmed stimulation was related to arrhythmia presentation. In all patients in group 1 sustained, uniform VT was induced, compared with 1 patient in group 2 and 2 patients in group 3 (p less than 0.001). There were 14 sudden cardiac deaths and 1 cardiac arrest during a mean follow-up of 18 +/- 14 months. The only 4 patients who presented with sustained VT or a cardiac arrest in whom sustained arrhythmia induction was suppressed with antiarrhythmic therapy remain alive. Nine of the 23 patients (4 in group 2 and 5 in group 3) in whom no sustained ventricular arrhythmia was induced died suddenly, with 5 of the 9 receiving empiric antiarrhythmic therapy. Three other patients, who had a slower and hemodynamically tolerated VT at the time of arrhythmia induction, died suddenly. Thus, in patients with nonischemic DC, uniform, sustained VT is always and almost solely initiated in patients who present with this arrhythmia; although few patients presenting with sustained VT or cardiac arrest have inducibility of the arrhythmias suppressed with therapy, if it is suppressed the patient appears to have a good prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Implantable defibrillator event rates in patients with unexplained syncope and inducible sustained ventricular tachyarrhythmias: a comparison with patients known to have sustained ventricular tachycardia

OBJECTIVES

To assess the clinical significance of inducible ventricular tachyarrhythmias among patients with unexplained syncope.

BACKGROUND

Induction of sustained ventricular arrhythmias at electrophysiology study in patients with unexplained syncope and structural heart disease is usually assigned diagnostic significance. However, the true frequency of subsequent spontaneous ventricular tachyarrhythmias in the absence of antiarrhythmic medications is unknown.

METHODS

In a retrospective case-control study, the incidence of implantable cardiac defibrillator (ICD) therapies for sustained ventricular arrhythmias among patients with unexplained syncope or near syncope (syncope group, n = 22) was compared with that of a control group of patients (n = 32) with clinically documented sustained ventricular tachycardia (VT). Sustained ventricular arrhythmias were inducible in both groups and neither group received antiarrhythmic medications. All ICDs had stored electrograms or RR intervals. Clinical variables were similar between groups except that congestive cardiac failure was more common in the syncope group.

RESULTS

Kaplan-Meier analysis of the time to first appropriate ICD therapy for syncope and control groups produced overlapping curves (p = 0.9), with 57 ± 11% and 50 ± 9%, respectively, receiving ICD therapy by one year. In both groups, the induced arrhythmia was significantly faster than spontaneous arrhythmias, but the cycle lengths of induced and spontaneous arrhythmias were positively correlated (R = 0.6, p < 0.0001). During follow-up, three cardiac transplantations and seven deaths occurred in the syncope group, and two transplantations and five deaths occurred in the control group (36-month survival without transplant 52 ± 11% and 83 ± 7%, respectively, p = 0.03).

CONCLUSIONS

In patients with unexplained syncope, structural heart disease and inducible sustained ventricular arrhythmias, spontaneous sustained ventricular arrhythmias occur commonly and at a similar rate to patients with documented sustained VT. Thus, electrophysiologic testing in unexplained syncope can identify those at risk of potentially life-threatening tachyarrhythmias, and aggressive treatment of these patients is warranted.     

Spontaneous Variability of Ventricular Ectopic Activity in Patients with Sustained Ventricular Tachycardia and in Survivors of Cardiac Arrest

Background: Spontaneous variability of ventricular arrhythmia has been described in patients with chronic stable ventricular arrhythmias and in patients with chronic heart failure. However, no data are available on spontaneous variability in patients with sustained ventricular tachyarrhythmias. Thus, the present study was designed to prospectively determine the extent of spontaneous variability of ventricular arrhythmia in patients with sustained ventricular tachyarrhythmias and in survivors of cardiac arrest. Methods: Ventricular arrhythmia variability was determined in 470 patients (413 men, 57 women), age (mean ± SD) 64.6 ± 9.5 years with documented ventricular tachycardia (VT), cardiac arrest, or syncope who were prospectively enrolled in a randomized trial of the comparison of electrophysiological testing with Holter monitoring to predict antiarrhythmic drug efficacy. Coronary artery disease was present in 398 (85%) patients, and the mean left ventricular ejection fraction was 0.32 ± 0.13. They underwent two 24-hour ambulatory recordings separated by 1 day. Spontaneous variability was determined for total premature ventricular complexes (PVCs), pairs, and VT events. Results: Arithmetic mean of hourly total PVCs on day 1 was 315 ± 425. The 95% confidence limit of spontaneous reduction in total PVC count was 71%. Corresponding values for pairs, VT events of 3–15 beats, < 15 beats, or < 15 seconds were 72%, 80%, 94%, and 95%, respectively. The percentage increases in total PVCs, pairs, and VT events 3–15 beats, < 15 beats, and < 15 seconds were 243%, 259%, 397%, 1553%, and 1756%, respectively. The percentage reduction required to show a true drug effect was 63% for patients with an ejection fraction > 0.32 and 76% for those with an ejection fraction ltm 0.32 (P = 0.024). Patients who presented with unmonitored syncope showed less spontaneous variability than either patients with documented, sustained VT or cardiac arrest. Conclusions: Marked spontaneous variability of ventricular arrhythmias is observed in patients with sustained ventricular tachyarrhythmias. Variability is affected by the degree of left ventricular dysfunction. The lowest variability was observed in patients presenting with unmonitored syncope. Thus, large changes in arrhythmia frequency must be observed in this population, as in others, to be ascribed to drug effect.     

Unexpected cardiac arrest in patients after surgical correction of tetralogy of Fallot.

Four of 220 patients without bifasicular block (complete right bundle branch block and left anterior hemiblock) or transient complete heart block immediately after surgery had an unexpected cardiac arrest one to 15 years after satisfactory surgical repair of tetralogy of Fallot. The postoperative electrocardiograms (ECG) revealed complete right bundle branch block in two patients and no intraventricle conduction abnormality in two patients. Each of the four patients had premature ventricular contractions on previous postoperative ECG. The cardiac arrest occurred during normal activity in three patients and mild exercise in one. Following the cardiac arrest, three patients died and one patient survived. Eighteen months before the cardiac arrest, the survivor had a stress test which revealed multifocal premature ventricular contractions with short bursts of ventricular tachycardia after exercise. This ventricular arrhythmia was suppressed with quinidine therapy. Although complete heart block cannot be excluded in these four patients, we reasoned that the cardiac arrests were probably preceded by ventricular tachyarrhythmia. Because of this experience, we believe that any patient who has had intraventricular surgery should be evaluated for ventricular arrhythmia. If frequent premature ventricular contractions or serious ventricular arrhythmias are documented, we seriously consider antiarrhythmic therapy in an attempt to prevent ventricular tachyarrhythmias and sudden death.     

Comparison of arrhythmia recurrence in patients presenting with ventricular fibrillation versus ventricular tachycardia in the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial

Because many episodes of ventricular fibrillation (VF) are believed to be triggered by ventricular tachycardia (VT), patients who present with VT or VF are usually grouped together in discussions of natural history and treatment. However, there are significant differences in the clinical profiles of these 2 patient groups, and some studies have suggested differences in their response to therapy. We examined arrhythmias occurring spontaneously in 449 patients assigned to implantable cardioverter-defibrillator (ICD) therapy in the Antiarrhythmics Versus Implantable Defibrillators (AVID) trial to determine whether patients who receive an ICD after VT have arrhythmias during follow-up that are different from patients who present with VF. ICD printouts were analyzed both by a committee blinded to the patients' original presenting arrhythmia and by the local investigator. During 31 +/- 14 months of follow-up, 2,673 therapies were reported. Patients who were enrolled in the AVID trial after an episode of VT were more likely to have an episode of VT (73.5% vs 30.1%, p <0.001), and were less likely to have an episode of VF (18.3% vs 28.0%, p = 0.013) than patients enrolled after an episode of VF. Adjustment for differences in ejection fraction, previous infarction, and beta-blocker and antiarrhythmic therapy did not appreciably change the results. Ventricular arrhythmia recurrence during follow-up is different in patients who originally present with VT than in those who originally present with VF. These findings suggest there are important differences in the electrophysiologic characteristics of these 2 patient populations.     

Autonomic Modulation for the Treatment of Ventricular Arrhythmias: Therapeutic Use of Percutaneous Stellate Ganglion Blocks

Ventricular tachycardia (VT), ventricular fibrillation (VF), and electrical storm are commonly encountered emergency conditions in cardiac and surgical intensive care units. In most cases, recurrent ventricular arrhythmias or electrical storm are associated with a heightened sympathetic tone. These arrhythmias can be difficult to treat and may be refractory to beta‐blockade, antiarrhythmic therapy, sedation, and mechanical hemodynamic support. While monomorphic ventricular tachycardia and PVC‐triggered polymorphic ventricular tachycardia may sometimes be amenable to successful ablation, some patients may be too critically ill to make such an approach feasible. We present 2 cases of minimally invasive stellate ganglion blocks for the treatment of electrical storm in patients with advanced heart failure on mechanical life support. These cases are part of a collaborative initiative at our institution to use percutaneous stellate ganglion block as an adjunctive intervention to achieve control of life‐threatening ventricular arrhythmias.     

Rhythmusstörungen bei Schwangeren

Atrial premature beats are frequently diagnosed during pregnancy (PR) and supraventricular tachycardia (SVT) (atrial tachycardia, AV nodal reentrant tachycardia, circus movement tachycardia) less frequently. For acute therapy, electrical cardioversion with 50–100 J is indicated in all unstable patients. In stable SVT the initial therapy includes vagal maneuvers to terminate breakthrough tachycardias. For short-term management, when vagal maneuvers fail, intravenous adenosine is the first choice drug and may safely terminate the arrhythmia. For long-term therapy, ß-blocking agents with β₁ selectivity are first-line drugs; class Ic agents or the class III drug sotalol (sot) are effective and therapeutic alternatives. Ventricular premature beats are also frequently present during PR and benign in most of the patients; however, malignant ventricular tachyarrhythmias [sustained ventricular tachycardia (VT), ventricular flutter (VFlut), ventricular fibrillation (VF)] were observed less frequently. Electrical cardioversion is necessary in all patients with hemodynamically unstable situation and life-threatening ventricular tachyarrhythmias; in hemodynamically stable patients, initial therapy with ajmaline, procainamide or lidocaine is indicated. If prophylactic therapy is needed, ß-blocking agents with ß₁ selectivity are considered as first choice drugs. If this therapy is ineffective, class Ic agents or sot can be considered. In patients with syncopal VT, VF, VFlut or aborted sudden death an implantable cardioverter-defibrillator is indicated. In patients with symptomatic bradycardia, a pacemaker can be implanted using echocardiography at any stage of PR. The treatment of the pregnant patient with cardiac arrhythmias requires important modification of the standard practice of arrhythmia management. The goal of therapy is to protect the patient and fetus through delivery, after which chronic or definitive therapy can be administered. In addition, antiarrhythmic therapy is also possible during breastfeeding.