Current concepts in diagnosis and treatment of tachyarrhythmias

A diagnostic and therapeutic approach of supraventricular and ventricular tachyarrhythmia is always challenging. Several criteria serve to discriminate correctly between these two types of tachycardia. Cardiac arrhythmias are terminated reliably by intravenous (IV) application of antiarrhythmic drugs: adenosine for supraventricular arrhythmia, amiodarone or ajmaline for ventricular tachycardia. Furthermore, AV-nodal tachycardia, atrioventricular reciprocating tachycardia, and typical atrial flutter is treated curatively by radiofrequency ablation during an electrophysiological study. This interventional therapy is well established in patients suffering from ventricular premature contractions or tachycardia originating in the right or left ventricular outflow tract. Aside treatment with an implantable defibrillator, patients with coronary artery disease highly benefit from adjusted pharmaceutical treatment.     

Management of fetal tachyarrhythmias

Opinion statement Fetal tachyarrhythmias are an important cause of fetal morbidity and mortality. The majority of fetal tachyarrhythmias are due to atrioventricular reentrant type of supraventricular tachycardia and atrial flutter. Fetal echocardiography remains the main tool of diagnosing and discerning the mechanism of tachyarrhythmia. The goals of therapy for fetal arrhythmias are to restore sinus rhythm, resolve heart failure, and postpone delivery before term. Although there is no anonymity in the approach to the drug treatment of fetal tachycardia, digoxin is the most commonly employed first-line antiarrhythmic drug for supraventricular tachycardia. In digoxin nonresponders, flecainide (± digoxin) controls tachyarrhythmia with high conversion rate. A combination of digoxin and sotalol has proved effective therapy for atrial flutter, but the proarrhythmic side effect of sotalol on the fetus has been a concern. Amiodarone has emerged as a second-line treatment after digoxin failure in nonhydropic fetuses and the most effective treatment for drug-refractory fetal tachycardia accompanied by hydrops. Both the fetus and mother should be closely monitored for the response and adverse effect of the treatment. The antiarrhythmic treatment for supraventricular tachycardia should be continued after birth and during infancy due to the high incidence of postnatal recurrence.     

The contribution of artificial pacemaking to understanding the pathogenesis of arrhythmias

Right atrial or ventricular pacing was performed on 36 occasions in 26 patients in an attempt to terminate a variety of tachyarrhythmias. Of 16 episodes of atrial flutter, 13 were terminated successfully; in 9 of the 13, sinus rhythm or the patient's pre-flutter rhythm was restored immediately, whereas in 4 patients, intervening atrial fibrillation or unstable atrial flutter occurred. Pacing terminated paroxysmal atrioventricular junctional or paroxysmal atrial tachycardia on 3 occasions; in a fourth patient, this tachyarrhythmia terminated during catheter manipulation. Six episodes of pacemaker-induced ventricular tachycardia were abolished by ventricular pacing. In 2 patients, atrial tachycardia was only transiently suppressed, and in 1 of these patients, d-c cardioversion produced a similar effect. Atrial fibrillation, spontaneously converting to atrial flutter, resulted during pacing for atrial tachycardia with block; the latter arrhythmia returned when the atrial flutter was terminated. Atrial fibrillation in 7 patients remained unaffected by atrial pacing. Based on the different electrophysiologic mechanisms responsible for reentrant excitation and automatic pacemaker discharge, an attempt has been made to determine the pathogenesis of the tachyarrhythmia by its response to pacing.     

Arrhythmogenic effect of ajmaline on the atrial level

The aim of this study was to determine whether an antiarrhythmic, Ajmaline, could have proarrhythmic effects on the atrium and to compare the results with those of other antiarrhythmic drugs. A total of 1950 patients without cardiac failure or recent (less than 6 weeks) myocardial infarction were given 1 mg/kg of Ajmaline intravenously during electrophysiological investigation. A proarrhythmic effect was defined as the occurrence of supraventricular tachycardia (SVT) in a patient without this arrhythmia before the test or the facilitation of its induction. Fifty five patients developed SVT (mainly atrial tachyarrhythmias: 48 cases, and some junctional tachycardia: 7 cases) which occurred spontaneously in 22 patients and during fixed atrial pacing in 33 patients. Fifteen patients developed ventricular tachycardia (VT). The predisposing factors for the development of SVT were: a previous history suggesting spontaneous SVT (28 patients; 51 p. 100); sinoatrial block (14 patients--the only abnormality in 10 cases). Seventeen patients had none of these factors but 8 had known cardiac pathology and the other 9 were relatively elderly patients (79 years). Twelve of the patients developing VT had known cardiac disease, bundle branch block in 12 cases and previous VT in 6 cases. In conclusion, proarrhythmic effects of Ajmaline are infrequent if its contraindications are respected, but they do exist at both atrial (2.8 p. 100) and ventricular levels (0.8 p. 100): the risk factors are comparable: previous spontaneous arrhythmias or ECG changes (SA block at the atrial and bundle branch block at the ventricular level).     

Catheter Ablation of Inducible Atrial Flutter, in Combination with Atrial Pacing and Antiarrhythmic Drugs (“Hybrid Therapy”) Improves Rhythm Control in Patients with Refractory Atrial Fibrillation

Atrial flutter or tachycardia may coexist with atrial fibrillation [AF] and can be treated with ablation techniques in attempt to reduce the total AF burden. The role of ablation of latent atrial tachyarrhythmias elicited at electrophysiologic study in conjunction with atrial pacing and antiarrhythmic drugs in patients with refractory AF has not been evaluated. We evaluated the efficacy of catheter ablation of electrically induced atrial flutter or atrial tachycardia in improving rhythm control in patients with refractory AF. Methods: Consecutive patients with refractory AF, and spontaneous atrial flutter (Group 1) or without spontaneous atrial flutter (Group 2) underwent programmed stimulation in a baseline drug-free state. All patients had electrically induced atrial flutter or tachycardia. Radiofrequency ablation of the arrhythmia substrate was performed in all patients. Primary endpoints evaluated for patient outcome in both groups included maintenance of rhythm control and freedom from recurrent atrial tachyarrhythmias. Results: Forty-three patients, with a mean age of 66±13 years were studied. Group 1 consisted of 22 patients while Group 2 had 21 patients. Ablation of the tricuspid valve-inferior venacaval isthmus was performed in 41 patients who had common atrial flutter induced at electrophysiologic study. Ablation of other atrial sites was performed in 8 patients with induced atypical flutter and 4 patients with induced atrial tachycardia. Ten of these patients had ablation of more than one arrhythmia. 17 patients (40%) had atrial pacing instituted and 28 patients remained on a class 1/3 antiarrhythmic drug. During a mean follow-up of 26±14 months, 33 patients (82.5%) remained in rhythm control. Actuarial analysis showed 96% of patients in rhythm control at 6 months, 94% at 12 months, and 90% at 24 months. Freedom from symptomatic AF recurrence was 64% at 6 months, 58% at 12 months, and 42% at 24 months. The outcome for both of these endpoints was similar for Group 1 and Group 2 (p = NS). The AF free interval increased significantly from 7±9 days to 172±121 days (p < 0.01) after ablation. This increase was again similar in both the groups. In the 14 patients were who did not receive atrial pacing and who remained on the same class 1/3 antiarrhythmic drug, the AF free interval increased from 18±17 days to 212±102 days (p < 0.01). Conclusions: We conclude that electrophysiologic studies can elicit latent atrial flutter or tachycardia in patients with refractory AF without spontaneous monomorphic atrial tachyarrhythmias. Catheter ablation of electrically induced atrial flutter or tachycardia either alone, or with atrial pacing and with antiarrhythmic drug may improve rhythm control and reduce AF recurrences. This is similar in patients with and without spontaneous atrial flutter and refractory AF.     

Combining Antiarrhythmic Drugs and Implantable Devices Therapy: Benefits and Outcome

At least 50% of patients who received an ICD have been treated with antiarrhythmic drugs (AAD). The potential indications for combining antiarrhythmic drugs and ICD are generally the following: reduction of the number of episodes of ventricular tachycardia or ventricular fibrillation and therefore of the number of shocks, improving patient's quality of life and extending the battery life of the ICD, prevention of supraventricular arrhythmias and/or control of their rate, lengthening of the tachycardia cycle length to allow ventricular tachycardia conversion by antitachycardia pacing and reduction of the number of episodes of syncope.Although previous papers reported conflicting results about pharmacologic therapy in reducing the frequency of iCD shocks, some recent randomized prospective studies showed the efficacy of pharmacologic therapy in reducing the frequency of ICD shocks.The use of antiarrhythmic drugs can have also adverse effect: an increase in the defibrillation threshold, an increase in the pacing threshold and an increase in the VT cycle length leading to detection failure. We have also to consider that some advantages derived from antiarrhythmic drugs can be reached by the new devices with atrial sensing and pacing and/or the possibility of atrial defibrillation or by using catheter ablation as adjunctive therapy to ICD.For these reasons, the concomitant use of antiarrhythmic drugs and ICD should be evaluated in each patient in relation to specific clinical and electrophysiologic features including: the frequency, the rate and the clinical presentation of the ventricular arrhythmia, the effect of the selected drug on the defibrillation threshold, the defibrillation threshold at the implant, the effect of the selected drug on the ventricular function and the likelihood of proarrhythmic events.     

Wolff-Parkinson-White syndrome with orthodromic supraventricular tachycardia associated with a "hyper-conductor" atrio-ventricular node. A therapeutic challenge

One case of Wolff-Parkinson-White Syndrome with paroxysmal supraventricular tachycardia related to orthodromic atrioventricular reentry using an accessory pathway for retrograde conduction an a rapidly conducting AV node for anterograde conduction is present. The pharmacological therapy with Digoxin, Propranolol, Quinidine, Disopyramide and Propafenone was not effective. An electrophysiologic study showed a reciprocating tachycardia induced by spontaneous ventricular beats. Both the effective refractory period of the AV node and the anterograde effective refractory period of the accessory pathway were minor or equal to 220 msec which made the control of the arrhythmia difficult. Amiodarone was able to suppress the premature ventricular beats, depress conduction and prolong refractoriness in both, the AV node and accessory pathway to prevent recurrences of atrioventricular reentry. In this patient a false positive test with ajmaline was documented. The electrophysiologic study showed the association of Wolff-Parkinson-White Syndrome with an enhanced atrioventricular nodal-conduction and allowed the selection of an appropriate antiarrhythmic agent.     

Quantitation of day to day variability in mode of induction of ventricular tachyarrhythmias by programmed stimulation

Spontaneous day to day variability in the mode of induction of ventricular tachycardia at programmed stimulation in the drug-free state has been described but not quantitated. To quantitate this variability, this study employed a new protocol of programmed stimulation in which the number of extrastimuli required for tachycardia induction was the only major stimulation variable. This protocol was applied to 18 consecutive patients with previously documented sustained ventricular tachyarrhythmia due to coronary artery disease. One to seven extrastimuli were available for arrhythmia induction if required. Each patient underwent programmed stimulation in the absence of antiarrhythmic drugs on 3 separate days with a mean interval of 5 ± 2.7 days between studies.A sustained ventricular tachyarrhythmia was inducible in all studies with ≤4 extrastimuli; the mean number of extrastimuli required was 2.4 ± 0.8. Day to day variability in the number of extrastimuli required for tachycardia induction was observed in the majority of patients (72%). Eleven patients (61%) varied by one extrastimulus over the three control studies, and two patients (11%) varied by two extrastimuli. At analysis of variance, the 95% confidence interval for the degree of day to day variability was ± 1 extrastimulus from the mean number required in the three studies. Multiple configurations of induced ventricular tachycardia were frequently observed at repeat studies and occurred in 15 patients (83%).In conclusion, spontaneous day to day variability in mode of induction of ventricular tachycardia in the absence of drugs is common. The 95% confidence limit is a sizable ±1 extrastimulus from the mean, representing a variability of ± 46% of the mean value. Failure to allow for this variability will cause false estimations of antiarrhythmic drug efficacy at electrophysiologic testing.     

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.     

Utility of transesophageal atrial pacing in the diagnostic evaluation of patients with unexplained syncope associated or not with palpitations

BACKGROUND: Noninvasive studies are often negative in patients with syncope, normal surface ECG and without heart disease. The purpose of the study was to determine the diagnostic impact of an esophageal electrophysiological study performed during a consultation. METHODS: A total of 154 patients aged from 16 to 87 years were consecutively recruited for unexplained syncope; they had a normal ECG in sinus rhythm, no documented arrhythmia and no patent heart disease. Half of them complained of palpitations. Electrophysiologic study was performed during a consultation by transesophageal route: rate of 2nd d AV block occurrence during atrial pacing and sinus node recovery time were determined; programmed atrial stimulation using one and two atrial extrastimuli were delivered in control state and then after infusion of 0.02-1 microg/min of isoproterenol; arterial blood pressure was monitored. RESULTS: (1) Electrophysiologic study was positive in 107 patients (69%); (2) sinus node dysfunction was noted in 9 patients (6%); (3) atrioventricular conduction disturbances were noted in 2 patients (1%); (4) vasovagal reaction which associated a junctional bradycardia and a fall of arterial blood pressure and which reproduced spontaneous symptoms was provoked by isoproterenol infusion in 21 patients (14%); (5) sustained atrial fibrillation was induced in 23 patients (15%); and (6) paroxysmal junctional tachycardia was induced in 52 patients (34%). Patients with negative study were younger (44+/-21.5 years) than those with sinus node dysfunction or atrial fibrillation (71+/-9 and 63+/-14 years, respectively). The treatment was guided by these data: patients with inducible atrial fibrillation were treated by antiarrhythmic drugs and those with inducible paroxysmal junctional tachycardia by the radiofrequency ablation of reentrant circuit. Syncope disappeared in all patients but 2. CONCLUSION: Esophageal electrophysiologic study performed during a consultation was a safe, rapid and economic means to detect an arrhythmia (sinus node dysfunction or supraventricular tachycardia) in patients with dizziness/syncope and palpitations in half cases. Supraventricular tachycardia was clearly an underestimated cause of syncope in this population.     

Electrophysiologic effects of penticainide in patients with supraventricular tachycardia

The electrophysiologic effects of the new class-I antiarrhythmic drug pentisomide were investigated after intravenous (5 mg/kg) application in nine patients with atrioventricular nodal reentrant tachycardia and six patients with atrioventricular tachycardia. Pentisomide did not change sinus cycle length, effective refractory period of the right ventricle (ERP-RV), the AV-node (ERP-AVN) and QT interval. Intranodal (AH-interval) and infranodal conduction time (HV-interval), effective refractory period of the right atrium (ERP-A), QRS duration, antegrade effective refractory period of the accessory pathway (ERP-Kent), ventricular cycle length during atrial fibrillation and tachycardia cycle length were significantly (P less than 0.05) increased. Intravenous pentisomide prevented induction of the tachycardia in 5/9 patients with atrioventricular nodal tachycardia and in 2/6 patients with atrioventricular tachycardia. The electrophysiologic properties of pentisomide indicate that it might be a useful drug in the treatment of supraventricular tachycardia.     

External cardiac programmed stimulation for noninvasive termination of sustained supraventricular and ventricular tachycardia

To examine the feasibility of using a noninvasive temporary pacemaker for termination of well-tolerated supraventricular (SVT) and ventricular tachycardia (VT), a standard external demand pacemaker was modified to allow stimulation with single or multiple extrastimuli and overdrive pacing. To evaluate the efficacy, safety and tolerance of external cardiac programmed stimulation, a standard arrhythmia termination protocol was used in 223 tachycardias in 22 patients. The technique of external cardiac programmed stimulation was used in 209 episodes of SVT in 13 patients. It terminated 95% of the episodes with success in 19 of 20 episodes of atrioventricular nodal reentrant tachycardia and 179 of 189 episodes of atrioventricular reciprocating tachycardia. Of 198 episodes of SVT terminated by the technique 168 (85%) were terminated by a single extrastimulus and 28 (14%) by double extrastimuli. Only 2 episodes of SVT required overdrive pacing for termination. External cardiac programmed stimulation did not result in atrial fibrillation or arrhythmia acceleration. Of 14 episodes of sustained monomorphic VT 5 were terminated by external cardiac programmed stimulation. One tachycardia was terminated by a single extrastimulus, 1 by double extrastimuli and 3 by overdrive pacing. Arrhythmia acceleration occurred once and was terminated by endocardial pacing. On 27 separate occasions patient evaluation of maximal discomfort included 4 ratings of mild, 10 of moderate, 11 of severe and 2 of intolerable discomfort. External cardiac programmed stimulation is effective and safe in patients with well-tolerated sustained supraventricular or ventricular arrhythmias.     

An approach to therapy of supraventricular tachyarrhythmias: An algorithm versus individualized therapy

Approaches to the treatment of supraventricular arrhythmias, including atrial fibrillation, atrial flutter, atrial tachycardia, atrioventricular (AV) reentrant tachycardia, and AV nodal reentrant tachycardia, continue to evolve. Within the past two decades, many new and effective treatments have become available. These include several new antiarrhythmic agents, ablative therapies, pacing and surgical modalities, and cardioversion/defibrillation techniques. This paper provides an algorithm for the treatment of these supraventricular arrhythmias which includes therapy for the acute episode as well as the prevention of subsequent episodes of the tachyarrhythmia.     

Reversion of supraventricular tachyarrhythmias by means of atrial stimulation.

Thirteen patients with different forms of supraventricular tachyarrhythmia were treated by means of right atrial pacing. Reversion of arrhythmia was obtained in nine out of ten patients with atrial tachycardia or flutter. The remaining three patients, with atrial fibrillation, did not respond to the procedure. The effective pacing rate in converting arrhythmia ranged from 110 to 2400/min, however in five cases it was lower than the atrial rate. The duration of pacing at an effective rate ranged from 20 seconds to 5 minutes in 5 cases, while in the remaining patients it lasted 10 minutes. In two patients the original arrhythmia was converted to atrial fibrillation during stimulation, but in one it disappeared with pacing at 110/min, and in the other, reversion to sinus rhythm occurred spontaneously 4 hours later. No complications were observed. It is concluded that atrial pacing may be useful aid to treat paroxysmal atrial tachycardia or flutter, and can be considered as an alternative procedure whenever there is no response to customary medical treatment or when transthoracic direct current cardioversion is potentially dangerous.     

Idiopathic ventricular fibrillation: inducibility and beneficial effects of class I antiarrhythmic agents

Ventricular fibrillation in patients without recognizable heart disease is uncommon and electrophysiologic data on such patients is limited. Over a 7 year period, five patients (three men and two women, ranging in age from 24 to 52 years) without demonstrable heart disease underwent electrophysiologic studies with pharmacologic drug testing because of single (four patients) or multiple (one patient) documented episodes of ventricular fibrillation. The arrhythmic event was unrelated to myocardial ischemia or infarction, metabolic or electrolyte disturbances, drug toxicity, preexcitation, or prolonged QT syndromes. In all three patients receiving no antiarrhythmic drugs and in two pretreated with amiodarone, a rapid poorly tolerated ventricular tachyarrhythmia requiring cardioversion was induced by programmed ventricular stimulation with up to two extrastimuli. In all instances, addition of either oral quinidine or oral disopyramide prevented the induction of sustained ventricular arrhythmias. All five patients were placed on antiarrhythmic drug regimens found effective during electrophysiologic studies and remained asymptomatic during follow-up periods ranging from 12 to 93 (mean 52) months. We conclude that in the patients with idiopathic ventricular fibrillation in our study: programmed ventricular stimulation reliably replicated the spontaneous arrhythmia, class I antiarrhythmic agents effectively prevented induction of the arrhythmia in the laboratory, and in contrast to the severity of the presenting arrhythmia, a benign clinical course was observed during long-term therapy with class I antiarrhythmic agents.     

Termination of recurrent supraventricular tachycardia by right ventricular endocardial pacing but not by left ventricular epicardial pacing

Externally controlled ventricular pacing was employed in a patient with recurrent disabling supraventricular tachycardia and frequent sinus pauses between attacks of tachyarrhythmia. A permanent transthoracic demand pacemaker was inserted after electrophysiologic study demonstrated the effectiveness of ventricular stimulation in terminating induced supraventricular tachycardia. Subsequently, spontaneous recurrences of tachyarrhythmia failed to respond to fixed rate left ventricular stimulation accomplished by placing a magnet externally over the pacemaker pack. During an induced supraventricular tachycardia, repeat electrophysiologic study demonstrated that paced left ventricular beats failed to invade the A-V junctional area before it was depolarized previously by the corresponding tachycardia beat. Right ventricular stimulation from a transvenous pacemaker could depolarize the site of the reentrant circuit and terminate an induced supraventricular tachycardia. The addition of propranolol increased the ease by which spontaneous attacks of tachyarrhythmia could be terminated by right ventricular endocardial pacing.     

Ablation of cardiac tissues by an electrode catheter technique for treatment of ectopic supraventricular tachycardia in adults

Five patients with chronic or recurrent ectopic supraventricular tachycardias unresponsive to drugs underwent programmed stimulation, endocardial mapping, and attempted catheter ablation of the arrhythmia focus. For attempted ablation, an intracardiac electrode catheter was positioned near the exit point of the tachycardia and served as the cathode while a chest wall patch served as the anode. In two patients with tachycardia originating near the coronary sinus, discharges of 200 or 400 J each were delivered to two electrodes at the earliest area of endocardial activation. These two patients with incessant tachycardia remain free of tachycardia for 17 and 11 months, respectively. In one patient with tachycardia originating from the right atrial appendage, both catheter and surgical ablation proved unsuccessful in that a new focus of atrial tachycardia supervened. This patient subsequently underwent successful catheter ablation of the atrioventricular junction. Two patients with junctional tachycardia underwent catheter ablation of the atrioventricular junction. Complete atrioventricular block followed atrioventricular junctional ablation and these patients required permanent cardiac pacing. The junctional tachycardia was replaced by sinus rhythm with episodes of unsustained atrial tachycardia. However, after 13 +/- 5 months follow-up, neither of the patients require antiarrhythmic drugs. Catheter ablation can be effective for atrial foci near the coronary sinus os, and can be performed with preservation of atrioventricular conduction. Arrhythmia ablation is possible in those with atrioventricular junctional tachycardia but requires the sacrifice of atrioventricular conduction. After ablation, other automatic atrial foci may become operative and complicate use of dual-chamber pacemakers.     

Clinical types of proarrhythmic response to antiarrhythmic drugs

The problem of drug-induced or drug-aggravated cardiac arrhythmias has been recognized for many years. Digitalis glycosides and class I, II, III, or IV antiarrhythmic drugs can cause severe sinus node dysfunction or atrioventricular block. Digitalis can cause a variety of supraventricular arrhythmias; atrial tachycardia with block and nonparoxysmal atrioventricular junctional tachycardia are the most characteristic. Recognition that class IA and class III antiarrhythmic drugs can aggravate arrhythmias or cause new arrhythmias in patients being treated for potentially malignant or malignant ventricular arrhythmias has intensified the interest in proarrhythmia in recent years. Several characteristic types of proarrhythmic response have been described. Torsades de pointes (multiform) ventricular tachycardia (VT) accompanied by prolongation of the QT interval can be caused by class IA and class III antiarrhythmic drugs as well as other drugs that bind to the membrane sodium channels of ventricular cells, for example, tricyclic antidepressants. Uniform VT in patients with malignant ventricular arrhythmias and poor left ventricular function is a characteristic proarrhythmic response to class IC antiarrhythmic drugs. Bidirectional VT or accelerated idioventricular rhythm are characteristic of digitalis toxicity. More difficult to establish as proarrhythmic responses are increased frequency of ventricular premature depolarizations and increased ease of inducing VT with programmed ventricular stimulation.     

Bradycardia-mediated tachyarrhythmias in congenital heart disease and responses to chronic pacing at physiologic rates

The coexistence of bradycardia and a tachyarrhythmia may preclude effective pharmacologic treatment of 1 arrhythmia without paradoxic aggravation of the other. This study evaluated the potential relation between the 2 types of arrhythmias and the effect of conventional modes and rates of pacing for bradycardia on the frequency of the associated tachyarrhythmias. Twenty-one young patients, aged 2 to 19 (mean 11) years with congenital heart disease and a tachyarrhythmia occurring in the setting of chronic bradycardia were studied. The effects of pacing were evaluated by comparison of the number of episodes of clinical tachycardia during the 12-month intervals before and after pacemaker implantation. During these intervals, antiarrhythmic drug therapy was not altered. Patients were analyzed as independent groups, based on the type of tachyarrhythmia: supraventricular (n = 5), atrial flutter (n = 9) and ventricular (n = 7). The modes of chronic pacing were AAI (n = 4), DDD (n = 6) and VVI (n = 11). The prevention of bradycardia by pacing was associated with a significant decrease in the frequency of supraventricular (p = 0.008) and ventricular (p = 0.02) tachyarrhythmias. However, the frequency of atrial flutter was not altered. Prevention of tachycardia was more frequently associated with the AAI and DDD modes of pacing compared to VVI (p = 0.08). Pacing represents an effective therapy for certain tachyarrhythmias associated with chronic bradycardia, although critical modes may be required.     

Functional abnormalities of the conduction system in children with an atrial septal defect

We performed an electrophysiologic study in 40 children with an atrial septal defect and analyzed their pre- and postoperative electrocardiograms and 24-hour Holter recordings. The electrophysiologic study showed a prolonged corrected sinus node recovery time in 83% and an abnormal sinuatrial conduction time in 25% of the children. An early Wenckebach response to atrial pacing was seen in 18%. Sixteen percent had a prolonged atrial conduction time. The atrial functional refractory period was abnormal in 35%. Two children developed nonsustained supraventricular tachycardia during the electrophysiologic study. The preoperative electrocardiogram showed first-degree atrioventricular block in 15% of the children; prolonged periods of accelerated atrial rhythm were found in 35% of the preoperative 24-hour Holter recordings. The incidence of first-degree atrioventricular block and accelerated atrial rhythm decreased postoperatively. We could not find a significant correlation between age or shunt size and the presence of electrophysiologic abnormalities or arrhythmias. These results indicate that the sinus node, atrioventricular node and atrial myocardium show some degree of dysfunction in patients with an atrial septal defect. An early operation may prevent further progression of electrophysiologic abnormalities and the development of symptomatic arrhythmias.