The diagnosis and management of supraventricular tachycardia by transesophageal cardiac stimulation and recording

Twenty-two consecutive patients underwent esophageal stimulation and recording for the diagnosis and management of supraventricular tachycardia. In 13 of these patients, the resting electrocardiogram was normal and in nine it showed pre-excitation. Of the 13 patients with a normal resting electrocardiogram, supraventricular tachycardia was initiated in all. Seven patients had a ventricular-to-atrial interval greater than 70 ms during supraventricular tachycardia suggesting the presence of a concealed accessory pathway, and six patients had a ventricular-to-atrial interval less than 70 ms during supraventricular tachycardia suggesting reentry within the atrioventricular node. Supraventricular tachycardia was initiated in four of nine patients with pre-excitation on the resting electrocardiogram and the accessory pathway was confirmed by a ventricular-to-atrial interval of greater than 70 ms during supraventricular tachycardia in these four patients. Atrial fibrillation was initiated in eight of the nine patients with pre-excitation on the resting electrocardiogram and the shortest R-R interval during atrial fibrillation was measured. The response to therapy was assessed in seven of these nine patients by further measurement of the shortest R-R interval during atrial fibrillation following treatment. Esophageal stimulation and recording provides a simple noninvasive procedure which can be utilized as a screening technique to identify patients with intranodal reentry and those with reentry utilizing an accessory pathway. Sequential assessment of the response to therapy, especially in those patients with pre-excitation, is of considerable value in treatment.     

Radiofrequency ablation for treating paroxysmal supraventricular tachycardia complicated by atrial fibrillation:A single-center retrospective analysis

Background The effect of selective radiofrequency ablation for treating paroxysmal supraventricular tachycardia(PSVT) and its associated paroxysmal atrial fibrillation(PAF) was assessed. Methods Data were collected retrospectively from patients diagnosed of PSVT and subsequently treated with radiofrequency ablation. Regular monthly follow-up by dynamic electrocardiography(ECG) was performed. Incident rates of atrial fibrillation before and after ablation were compared. Results 382 PSVT patients with 58 having atrial fibrillation were enrolled. The order of complicated PAF from high to low in these patients was displayed as: atrial tachycardia(AT),atrioventricular reentrant tachycardia(AVRT) and atrioventricular nodal reentrant tachycardia(AVNRT). Among AVRT patients, PAF was more frequent in patients having accessory pathways. AVNRT patients had significantly lower PAF rate comparing to other patients. PAF incident rate was significantly reduced by radiofrequency ablation therapy. Conclusion We advise regular dynamic ECG for PSVT patients, especially those with atrial flutter, AT or pre-excitation syndrome. Selective radiofrequency ablation is a feasible approach for treating AF complicated PSVT patients.     

Internal transvenous low energy cardioversion for the treatment of cardiac arrhythmias

Low energy endocardial cardioversion was attempted in 23 patients with 30 arrhythmias, of whom only four were receiving additional drug treatment. Four had atrial flutter, five atrial fibrillation, three intra-atrioventricular nodal tachycardia, two atrioventricular re-entrant tachycardia, 13 ventricular tachycardia, and three ventricular fibrillation. A pacing lead with special large surface area electrodes--the active electrode positioned either in the right atrium or in the right ventricular apex and the indifferent electrode in the right atrium, superior vena cava, or inferior vena cava--was used together with a low energy defibrillator. A total of 114 shocks was delivered, 26 of which were atrial. One episode of atrial flutter was terminated, but atrial fibrillation and atrioventricular nodal tachycardia were not terminated in any of the patients. Both patients with atrioventricular tachycardia were successfully treated, as were eight of the patients with ventricular tachycardia. Atrial fibrillation was produced in three patients and non-sustained ventricular tachycardia in one, ventricular tachycardia was accelerated in two, and ventricular fibrillation induced in five. Fourteen patients experienced severe discomfort and seven mild or moderate discomfort, and only one found the procedure painless. One patient was anaesthetised throughout the procedure. Low energy endocardial cardioversion is not universally successful even at the highest energies tolerable, and with the present electrode and pulse waveforms some patients may suffer considerable discomfort.     

Catheter ablation of atrial flutter due to amiodarone therapy for paroxysmal atrial fibrillation.

AIMS: Antiarrhythmic drug treatment for atrial fibrillation can cause atrial flutter-like arrhythmias. The aim of this study was to clarify the effect of catheter ablation of the tricuspid annulus-vena cava inferior isthmus on amiodarone-induced atrial flutter and to determine the incidence of atrial fibrillation after catheter ablation of amiodarone-induced atrial flutter in comparison to regular typical flutter. METHODS AND RESULTS: Among 92 consecutive patients with typical atrial flutter who underwent isthmus ablation 28 patients had atrial flutter without a history of previous atrial fibrillation (group I), 10 patients had atrial flutter following the initiation of amiodarone therapy for paroxysmal atrial fibrillation (group II) and 54 patients had atrial flutter and atrial fibrillation (group III). Atrial cycle length during atrial flutter in amiodarone-treated patients (group II) (277+/-24 ms) was significantly longer as compared to the cycle length of atrial flutter in group I (247+/-33 ms) and group III patients (235+/-28 ms). The rate of successful transient entrainment and overdrive stimulation to sinus rhythm was not different between patients with (60%) or without amiodarone therapy (group I: 71%, group III: 53%). Successful isthmus ablation with bidirectional conduction block eliminating right atrial flutter was achieved in 90% of amiodarone-treated patients and 93% of patients without amiodarone therapy. In the amiodarone-treated patient group atrial conduction times during pacing in sinus rhythm were significantly prolonged by 20-30% before and after ablation in all regions of the reentrant circuit. During a mean follow-up of 8+/-3 months post-ablation, atrial fibrillation recurred in two of 10 patients on continued amiodarone therapy after successful isthmus ablation. Thus, successful catheter ablation of atrial flutter due to amiodarone therapy was associated with a markedly lower recurrence rate of paroxysmal atrial fibrillation (20%) as compared to patients with atrial flutter plus preexisting paroxysmal atrial fibrillation (76%) and was similar to the outcome of patients with successful atrial flutter ablation without preexisting atrial fibrillation (25%). CONCLUSION: These data suggest that isthmus ablation with bidirectional block and continuation of amiodarone therapy is an effective therapy for the treatment of atrial flutter due to amiodarone therapy for paroxysmal atrial fibrillation.     

Internal transvenous low energy cardioversion for the treatment of cardiac arrhythmias.

Low energy endocardial cardioversion was attempted in 23 patients with 30 arrhythmias, of whom only four were receiving additional drug treatment. Four had atrial flutter, five atrial fibrillation, three intra-atrioventricular nodal tachycardia, two atrioventricular re-entrant tachycardia, 13 ventricular tachycardia, and three ventricular fibrillation. A pacing lead with special large surface area electrodes--the active electrode positioned either in the right atrium or in the right ventricular apex and the indifferent electrode in the right atrium, superior vena cava, or inferior vena cava--was used together with a low energy defibrillator. A total of 114 shocks was delivered, 26 of which were atrial. One episode of atrial flutter was terminated, but atrial fibrillation and atrioventricular nodal tachycardia were not terminated in any of the patients. Both patients with atrioventricular tachycardia were successfully treated, as were eight of the patients with ventricular tachycardia. Atrial fibrillation was produced in three patients and non-sustained ventricular tachycardia in one, ventricular tachycardia was accelerated in two, and ventricular fibrillation induced in five. Fourteen patients experienced severe discomfort and seven mild or moderate discomfort, and only one found the procedure painless. One patient was anaesthetised throughout the procedure. Low energy endocardial cardioversion is not universally successful even at the highest energies tolerable, and with the present electrode and pulse waveforms some patients may suffer considerable discomfort.     

持续性心房颤动经导管射频消融治疗的方法探讨(附三例报告)

探讨经导管射频消融治疗持续性心房颤动 (简称房颤 )的可行性。 3例房颤患者房颤持续时间 2个月至 1年4个月。术前口服胺碘酮 ,1例转为窦性心律伴频发房性早搏 (简称房早 ) ,1例转为房早与短阵房颤和阵发心房扑动 (简称房扑 ) ,1例转为房早与阵发房性心动过速 (简称房速 )。经导管作点状消融或点状消融加房扑线性消融 ,2例术中房早消失 ,1例房早显著减少 ,经快速心房刺激或静脉点滴异丙肾上腺素均不能诱发房颤。 1例术后有短阵房颤发作 ,服用莫雷西嗪 ,房颤未再发作。结论 :某些持续性房颤用药物后可转复成窦性心律伴频发房早、房扑或房速 ,局部单点消融或单点消融加线性消融可以达到治疗目的。     

Use of Propafenone in Patients With Supraventricular Tachycardia

Propafenone prolongs refractoriness and slows conduction of the atrium, atrioventricular node, and accessory atrioventricular pathway. By interfering with conduction in locations necessary to support supraventricular tachycardia, propafenone effectively treats several mechanisms of rhythm disturbance. Early experience shows that propafenone, when administered in the electrophysiology laboratory, effectively terminates or prevents reinduction of paroxysmal supraventricular reentrant tachycardia in 50% to 75% of patients. The most effective dose associated with the fewest side effects has been 2 mg/kg infused over 10 minutes. Long-term success with propafenone has been demonstrated in patients with paroxysmal atrial fibrillation, paroxysmal atrial flutter, atrioventricular node reentrant tachycardia, atrioventricular reentrant tachycardia using a concealed accessory pathway, and tachycardias associated with the Wolff-Parkinson-White syndrome, including paroxysmal atrial fibrillation and atrioventricular reentrant tachycardia. In 67% (range, 27% to 89%) of patients receiving long-term therapy with propafenone, episodes of supraventricular tachycardia have been either eliminated or significantly reduced in frequency and treatment has not had to be stopped because of side effects. The effective daily dose for longterm therapy has been 550 to 750 mg administered in three or four divided doses. Although the number of patients reported in the literature at this time is small, propafenone appears to be an effective agent for treating supraventricular tachycardia due to one of several mechanisms.     

Assessment and follow-up of pediatric survivors of sudden cardiac death

In the young patient resuscitated from sudden cardiac arrest, the risks of recurrence are uncertain and so are the criteria defining therapeutic efficacy for the presumed cause of the initial event. In this study, we analyzed the outcome of 15 consecutive young patients, who were resuscitated from pulseless ventricular tachycardia or ventricular fibrillation and who were evaluated by comprehensive hemodynamic and electrophysiological testing. Patients were 11.2 +/- 2.7 (mean +/- SD) years old at the time of their event, and each was known to have some form of heart disease before sudden cardiac arrest. Ventricular tachycardia or fibrillation was inducible by programmed electrical stimulation in eight patients. Accessory atrioventricular connections, with antegrade effective refractory periods less than 220 msec, were identified in three patients. Sustained atrial flutter was the only arrhythmia inducible in two patients, and no arrhythmias were inducible in two other patients. Surgical or electrophysiological-guided medical therapy resulted in noninducibility of the ventricular arrhythmias in six patients. Surgical division of the accessory atrioventricular connections was performed in three patients, and arrhythmias were not inducible after operation. The four patients with atrial flutter or without defined arrhythmia were treated with an empiric therapy. During 37 +/- 14 months of follow-up, the nine patients with documented noninducibility of a defined cause of sudden cardiac arrest were free of recurrent events. In contrast, during 18 +/- 10 months of follow-up, two of the six patients with empiric therapy or persistent inducibility of ventricular tachycardia died suddenly, and three others had recurrence of ventricular tachycardia or fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiac arrhythmias in patients with surgical repair of Ebstein's anomaly

Preoperative, perioperative and postoperative arrhythmias in 52 consecutive patients who underwent operation for Ebstein's anomaly were reviewed. There were 25 male and 27 female patients (mean age 18 years, range 11 months to 64 years). Thirty-four patients had one or more documented arrhythmias preoperatively (18 had paroxysmal supraventricular tachycardia, 10 had paroxysmal atrial fibrillation or flutter, 13 had ventricular arrhythmia and 3 had high grade atrioventricular block). Seven patients without documented arrhythmias had a history typical of tachyarrhythmias. During the perioperative and early postoperative periods, 14 patients had atrial tachyarrhythmias and 8 had ventricular tachycardia or ventricular fibrillation. There were seven deaths between day 1 and 27 months after operation. Five of these deaths were sudden (all in male patients, aged 12 to 34 years), and four of the patients had had perioperative ventricular tachycardia or ventricular fibrillation. One patient was taking one antiarrhythmic agent and another patient was taking two at the time of sudden death. Of the 18 patients with paroxysmal supraventricular tachycardia and 9 patients with paroxysmal atrial fibrillation or flutter preoperatively who were followed up for a mean of 40 and 36 months, respectively, 22 and 33% continued to have symptomatic tachycardia. Of the 11 patients (mean age 9 years) without preoperative documentation or symptoms of arrhythmia, follow-up data were obtained (range 1 to 144 months, mean 31) in 9 patients. None died suddenly or developed symptomatic arrhythmia.     

Paroxysmal supraventricular tachycardia induction in patients with Wolff-Parkinson-White syndrome.

In 54 patients with pre-excitation, 30 (56%) had inducible A-V re-entrant paroxysmal tachycardia. Of these 30, 20 had spontaneous paroxysmal tachycardia (four also had atrial fibrillation), four had spontaneous paroxysmal atrial fibrillation, five had a history of palpitation without arrhythmia, and one was asymptomatic. In 24 patients (44%), paroxysmal tachycardia was not inducible. Of these 24, none had documented paroxysmal tachycardia, four had atrial fibrillation, none had palpitation without arrhythmia, and 11 were asymptomatic. The incidence of documented paroxysmal tachycardia was higher in the patients with inducible tachycardia (P less than 0.001). Tachycardia induction was noted in 20 of 20 patients with spontaneous paroxysmal tachycardia, eight of 12 patients with paroxysmal atrial fibrillation, five of 14 patients with palpitation and no arrhythmia, and one of 12 asymptomatic patients. The frequency of ability to induce paroxysmal tachycardia was significantly higher in both the patients with documented spontaneous paroxysmal tachycardia and the patients with paroxysmal atrial fibrillation than in the asymptomatic group (P less than 0.01).     

Cryoablation of the accessory pathway in Wolff-Parkinson-White syndrome: initial results and long term follow up.

Cryoablation of the accessory pathway was used in the management of 20 patients with pre-excitation syndromes. All patients had presented with paroxysmal atrioventricular reentrant tachycardia; in addition, six had experienced atrial fibrillation. In 16 patients pre-excitation was overt and in four the accessory pathway was concealed. Intraoperative epicardial and endocardial mapping showed 10 left free wall pathways, seven septal pathways, and four right free wall pathways. One patient had two right free wall accessory pathways. There was one postoperative death (from a ruptured cerebral haemangioma) and one patient had transient hemiparesis. There was early recurrence of arrhythmia or pre-excitation in six patients and five of these were among the first ten in the series. Four of the six underwent successful reoperation; 17 patients remain symptom free of all antiarrhythmic treatment. Two patients did not undergo reoperation--one became symptom free on drugs that had previously been ineffective and the other received an antitachycardia pacemaker. The mean period of follow up was six years. Accessory pathway function was not restored and atrioventricular nodal function was preserved in all patients, demonstrating the feasibility of this technique in the long term management of patients with the pre-excitation syndrome.     

Cryoablation of the accessory pathway in Wolff-Parkinson-White syndrome: initial results and long term follow up

Cryoablation of the accessory pathway was used in the management of 20 patients with pre-excitation syndromes. All patients had presented with paroxysmal atrioventricular reentrant tachycardia; in addition, six had experienced atrial fibrillation. In 16 patients pre-excitation was overt and in four the accessory pathway was concealed. Intraoperative epicardial and endocardial mapping showed 10 left free wall pathways, seven septal pathways, and four right free wall pathways. One patient had two right free wall accessory pathways. There was one postoperative death (from a ruptured cerebral haemangioma) and one patient had transient hemiparesis. There was early recurrence of arrhythmia or pre-excitation in six patients and five of these were among the first ten in the series. Four of the six underwent successful reoperation; 17 patients remain symptom free of all antiarrhythmic treatment. Two patients did not undergo reoperation--one became symptom free on drugs that had previously been ineffective and the other received an antitachycardia pacemaker. The mean period of follow up was six years. Accessory pathway function was not restored and atrioventricular nodal function was preserved in all patients, demonstrating the feasibility of this technique in the long term management of patients with the pre-excitation syndrome.     

Effect of amiodarone in the Wolff-Parkinson-White syndrome

The effect of amiodarone in the Wolff-Parkinson-White syndrome was studied with programmed electrical stimulation of the heart in 15 patients. All 15 patients had circus movement tachycardias; 7 also had atrial fibrillation. Programmed electrical stimulation was performed before and after 14 days of oral administration of amiodarone. The effective refractory period of the accessory pathway lengthened in an atrioventricular direction in all patients and in a ventriculoatrial direction in eight patients. The effective refractory period of the atrium and ventricle lengthened in 14 and 12 patients, respectively. After administration of amiodarone, circus movement tachycardia could no longer be initiated in five patients. The zone of tachycardia narrowed in four patients, did not change in two and increased in seven. The effect of amiodarone on initiation of circus movement tachycardia could be related to differences in effect of the drug and in the mechanism of tachycardia in individual patients. In all patients in whom tachycardias could still be initiated after treatment with amiodarone the heart rate during tachycardia was slower than before treatment. This slowing was caused by a decrease in conduction velocity of the circulatory wave in different parts of the tachycardia circuit. The effect of amiodarone in prolonging the refractory period of the accessory pathway makes this drug especially useful in patients with the Wolff-Parkinson-White syndrome and atrial fibrillation.     

Advances in the acute pharmacologic management of cardiac arrhythmias

Safe and effective control of rapid ventricular rates in acute-onset atrial fibrillation (AF) can be accomplished with intravenous calcium antagonists, beta-blockers or amiodarone; digoxin is less effective. If pharmacologic cardioversion of AF is desired, single oral doses of propafenone or flecainide are safe and effective in patients without structural heart disease. Intravenous ibulitide is moderately effective in the conversion of persistent AF or atrial flutter, with a small risk of proarrhythmia. In wide QRS complex tachycardia of uncertain origin, adenosine and lidocaine are no longer recommended. Procainamide or amiodarone are the treatment options, but attempts should be made to define the origin of tachycardia. In the treatment of monomorphic ventricular tachycardia, lidocaine is no longer recommended; procainamide or amiodarone are the recommended therapies. In polymorphic ventricular tachycardia with a normal QT interval, beta-blockers are recommended. In shock-refractory ventricular fibrillation, lidocaine, and magnesium are ineffective; intravenous amiodarone should be the treatment of choice.     

Paroxysmal Atrial Fibrillation on Flecainide Therapy

Flecainide pill-in-the-pocket therapy is a pharmacologic treatment option for patients with infrequent episodes of symptomatic atrial fibrillation. We report a case of wide complex tachycardia due to atrial flutter with 1:1 atrioventricular conduction in a patient who took pill-in-the-pocket flecainide without concomitant atrioventricular nodalblockade.     

Regular ventricular rhythms in patients with symptomatic paroxysmal atrial fibrillation

Paroxysmal atrial fibrillation is a grossly irregular tachycardia. Forty-nine patients with paroxysmal atrial fibrillation who were taking a variety of antiarrhythmic medications including the class IC agents propafenone and flecainide were followed up for a median of 371 days with use of transtelephonic electrocardiogram (ECG) monitoring to document symptomatic rhythms. Eighteen patients had 96 episodes of regular tachycardia; the cumulative incidence rate was 25% at 6 months, 33% at 1 year and 41% at 18 months. Eighty of the 96 episodes occurred with a heart rate less than or equal to 180 beats/min and could have been explained by atrial flutter with 2:1 block. However, nine patients had a total of 16 episodes with a rate greater than 180 beats/min that were probably not due to atrial flutter with block; the cumulative incidence rate of these fast regular tachycardias was 14% at 6 months, 17% at 1 year and 25% at 18 months. QRS duration during the first episode of regular tachycardia was significantly longer in patients taking a class IC drug (median 105 vs 90 ms, p less than 0.001 Wilcoxon rank sum test). In contrast to drug therapy with amiodarone or the combination of digoxin and verapamil, the QRS duration of regular tachycardias during class IC therapy was directly related to the tachycardia heart rate (Spearman's rank, p less than 0.01). All episodes of fast, regular tachycardias with a QRS duration greater than 120 ms occurred in patients taking a class IC drug. Clinicians treating patients with paroxysmal atrial fibrillation should expect a substantial incidence of regular tachycardia in addition to atrial fibrillation.     

Intravenous amiodarone in the acute termination of supraventricular arrhythmias

This study was performed to ascertain whether intravenous amiodarone would revert supraventricular tachycardias to sinus rhythm, and if so, whether this effect depended upon the underlying mechanism of the arrhythmia. Fourteen patients were studied. Seven had Wolff-Parkinson-White (WPW) syndrome, 1 had dual atrioventricular nodal pathways and 1 an ectopic atrial tachycardia. Five patients had atrial fibrillation without accessory pathways. An atrial electrode was inserted to initiate tachycardias and record the electrogram. If tachycardias were stable for more than 5 min, amiodarone (5 mg/kg) diluted with dextrose saline was infused intravenously over 5 min. Two electrocardiographic leads and the right atrial electrogram were monitored. In 7 patients with atrial fibrillation (2 with accessory pathways), 6 did not revert to sinus rhythm, 1 reverted only after 1 hr. In 5 cases without accessory pathways the ventricular rate fell 5-10 min after commencing amiodarone. Four of the 5 patients with WPW syndrome and re-entrant tachycardias returned to sinus rhythm within 6 min of commencing the infusion (atrioventricular and ventriculoatrial times increased by 0-38% and 0-14% respectively). (Tachycardias terminated in the anterograde limb.) Three patients underwent intermittent right atrial stimulation for 1 hr. No tachycardias could be initiated for 30 min post amiodarone. The ectopic atrial tachycardia and that due to dual atrioventricular nodal pathways terminated within 7 and 2 min, respectively, of commencing intravenous amiodarone. Thus the use of intravenous amiodarone would be appropriate in the acute management of sustained supraventricular tachycardias.     

Treatment of recurrent supraventricular tachyarrhythmias with flecainide or a flecainide and amiodarone combination

The acute electrophysiologic effects and therapeutic efficacy of intravenous and oral flecainide were assessed in 18 patients with recurrent supraventricular tachyarrhythmias, resistant to conventional antiarrhythmic agents. They were 22 to 76 years old (mean 50). Twelve patients underwent electrophysiologic study for the investigation of tachyarrhythmias. Of the whole four patients had functional longitudinal AH dissociation (dual AV pathways). These patients had provocable intra-AV nodal reentrant tachycardia (Group I). Six patients had a direct accessory AV pathway, that showed bidirectional conduction in 5 and retrograde conduction alone in 1 (Group II). These patients had provocable atrioventricular reentrant tachycardia using the accessory pathway as the retrograde limb of the tachycardia circuit. Two patients suffered from automatic supraventricular tachycardia (Group III). Group IV included patients with paroxysmal atrial flutter or fibrillation. The patients of this group did not discontinue chronic treatment with amiodarone. After baseline electrophysiologic evaluation, intravenous flecainide (2 mg/Kg body weight over 5 minutes) was given to patients of I and II group during induced reentrant tachycardia. Flecainide was administered to other patients during spontaneous episodes of tachyarrhythmias. Flecainide resulted in tachycardia termination in all patients of group I and in 4 patients of group II (66%). Tachycardia termination was due to block in the retrograde limb of the circuit. Before termination tachycardia cycle length increased significantly, mainly as the result of an increase in ventriculo-atrial conduction time. After intravenous flecainide therapy, reentrant SVT was non inducible in the patients of group I and in 4 patients of group II. Flecainide was successful in the acute termination of 100% of automatic supraventricular tachycardia and 75% of fibrillation. The patients with atrial flutter developed a faster ventricular rate.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Amiodarone therapy in symptomatic,sustained refractory atrial and ventricular tachyarrhythmias

Amiodarone was utilized in 70 patients with symptomatic, sustained refractory tachyarrhythmias. Of these, 29 had atrial arrhythmia (20 recurrent atrial fibrillation and nine sustained supraventricular tachycardia). Control was achieved in eight with supraventricular tachycardia and in 16 with atrial fibrillation. Recurrence has been prevented in these 24 patients (83%) during an average follow-up of 13.4 months. An additional 41 patients had recurrent ventricular tachycardia. In 19 with symptoms consisting of dizziness or lightheadedness without syncope or clinically apparent hemodynamic compromise, treatment was limited to amiodarone. Of these, 14 responded (74%) and have been free of arrhythmia during an average follow-up of 13 months. In 22 who experienced either syncope or life-threatening hemodynamic impairment, amiodarone was added to those agents which had only partially suppressed advanced grades of ventricular premature beats. Fourteen of these patients (64%) have remained free of recurrent ventricular arrhythmia during an average follow-up of 12 months. After drug loading, maintenance therapy consisted of a daily dose ranging from 200 to 600 mg. Only mild side effects have been encountered in the 17 patients (23%) with any untoward responses. This experience confirms that oral amiodarone is an effective and safely applied agent against recurrent refractory atrial tachyarrhythmia and sustained intractable ventricular tachycardia with moderate symptoms. While also efficacious in refractory sustained life-threatening ventricular tachyarrhythmia, usage of the agent is often difficult in this condition owing in part to insufficient information concerning amiodarone pharmacokinetics.