Oral flecainide in the treatment of refractory arrhythmias. Long-term follow-up of 98 patients

Oral flecainide was administered to 98 patients with arrhythmias regarded as resistant to other antiarrhythmic agents: quinidines (82), propafenone (40), beta-blockers (30), amiodarone alone (38) or combined with a class I compound (19). Therapeutic effectiveness was assessed on clinical date, repeated Holter recordings (64 patients), exercise tests (8) and electrophysiological exploration (15). Mean follow-up was 11.7 +/- 11 months; the patients treated have now been followed up for 18.2 +/- 12 months (range: 7-58 months). Fifty-three patients had atrial arrhythmia (fibrillation or flutter in 45, atrial tachycardia in 8). Flecainide was effective in 26 patients (49%) and ineffective in 27 (51%). There was no significant difference in dosage between these 2 groups: 231 +/- 62 mg/day and 265 +/- 61 mg/day respectively. Paroxysms of re-entrant junctional tachycardia were controlled in 6 of the 8 cases observed. Eleven patients presented with Wolff-Parkinson-White syndrome: treatment was successful in the 3 patients with atrial fibrillation and in 8 of the 10 patients with orthodromic reciprocating rhythms. Among 30 patients with episodes of ventricular tachycardia, 9 (30%) responded to flecainide and 21 (70%) failed to respond. Flecainide reduced the repetitive forms by more than 90% in 7/15 patients and suppressed exercise-induced ventricular tachycardia in 2/8 patients. Fifteen out of 18 patients had ventricular tachycardia reproducible by programmed stimulation; under flecainide, the ventricular tachycardia spontaneously recurred in 4 cases, was provoked by stimulation in 5 other cases, was more easily inducible in 3 cases and was not inducible in a sustained manner in the last 3 cases.(ABSTRACT TRUNCATED AT 250 WORDS)     

Anti-arrhythmia efficacy of propafenone in children. Apropos of 30 cases

Thirty children aged from 3 months to 20 years were treated with propafenone 250 to 650 mg/m2 divided into 2 to 4 daily doses, for a mean period of 14 months (range: 4 days to 5 years); 8 had chronic atrial tachycardia, 9 had junctional arrhythmia and 13 had ventricular arrhythmia. There were 17 good results (suppression of the arrhythmia), 7 fair results (good clinical effect but partial persistence of the arrhythmia) and 6 failures, either because the drug proved ineffective (3 cases) or on account of side-effects (3 cases). In the treatment of chronic atrial tachycardia propafenone seemed to be more effective than amiodarone in 3 cases and as effective as that drug in 2 cases. In junctional arrhythmia propafenone was certainly effective but unpredictably so (3 good results, 2 fair results, 4 failures). Among ventricular arrhythmias, ventricular tachycardia in bursts was the one which benefited most regularly from treatment with propafenone: the results in 8 patients were better than those obtained with other antiarrhythmic agents (class I drugs, beta-blockers, calcium antagonists); only amiodarone proved superior to propafenone in this type of arrhythmia. Despite a 27% incidence of side-effects, propafenone was generally well tolerated by the children, with no significant gastrointestinal disorders. No depressive effect on the myocardium was noted in 6 children with moderate heart failure well controlled by digitalis and diuretics. However, since overdosage may cause severe disorders of conduction with widened ventriculogram, we recommend regular ECG monitoring during the first 3 days of treatment at least: although there is little slowing down of sinus rate (12%) and little modification of the slow phase under treatment, serious toxicity is possible. Thus, propafenone is a drug that should be handled with caution, but it constitutes a major addition to the range of antiarrhythmic agents which can be used in paediatrics.     

Anti-arrhythmic effect of oral propafenone. Apropos of 70 cases

During a 3 year period, seventy patients aged 53 +/- 16 years with a total of 73 arrhythmias were treated over a mean period of 6.8 months (maximum 27 months) with oral propafenone, the usual dose being 900 mg/day. The study covered the whole spectrum of cardiac arrhythmias (32 supraventricular, 41 ventricular), and their relation to the autonomic nervous system. The efficacy was scored from 1 (no effect) to 5 (complete control) as judged by the clinical response, the results of Holter monitoring (175 control and 133 test recordings on therapy), and a comparison was made between the effects of propafenone and other antiarrhythmics: quinidine-like drugs, beta-blockers and amiodarone. With respect to supraventricular arrhythmias: 9 cases of vagally-induced atrial flutter and fibrillation were unaffected by propafenone (mean score = 1.1). On the other hand, the drug was very effective (mean score = 4.1) in 8 cases of adrenergic atrial arrhythmias. In 12 arrhythmias with more varied mechanisms (extrasystoles, tachysystole, paroxysmal atrial fibrillation) an intermediate score was obtained (2.8). Three cases of resistant junctional tachycardia due to reentry were improved. At ventricular level, 5 cases of extrasystole sensitive to quinidine were also improved by propafenone (4.6); the difference was more clearcut in 8 cases of benign idiopathic tachycardia (propafenone: 4.1, and quinidine: 2.4). This was more marked in 13 cases of more severe arrhythmia in diseased hearts in which the effect of propafenone (4.1) was superior even to that of amiodarone. However, propafenone was less effective (3.3) than amiodarone in 4 cases of severe polymorphic idiopathic ventricular tachycardia closely related to the autonomic nervous system. The antiarrhythmic effect of propafenone was appreciable in 10 cases of resistant post-infarction ventricular tachycardia, eventually in association with amiodarone. Slowing of the sinus rhythm (-11.6%) with no change in the day/night ratio was due to beta-inhibition. However, in toxic doses this may progress to sinoatrial block (9 cases). A lengthening of the PR interval and duration of QRS was common, but this was not complicated by torsade de pointes, one case of which was successfully treated by propafenone. Secondary gastro-intestinal effects and vertigo were rarely severe enough to warrant stopping therapy. In conclusion, these results show that the introduction of propafenone is a valuable therapeutic advance in the treatment of arrhythmias, especially in those with a favoring adrenergic mechanism.     

European experience with the antiarrhythmic efficacy of propafenone for supraventricular and ventricular arrhythmias

Seventy-one patients (mean age 53 years) were treated with oral propafenone, 900 mg/day, for a mean of 6.6 months. A large spectrum of arrhythmias was encountered, and particular attention was paid to their relation with the autonomic nervous system. Drug efficacy was graded from 1 (no effect) to 5 (complete control) according to the clinical result and Holter recording. This method permitted comparisons to be made between propafenone and 3 other antiarrhythmic agents: quinidine, beta-blockers and amiodarone. Among the 32 patients with supraventricular arrhythmias, 9 cases of vagally dependent atrial flutter and fibrillation were less sensitive to propafenone (mean effect 1.4) than to quinidine (mean effect 2.0) or amiodarone (mean effect 2.3). However, 8 cases of adrenergically dependent atrial tachycardia and fibrillation were more sensitive to propafenone (mean effect 4.1) than to beta blockers (3.0) or amiodarone (mean effect 3.5). In 12 cases of miscellaneous atrial arrhythmias the response to propafenone was intermediate. However, 3 patients with resistant junctional tachycardia were improved with propafenone. Among 42 ventricular arrhythmias, 5 patients with extrasystole who were responsive to quinidine (mean effect 3.8) were also improved with propafenone (mean effect 4.6). Propafenone (mean effect 4.1) was much more effective than quinidine (mean effect 2.4) in treating 8 cases of idiopathic benign ventricular tachycardia and even more successful in treating 13 cases of more severe arrhythmias in diseased hearts (propafenone's mean effect 4.1, quinidine's mean effect 1.9 and amiodarone's mean effect 1.9). Propafenone was less effective (mean effect 3.3) than amiodarone (mean effect 4.0) in 4 cases of severe, adrenergically dependent idiopathic ventricular tachycardia (VT).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Clinical experience with propafenone for cardiac arrhythmias in the young

Seventy-two children were treated with propafenone between 1980and 1990. The mean age was 34 months (range 0.192). Arrhythmiasincluded atrioventricular re-entry tachycardia in 32 patients(44%), atrial flutter in 16 (22%), atrial or junctional ectopictachycardia in 10 (14%), atrial re-entry tachycardias in three(4%) and ventricular arrhythmias in 11 patients (16%). The efficacyof oral treatment was good in patients with atrio-ventricularre-entry tachycardia (80%), atrial flutter (71%) and atrialectopic tachycardia (83%); it was poor in ventricular arrhythmias(40%). The mean oral dose was 13.5 mg. kg^–1. day^–1. Dosageand serum levels of propafenone did not differ whether the patientswere treated successfully or not. No correlation between dosageand serum level was observed. Intravenous propafenone administrationwas only partially successful in suppressing supraventriculartachycardias (6 of 11 patients). The presence of a congenital heart defect and the time of onsetof the arrhythmias had a significant influence on the efficacyof propafenone. Better results were observed in patients withnormal hearts and in whom onset of arrhythmia was pre-natal(success 80%) as well as in patients with arrhythmias seen earlyafter surgery for congenital heart defects (success 87%). Success(65%) was also observed in patients without congenital heartdefects and postnatal onset of supraventricular arrhythmias.Patients with ventricular or supraventricular arrhythmias lateafter corrective surgery showed the poorest response (31%).     

Clinical Comparison of Ibutilide and Propafenone for Converting Atrial Flutter

Objective: To evaluate the efficacy and safety of intravenous ibutilide and propafenone for immediate treatment of atrial flutter.Methods: Forty patients with atrial flutter with an arrhythmia duration of three hours to 90 days were randomized to receive up to two 10-minute infusions of ibutilide (1 and 1 mg) or propafenone (70 and 70 mg) with a 10-minute interval.Results: Ibutilide was superior to propafenone for treating atrial flutter (90% vs. 30%, p < 0.01). The median conversion time in the ibutilide group was 11 min (the 25th and 75th percentile was 10 and 45 min), and the median conversion time in the propafenone group was 35 min (range 20–55 min). In all patients, the duration of arrhythmia before treatment was a predictor of arrhythmia termination, although this was more obvious in the group that received ibutilide. Conversion of atrial flutter by ibutilide was characterized mainly by increased cycle length variability. Bradycardia (2/20) and hypotension (4/20) were more common side effects with propafenone. Of 20 patients given ibutilide, 8 (40%) who developed monomorphic ventricular extrasystoles or repetitive atrial flutter with aberrant conduction tachycardia, no one required any specific treatment except for the interruption of ibutilide infusion.Conclusion: Ibutilide is highly effective for rapidly terminating atrial flutter. This new class III drug, under monitored conditions, is a potential alternative to currently available cardioversion options.     

Inducible ventricular flutter and fibrillation predict for arrhythmia occurrence in coronary artery disease patients presenting with syncope of unknown origin

INTRODUCTION: Ventricular fibrillation and ventricular flutter (cycle length < or = 230 msec) induced at electrophysiologic studies are thought to be nonspecific findings in patients presenting with syncope of unknown origin. However, there are limited data on the prognosis of these patients in long-term follow-up. METHODS AND RESULTS: We followed 274 consecutive patients with coronary artery disease presenting with syncope or presyncope who underwent electrophysiologic studies from January 1992 to June 1999 and assessed the risk of subsequent arrhythmias stratified by the electrophysiologic result at the time of their presentation with syncope. Ventricular fibrillation was induced in 23 patients (8%); ventricular flutter in 24 (9%), sustained ventricular tachycardia in 41 (15%); and nonsustained ventricular tachycardia 42 (15%). In 37 +/- 25 months of follow-up, there have been ventricular arrhythmias in 34 patients, including 3 (13%) of 23 who had induced ventricular fibrillation, and 7 (30%) of 24 with induced ventricular flutter, compared to 13 (32%) of 41 with sustained ventricular tachycardia, 7 (17%) of 42 with nonsustained ventricular tachycardia, and only 4 (3%) of 144 noninducible patients (P < 0.001 for induced ventricular fibrillation and ventricular flutter vs noninducible patients). The inducibility of ventricular fibrillation and ventricular flutter were independent risk factors for arrhythmia occurrence in follow-up. CONCLUSION: Ventricular fibrillation and ventricular flutter induced at electrophysiologic studies have prognostic significance for arrhythmia occurrence in patients presenting with syncope. These induced arrhythmias may not be as nonspecific as previously thought and treatment should be considered for these patients.     

Effectiveness of intravenous propafenone for conversion of atrial fibrillation and flutter of recent onset

The efficacy of intravenous propafenone (2 mg/kg) was assessed in 83 consecutive patients: 68 with atrial fibrillation (AF) and 15 with atrial flutter lasting less than 15 days. Conversion to sinus rhythm occurred in 47 patients (57%), including 42 (62%) of those with AF and 5 (33%) of those with atrial flutter (p less than 0.05). The mean time to conversion was 29 +/- 24 minutes. The success rate was strongly affected by arrhythmia duration. Thus, conversion occurred in 40 patients (71%) among the 56 with arrhythmia lasting less than 48 hours but in 7 patients (26%) among the 27 with a longer lasting arrhythmia (p less than 0.0005). Left atrial size (determined echocardiographically in 56 patients) was significantly larger in nonconverters (49 +/- 12 vs 39 +/- 7 mm, p less than 0.0005). In nonconverters the mean ventricular rate decreased from 141 +/- 26 to 104 +/- 22 beats/min (p less than 0.0005). Except for reversible low output state in 3 patients already hemodynamically compromised, no significant side effects were observed. In conclusion, (1) intravenous propafenone allows a quick restoration of sinus rhythm in the majority of patients with AF of recent onset, whereas it seems less effective in atrial flutter; (2) its efficacy is influenced by the duration of the arrhythmia and by left atrial dimensions; (3) the drug allows control of ventricular rate; and (4) its use seems to be safe except in patients with severe cardiac failure.     

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.     

Pharmacological treatment of young children with permanent junctional reciprocating tachycardia

Our objective was to assess the efficacy of pharmacological treatment in reducing the incidence of permanent junctional reciprocating tachycardia in young children, or to bring the mean heart rate over 24 h to a normal level. We included 21 children with a median age of 0.05 year seen with permanent junctional reciprocating tachycardia over the period 1990 through 2001. Of these children, two had abnormal left ventricular function. Follow-up visits were made at least every 6 months. We registered the presence of the tachycardia over 24 h, the mean heart rate over 24 h, and cardiac function. Treatment was started with propafenone alone, or in combination with digoxin as the first choice. Treatment was effective in 14 cases (67%), with either complete disappearance of the tachycardia after discontinuation of medication, or continuation in sinus rhythm with medication; partially effective in 4 cases (20%) when the mean heart rate over 24 h on the last Holter recording was less than 1 standard deviation above the normal for age; but was not effective in the remaining 3 cases (14%). In 3 patients treated with propafenone, or 13 given propafenone and digoxin, treatment was effective in 12 (75%), partially effective in 2 (13%), and ineffective in the other 2 (13%). All 21 children had a normal left ventricular function at the end of follow-up. The median duration of follow-up was 2.4 years. Permanent junctional reciprocating tachycardia had disappeared spontaneously in one-third of the children, 5 being less than 1 year old. Adverse effects, seen in 5 cases, were mild or asymptomatic. No signs of proarrhythmia were registered. Pharmacological treatment, either with propafenone alone, or in combination with digoxin, is safe and effective in young children with permanent junctional reciprocating tachycardia. The mean heart rate is normalized, and cardiac function is restored and preserved. Radiofrequency ablation may be delayed to a safer age, with the arrhythmia disappearing spontaneously in one-third.     

Propafenone in the prevention of non-ventricular arrhythmias associated with the Wolff-Parkinson-White syndrome

The antiarrhythmic effect of oral propafenone was evaluated in 10 patients with Wolff-Parkinson-White syndrome presenting with non-ventricular arrhythmias (paroxysmal supraventricular tachycardia n = 7, atrial fibrillation or flutter n = 3). The mean age was 38 +/- 13 years, the dose varied from 300 to 900 mg three times a day (mean 450 +/- 188) and the mean follow-up period was 7 +/- 3.5 months. All patients' drug responses were assessed on 12-lead electrocardiograms and 24-hour ambulatory Holter monitoring. Electrophysiologic studies were performed in cases of sustained tachycardia while echocardiography identified 2 cases with mitral valve prolapse. Four of 10 (40%) patients became asymptomatic on a starting propafenone dose of 300 mg, while 6 (60%) had recurrences necessitating an increase in dose for the complete control of the symptoms. We observed a slight slowing of the heart rate and an increase of the mean Q-T interval (P less than 0.001). Three patients reported minor side effects including nausea, dizziness and constipation that were tolerable and dosage dependent. It is concluded that propafenone is an effective and well tolerated drug for the treatment of non-ventricular arrhythmias associated with the Wolff-Parkinson-White syndrome.     

Electrophysiological and electropharmacological studies in pre-excitation syndromes: results with propafenone therapy and isoproterenol infusion testing.

To study the electrophysiological effects of oral propafenone on accessory pathways and determine the potential for catecholamine-mediated reversal of these effects, comprehensive electrophysiology studies (EPS) were conducted in 11 patients with manifest (n = 9) or concealed (n = 2) pre-excitation syndrome. EPS were performed at baseline (in the drug-free state), after oral propafenone loading, and with isoproterenol infusion during propafenone therapy. The study group included 10 men and 1 woman with a mean age of 39 +/- 13 years, who presented with symptoms of palpitations (n = 6), presyncope (n = 3) and syncope (n = 2). The clinical arrhythmia was atrioventricular reciprocating tachycardia (n = 6), atrial flutter/fibrillation (n = 3), or both (n = 2). During the baseline EPS the accessory pathway location was identified as left (n = 6) or septal (n = 5). The mean anterograde effective refractory period was 265 +/- 42 ms, the shortest pre-excited RR interval 259 +/- 20 ms and the retrograde refractory period 258 +/- 39 ms. Orthodromic atrioventricular reciprocating tachycardia was induced in 10 patients (mean cycle length = 324 +/- 31 ms). Antidromic reciprocating tachycardia was induced in one patient (cycle length = 340 ms). In all the 11 patients EPS were repeated after 4 days of oral propafenone loading (668 +/- 226 mg daily) when drug steady state was expected to have been achieved. One additional patient had baseline EPS but developed clinical arrhythmia recurrences after propafenone loading and thus he was excluded from the study; follow-up EPS were conducted on procainamide.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effectiveness of oral sotalol for treatment of pediatric arrhythmias.

Sotalol is a beta blocker with class III activity. Few investigators have reported its use in pediatric patients. From August 1985 to May 1990, 66 patients (mean age 8.7 years; range 9 days to 24 years), including 14 infants aged less than 3 months, were treated with oral sotalol alone (n = 46) or in association with digoxin (n = 20). Supraventricular reentrant tachycardia was present in 38 patients (20 with documented preexcitation), atrial flutter in 10 and atrial ectopic tachycardia in 7. Three patients had other types of supraventricular tachycardia. Tachycardia was of ventricular origin in 6 patients and both of supraventricular and ventricular origin in the remaining 2. Mean dose of oral sotalol was 135 mg/m2/day given in 2 doses. Congenital heart disease was present in 28 patients, 14 with previous cardiac surgery, mostly at the atrial level. Prior treatment with 1 or more antiarrhythmic agent had been unsuccessful in 83% of patients. Mean duration of treatment was 13.3 months (range 2 months to 5 years). Overall, treatment was successful in 79% of cases. Highest rate of success was observed in patients with supraventricular reentrant tachycardia with or without preexcitation (89%) and in those with atrial ectopic tachycardia (85.5%). Atrial flutter could be controlled in 60% of cases. Sotalol seemed less effective in ventricular tachycardia with a complete control of the arrhythmia being achieved in only 17%; however, it decreased the number of runs of ventricular tachycardia and the number of ventricular premature complexes in 50% of patients. There were no adverse effects in 89% of patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Efficacy and safety of intravenous and oral propafenone in pediatric cardiac dysrhythmias

Propafenone was administered to 58 patients with a mean age of 3.2 years (range 0.1 to 16). Mean intravenous dose was 1.2 mg/kg body weight (range 0.3 to 1.5 mg). The final mean oral maintenance dose was 308 mg/m2 body surface area (range 200 to 600 mg/m2, 16.8 mg/kg body weight). After intravenous application, propafenone was effective in 21 of 36 patients; atrial flutter was converted in 1 of 5 patients, and reentry supraventricular tachycardia was controlled in 15 of 25 patients. Propafenone was partially or completely effective in 3 of 4 patients with chaotic atrial tachycardia. Junctional ectopic tachycardia was suppressed in 2 infants. Thirty-seven patients had oral treatment with a mean follow-up of 2.2 years. Propafenone was effective in 33 of 37 patients (89%); atrial flutter was controlled in 2 patients, ventricular ectopy was suppressed in 1 of 2 patients. In reentry supraventricular tachycardia, propafenone was effective in 25 of 28 patients. Chaotic atrial tachycardia (n = 3) and junctional ectopic tachycardia (n = 2) were controlled after successful intravenous therapy. Systemic side effects were rare. Two patients developed a proarrhythmic effect, and 1 patient with ventricular ectopy after repair of tetralogy of Fallot died suddenly during propafenone maintenance therapy.     

CARTO标测下导管消融治疗房性心律失常的效果

目的：探讨三维电磁导管定位系统（CARTO）指导下3种常见房性心律失常（房性心动过速、心房扑动和心房颤动）导管消融临床的疗效及电生理特征。方法：2008年7月～2013年7月在我院行CARTO指导下导管消融治疗的166例房性心律失常患者的临床应用和电生理资料进行回顾性分析。结果：①166例房性心律失常患者,其中32例为房性心动过速,26例心房扑动,108例心房颤动（阵发性心房颤动78例、持续性房颤30例）;②消融及随访结果：共计162例即刻消融成功,4例失败（房速3例、房扑1例）,总成功率为97．6％;随访6—60个月,复发30例,其中房速、房扑各2例,均再次消融成功;心房颤动复发24例（阵发性心房颤动14例、持续性心房颤动10例）,再次消融后8例成功,二次房颤消融成功率为85％;均未出现心包填塞、心房食管瘘等严重并发症。结论：CARTO三维标测下导管消融治疗房性心动过速、心房扑动、心房颤动等房性心律失常是安全有效的。     

Paroxysmal supraventricular tachycardia: experience with propafenone

The authors studied the efficacy of intravenous (IV) (1.5-2 mg/kg) and oral propafenone (450 to 900 mg/day) in 16 patients with paroxysmal, sustained, recurrent supraventricular tachycardia (SVT). In 5 patients IV propafenone was not given, because of intolerant SVT. Nine patients had Wolff-Parkinson-White syndrome. IV propafenone immediately stopped and prevented reinduction of SVT in 9/11 patients. Oral propafenone prevented SVT induction in 3 of 5 patients. In the 9 patients responsive to IV propafenone, oral propafenone was effective: in particular, in 6 patients SVT tachycardia was not induced by serial transesophageal pacings, and in the remaining 3 patients the arrhythmia was still induced but was slower and of brief duration (3-5 seconds). In 11/12 patients responsive to oral propafenone the minimum effective dosage in preventing the induction of the arrhythmia was 600 mg/day. In only 1 patient was the dose of 450 mg/day equally effective. Propafenone administration was not associated with major side effects. In conclusion, propafenone is very effective in the control of paroxysmal supraventricular tachycardia; intravenous propafenone can predict the efficacy of oral therapy.     

Intravenous cibenzoline in the management of acute supraventricular tachyarrhythmias

Summary Intravenous cibenzoline was evaluated in 37 patients with acute supraventricular tachyarrhytymias and a ventricular rate >120 beats/min. The presenting arrhythmia was atrial fibrillation in 15 patients, atrial flutter in 5, ectopic atrial tachycardia in 11, and paroxysmal atrioventricular (AV) junctional reentrant tachycardia in 6 patients. Intravenous cibenzoline was administered as a bolus given over 2 minutes, at a dose of 1 mg/kg in the first 26 patients and 1.2 mg/kg in the subsequent 11 patients, 15 minutes following failure of placebo (isotonic glucose). The results were evaluated 15 minutes after the intravenous injection. Restoration of sinus rhythm was obtained in 3 out of 6 patients with paroxysmal AV junctional tachycardia (50%) and in 7 out of 31 patients (23%) with atrial tachyarrhythmias (5 out of 15 patients with atrial fibrillation and 2 out of 16 patients with ectopic atrial tachycardia or atrial flutter). Five additional patients with atrial tachyarrhythmias had slowing of ventricular rate below 100 beats/min. Therefore, a satisfactory result, that is, restoration of sinus rhythm or slowing of ventricular rate, occurred in 15 patients (40.5%). Side effects were transient, including visual disturbance (one patient), asymptomatic widening of QRS complex (three patients), incessant reciprocating tachycardia (one patient), and acceleration of ventricular rate (eight patients), resulting in 1:1 flutter, with poor tolerance in two patients. In conclusion, intravenous cibenzoline may be useful in selected patients with supraventricular tachyarrhythmias. Careful monitoring is recommended during therapy in view of the possible occurrence of 1:1 atrial flutter.     

Efficacy of propafenone in Wolff-Parkinson-White syndrome: electrophysiologic findings and long-term follow-up

The efficacy and safety of intravenous propafenone was studied in 10 patients with Wolff-Parkinson-White syndrome and in 2 patients with a concealed accessory pathway. During electrophysiologic study, the effect of propafenone on the effective refractory period of the accessory pathway was determined, as well as its effect during orthodromic atrioventricular (AV) reentrant tachycardia and atrial fibrillation. Propafenone caused significant increases in the accessory pathway refractory period, both in the anterograde direction (290 +/- 19 versus 474 +/- 50 ms, p less than 0.05) and in the retrograde direction (238 +/- 15 versus 408 +/- 44 ms, p less than 0.05). Complete anterograde accessory pathway conduction block occurred in four patients. Sustained AV reentrant tachycardia was inducible in 11 patients before administration of propafenone. Drug infusion during AV reentrant tachycardia promptly terminated arrhythmia in 10 of these 11 patients and caused slowing of AV reentrant tachycardia in the remaining patient. Before propafenone, sustained atrial fibrillation was inducible in six patients and nonsustained atrial fibrillation in four patients. After propafenone, no patient had inducible sustained atrial fibrillation. Furthermore, propafenone caused a marked decrease in peak ventricular rate during atrial fibrillation. Eight patients have been treated with oral propafenone and followed up for 12 +/- 2 months. All have remained virtually free of recurrent arrhythmia and none has developed significant side effects. Propafenone is a very promising agent for emergency intravenous therapy as well as long-term oral therapy in patients with Wolff-Parkinson-White syndrome.     

Atrial arrhythmias following ostial or circumferential pulmonary vein ablation

Aims The incidence, clinical significance and optimum treatment of AF ablation-induced proarrhythmia is not entirely known. This report describes the incidence and management of atrial arrhythmias occurring after various techniques for the ablative therapy of atrial fibrillation (AF).Methods Five hundred and forty-four patients with paroxysmal atrial fibrillation were subjected to ostial pulmonary vein (PV) (n = 204), antral (n = 300), or circumferential (n = 40) ablation around the PV ostia.Results Atrial tachycardia or flutter during the first 6 months after AF ablation was detected in 14 patients and was more common among patients subjected to circumferential or circumferential and linear ablation (18% and 22%, respectively) than to other techniques (p < 0.001). The risk of atrial tachycardia or flutter among patients who underwent ostial, ostial with lines and antral ablation was 1%, 8% and 1%, respectively. No difference was observed in the risk of atrial arrhythmia between patients who underwent ablation with or without additional lines, either ostial (p = 0.17) or circumferential (p = 0.99). Re-ablation was performed in patients with sustained atrial arrhythmia (11 out of 14 patients). At 6 months, no recurrence was seen in 10 of these patients as well as in 3 patients with non-sustained atrial tachycardia or flutter.Conclusions The incidence of atrial tachycardia or flutter following AF ablation is lower for ostial than circumferential ablation. The addition of lines along the mitral isthmus and between the superior PVs does not significantly affect the risk of ablation-induced arrhythmia. Non-sustained atrial tachycardia or flutter following AF ablation procedures does not always require additional ablation.