Radioiodine ablation of the thyroid to prevent recurrence of amiodarone-induced thyrotoxicosis in patients with resistant tachyarrhythmias.

Amiodarone-induced thyrotoxicosis (AIT) is a common complication of amiodarone therapy. Although permanent withdrawal of amiodarone is recommended due notably to the risk of worsening of tachyarrhythmias, some patients may require the reintroduction of amiodarone several months after normalizing their thyroid function. We, retrospectively, assessed the effects of (131)I therapy to prevent recurrence of AIT in euthyroid patients requiring reintroduction of amiodarone. SUBJECTS AND METHODS: Amiodarone was required in 10 cases of recurrent symptomatic paroxysmal atrial fibrillation (AF) and in 5 cases of ventricular tachycardia (VT) (M = 12, F = 3, mean age: 63 +/- 14). The underlying heart disease was dilated cardiomyopathy (n = 4), ischaemic heart disease (n = 4), hypertensive heart disease (n = 2), arrhythmogenic right ventricular dysplasia (n = 27) and valvulopathy (n = 1). Two patients had idiopathic paroxysmal AF. RESULTS: A mean (131)I dose of 579 +/- 183 MBq was administered 34 +/- 37 after the episode of AIT. Amiodarone was reintroduced in 14 of 15 patients after a mean interval of 103 +/- 261 d. Fourteen patients developed definite hypothyroidism necessitating l-thyroxine but we observed no late recurrence of AIT. After a mean follow-up of 22 +/- 16 months, tachyarrhythmias were controlled in 12 of 14 patients. CONCLUSION: (131)I therapy appears to be an effective and safe approach to prevent the recurrence of AIT in a patient requiring the reintroduction of amiodarone for tachyarrhythmias.     

Tachyarrhythmias in young athletes

Nineteen young athletes with documented symptomatic tachyarrhythmia were systematically evaluated. There were 15 men and 4 women, aged 14 to 32 years (mean 22 +/- 6). Documented tachyarrhythmias were paroxysmal atrial fibrillation in five patients, paroxysmal supraventricular tachycardia in five, paroxysmal ventricular tachycardia in eight (sustained in five, nonsustained in three) and ventricular fibrillation in one patient. Abnormal substrates were demonstrated in 15 (79%) of the 19 athletes: 5 had an anomalous atrioventricular (AV) pathway and 10 had heart disease (mitral valve prolapse in 9 patients and dilated cardiomyopathy in 1 patient). In 13 (68%) of the 19 athletes, all spontaneous attacks of tachyarrhythmia had started during strenuous exercise. Tachyarrhythmia that closely resembled clinical arrhythmia was induced by programmed cardiac stimulation in 13 athletes (68%) and was reproducibly provoked by treadmill exercise in 8 athletes (42%). In four of seven athletes with ventricular tachycardia, tachycardia closely resembling clinical arrhythmia was provoked by infusion of isoproterenol. In summary: young athletes can have any of several tachyarrhythmias; abnormal substrates can be demonstrated in many athletes with symptomatic tachyarrhythmia; and tachyarrhythmias in young athletes frequently occur during exercise.     

Combination of disopyramide and mexiletine for better tolerance and additive effects for treatment of ventricular arrhythmias

The efficacy and tolerance of disopyramide and mexiletine used alone and in combination were studied in 21 patients with frequent (greater than or equal to 30/h) ventricular premature complexes. Ambulatory electrocardiographic monitoring was performed at baseline and during therapy with disopyramide alone, mexiletine alone and a combination of disopyramide and mexiletine. During single drug therapy, the dose of disopyramide was 602 +/- 152 mg/day and that of mexiletine was 738 +/- 144 mg/day. During combination therapy with smaller doses of disopyramide (524 +/- 134 mg/day) and mexiletine (652 +/- 146 mg/day), no patient had side effects. At baseline before therapy, the mean number of ventricular premature complexes per hour, was 608 +/- 757, of couplets per hour was 22.4 +/- 45.8 and of episodes of nonsustained ventricular tachycardia/24 h was 219.7 +/- 758.2. The mean number of ventricular premature complexes per hour was reduced to 156 +/- 217 with disopyramide alone, 188 +/- 298 with mexiletine alone and 76 +/- 144 with combination therapy (p less than 0.05 for combination therapy versus disopyramide or mexiletine alone; p = NS for disopyramide versus mexiletine). Individually, an effective regimen (greater than 83% reduction in ventricular premature complexes and abolition of nonsustained ventricular tachycardia) was found in 5 (24%) of 21 patients during therapy with disopyramide alone, in 3 (14%) receiving mexiletine alone and in 13 (62%) receiving combination therapy (p less than 0.05 for combination therapy versus disopyramide or mexiletine; p = NS for disopyramide versus mexiletine). Thus, the antiarrhythmic effects of disopyramide and mexiletine are additive.(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.     

Selective blockade of retrograde fast pathway by intravenous disopyramide in paroxysmal supraventricular tachycardia mediated by dual atrioventricular nodal pathways.

Electrophysiological effects of 2 to 2.5 mg/kg iv disopyramide were studied in 10 patients with dual nodal pathways who used a slow pathway for anterograde and a fast pathway for retrograde conduction during paroxysmal supraventricular tachycardia (mean cycle length 308.5 +/- 37 ms; range 260-370 ms). Disopyramide terminated the tachycardia in six cases by production of ventriculoatrial block in five and by sinus overdrive in one. In the remaining four patients cycle length of the paroxysmal supraventricular tachycardia increased significantly from 270 +/- 8 ms to 377.5 +/- 28 ms. In all 10 patients disopyramide depressed retrograde fast pathway conduction manifest by an increase in mean ventricular paced cycle length producing ventriculoatrial block from less than or equal to 296.5 +/- 25 ms to 358 +/- 60 ms, and increase in retrograde fast pathway effective refractory period from less than or equal to 246 +/- 34 ms to 325 +/- 36 ms; the drug abolished ventriculoatrial conduction in two cases. Anterograde slow pathway and fast pathway conduction properties were unchanged after disopyramide (atrial paced cycle length producing AH block 292 +/- 30 to 306.5 +/- 30 ms; effective refractory period of anterograde fast pathway less than or equal to 274 +/- 56 to 284 +/- 44 ms, before and after the drug, respectively) suggesting that anterograde conduction was not crucial either for sustainment or for failure to initiate paroxysmal supraventricular tachycardia after the drug. Paroxysmal supraventricular tachycardia could not be reinduced in six cases after disopyramide. In the other four the ventricular paced cycle lengths producing ventriculoatrial block (318 +/- 41 ms) and effective refractory period of retrograde fast pathway (320 +/- 28 ms) were shorter than the cycle length of reinduced paroxysmal supraventricular tachycardia (367.5 +/- 35 ms) allowing perpetuation of the tachycardia. We conclude that disopyramide breaks atrioventricular nodal re-entrant tachycardia by specific blockade of the retrograde fast pathway though the effect on anterograde atrioventricular nodal conduction is variable.     

Selective blockade of retrograde fast pathway by intravenous disopyramide in paroxysmal supraventricular tachycardia mediated by dual atrioventricular nodal pathways

Electrophysiological effects of 2 to 2.5 mg/kg iv disopyramide were studied in 10 patients with dual nodal pathways who used a slow pathway for anterograde and a fast pathway for retrograde conduction during paroxysmal supraventricular tachycardia (mean cycle length 308.5 +/- 37 ms; range 260-370 ms). Disopyramide terminated the tachycardia in six cases by production of ventriculoatrial block in five and by sinus overdrive in one. In the remaining four patients cycle length of the paroxysmal supraventricular tachycardia increased significantly from 270 +/- 8 ms to 377.5 +/- 28 ms. In all 10 patients disopyramide depressed retrograde fast pathway conduction manifest by an increase in mean ventricular paced cycle length producing ventriculoatrial block from less than or equal to 296.5 +/- 25 ms to 358 +/- 60 ms, and increase in retrograde fast pathway effective refractory period from less than or equal to 246 +/- 34 ms to 325 +/- 36 ms; the drug abolished ventriculoatrial conduction in two cases. Anterograde slow pathway and fast pathway conduction properties were unchanged after disopyramide (atrial paced cycle length producing AH block 292 +/- 30 to 306.5 +/- 30 ms; effective refractory period of anterograde fast pathway less than or equal to 274 +/- 56 to 284 +/- 44 ms, before and after the drug, respectively) suggesting that anterograde conduction was not crucial either for sustainment or for failure to initiate paroxysmal supraventricular tachycardia after the drug. Paroxysmal supraventricular tachycardia could not be reinduced in six cases after disopyramide. In the other four the ventricular paced cycle lengths producing ventriculoatrial block (318 +/- 41 ms) and effective refractory period of retrograde fast pathway (320 +/- 28 ms) were shorter than the cycle length of reinduced paroxysmal supraventricular tachycardia (367.5 +/- 35 ms) allowing perpetuation of the tachycardia. We conclude that disopyramide breaks atrioventricular nodal re-entrant tachycardia by specific blockade of the retrograde fast pathway though the effect on anterograde atrioventricular nodal conduction is variable.     

Effects of diltiazem in supraventricular paroxysmal tachyarrhythmias

Diltiazem (0.3 mg/kg body weight intravenous in 2 minutes) was administered to 40 patients (24 males, 16 females, mean age 51.55 years) with paroxysmal supraventricular tachyarrhythmias: 7 patients with atrial fibrillation, 6 patients with atrial flutter, 25 patients with paroxysmal supraventricular tachycardia, 2 patients with uncommon atrioventricular reciprocating tachycardia. In patients with atrial fibrillation intravenous diltiazem produced a significant decrease of ventricular response (from 160 +/- 11 to 113.57 +/- 10.34--p less than 0.01). In patients with atrial flutter intravenous diltiazem produced variable effects: an increase in atrio-ventricular block (from 2:1 to 3:1 atrio-ventricular conduction (2 patients); conversion to sinus rhythm (1 patient); change to atrial fibrillation (1 patient); no appreciable change of the basic rhythm (2 patients). In paroxysmal supraventricular tachycardia patients conversion to sinus rhythm occurred in 20/22 patients (91%) treated with intravenous diltiazem (mean conversion time 4.69 minutes). In the 2 patients with uncommon atrioventricular nodal reciprocating tachycardia diltiazem increased P'-R and R-P' intervals without appreciable change of the basic rhythm. No serious side effects from drug administration were noted. Intravenous diltiazem appears to be as a highly effective medication in conversion or control of paroxysmal supraventricular tachyarrhythmias.     

Reduction of ventricular tachyarrhythmia by treatment of atrial fibrillation in ICD patients with dual-chamber implantable cardioverter/defibrillators capable of atrial therapy delivery: the REVERT-AF Study.

AIMS: The purpose of this prospective, randomized, multicentre study was to investigate whether the incidence of ventricular tachyarrhythmia can be reduced in standard implantable cardioverter/defibrillator (ICD) patients by implanting a dual-chamber ICD capable of atrial therapy delivery. METHODS AND RESULTS: A Jewel AF or GEM III AT ICD (Medtronic Inc., Minneapolis, MN, USA) was implanted in 122 patients (62.3 +/- 10.5 years; 84.4% male; coronary artery disease 71.3%; left ventricular ejection fraction 39.7 +/- 13.6%; secondary ICD indication 91%). Overall, 31.2% of the patients had paroxysmal atrial fibrillation (AF)/atrial tachycardia (AT) before ICD implantation (n = 38). Implantable cardioverter/defibrillator therapies for AT/AF were activated and de-activated every 3 months in a cross-over study design. The mean follow-up was 18.5 +/- 7.7 months (6.29 +/- 2.2 cross-over/patient). Overall, there were 684 episodes of ventricular tachyarrhythmias in 48.4% of patients (n = 59). In 33.6% of patients (n = 41), 532 supraventricular tachyarrhythmias occurred. Activation of ICD therapies for AT/AF did not result in a reduction of ventricular tachyarrhythmias (P = 0.92). Patients with monomorphic ventricular tachycardias (mVTs) as index arrhythmia for ICD implantation or inducible mVTs in the electrophysiological study had the highest probability of recurrences of ventricular tachyarrhythmias. CONCLUSION: For patients with standard indications for ICD therapy and no indication for cardiac pacing, a dual-chamber ICD capable of atrial tachyarrhythmia treatment offers no benefit concerning a reduction of ventricular tachyarrhythmias.     

Effectiveness of rhythm control in persistent or permanent atrial fibrillation with overdrive atrial pacing and antiarrhythmic drugs after linear right atrial catheter ablation

Right atrial (RA) maze procedures using linear catheter ablation have had limited efficacy in paroxysmal atrial fibrillation (AF). We hypothesized that "hybrid" therapy using overdrive atrial pacing and antiarrhythmic drugs can improve efficacy of catheter RA maze and expand its role to persistent or permanent AF. Catheter RA maze procedures were performed in 26 patients with persistent or permanent AF refractory to 4.5 +/- 2.1 antiarrhythmic drugs. Overdrive dual-site RA pacing (21 patients) or high RA pacing (5 patients) was continued (n = 11) or instituted periablation (n = 15). All patients continued receiving previously ineffective antiarrhythmic drugs. Freedom from permanent AF (rhythm control), symptomatic and/or asymptomatic AF recurrences, the safety of hybrid therapy, and overall survival were assessed. There was no procedure-related mortality or stroke. Rhythm control was achieved in 24 patients (92%) within 3 months. During long-term follow-up (6 to 49 months, mean 17 +/- 10), rhythm control was maintained in 20 patients (77%). Nine patients (35%) had no AF recurrences, whereas 11 patients maintained rhythm control with infrequent AF recurrences. Device datalogs at the study cut-off point demonstrated no AF events in 6 patients, nonsustained atrial tachycardia in 2 patients, and brief asymptomatic paroxysmal AF in 12 patients. Actuarial patient survival was 95% at 1 year and 74% at 2 years of follow-up. Thus, hybrid therapy utilizing catheter RA maze procedures with overdrive atrial pacing and antiarrhythmic drugs can be performed safely and can reestablish rhythm control in selected patients with refractory persistent or permanent AF.     

Disopyramide-pyridostigmine interaction: selective reversal of anticholinergic symptoms with preservation of antiarrhythmic effect

This double-blind, randomized, placebo crossover study was used to evaluate the effects of a cholinesterase inhibitor--slow-release pyridostigmine (180 mg orally every 12 hours)--on the anticholinergic and antiarrhythmic properties of disopyramide. Quantitative side effects questionnaire scores were used to guide disopyramide administration in 20 men with ventricular tachycardia. Disopyramide was given to each patient both with placebo and with active pyridostigmine. The maximal administered dose for each regimen was used in conjunction with corresponding questionnaire scores to calculate an index or estimate of the maximal tolerable dose of disopyramide. Additional evaluations performed at baseline and at each maximal administered dose regimen included tear and saliva quantitation, 24 hour electrocardiogram (ECG), exercise testing and programmed ventricular stimulation. Results showed that the maximal administered dose of disopyramide was greater with active pyridostigmine than with placebo: 295 +/- 75 versus 245 +/- 100 mg every 6 hours (p less than 0.05). The calculated maximal tolerable dose was substantially greater in the presence of pyridostigmine: 355 +/- 90 versus 260 +/- 115 mg every 6 hours (p less than 0.001). Maximal side effects questionnaire scores also reflected decreased anticholinergic activity in the presence of pyridostigmine compared with placebo: 101.9 +/- 2.2 versus 104.6 +/- 2.8, respectively (p less than 0.005). Baseline tear and saliva production was significantly reduced during disopyramide therapy, but was restored toward normal by the addition of pyridostigmine.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical evaluation of oral mexiletine therapy in the treatment of ventricular arrhythmias

The effect of oral mexiletine therapy on ventricular arrhythmias was evaluated in 58 patients in whom conventional drugs had been unsuccessful. Mean daily dose of mexiletine was 652 mg (range 250 to 1,500) and mean duration of therapy was 14.4 months (range 0.1 to 34.4). Mexiletine was associated with a decrease of 52% in total premature ventricular complexes in 24 hours compared with control (6,841 +/- 1,053 [SEM] versus 3,248 +/- 734, p less than 0.005) and 19 patients (36.5%) had a greater than 83% decrease in ventricular ectopic rhythm. The drug was discontinued in 6 of these 19 patients because 5 of them (26%) experienced side effects after a mean period of 29.6 weeks (range 0.83 to 63.2) and sudden death occurred in 1 patient (5%); this indicates effective suppression of ventricular ectopic rhythm without significant side effects in 13 (25%) of 52 patients during long-term therapy. Adjustment of drug dosage to achieve therapeutic blood levels resulted in an efficacy on ventricular ectopic rhythm similar to that obtained with the maximal tolerated dose. There was no correlation between drug dose and therapeutic effectiveness. Mexiletine was associated with a 48% decrease in episodes of ventricular tachycardia (345.5 versus 179.3/24 h) and 5 of 10 patients with a history of cardiac arrest remained free of symptomatic ventricular tachyarrhythmias for 14.8 months (range 3.7 to 24.3).(ABSTRACT TRUNCATED AT 250 WORDS)     

Intravenous flecainide acetate for the clinical management of paroxysmal tachycardias

Intravenous flecainide acetate (2 mg/kg) was administered to 40 patients undergoing routine electrophysiological evaluation for the investigation of recurrent paroxysmal tachycardias. Ten patients had recurrent atrial flutter, 11 patients had recurrent atrial fibrillation, one of whom also had paroxysmal left atrial tachycardia, and 19 patients had recurrent ventricular tachyarrhythmias (17 with recurrent ventricular tachycardia and 2 with recurrent fascicular tachycardia). Flecainide was administered during tachycardia (over 5 to 10 minutes) to all patients with atrial flutter, to 10 patients with atrial fibrillation, and to 17 patients with ventricular tachyarrhythmias. In the remaining 3 patients with ill-sustained arrhythmias flecainide was administered during sinus rhythm and reinitiation of tachycardia was then attempted. Flecainide restored sinus rhythm in only 2 patients with atrial flutter (20%), in 9 patients with atrial fibrillation (90%), in 12 patients with ventricular tachycardia (80%), and in one of the 2 patients with fasicular tachycardia. Flecainide also successfully terminated the left atrial tachycardia. Two patients experienced proarrhythmic side effects during flecainide administration, one of whom required intervention by cardioversion. Minor dose effects included oral paresthesia, transient drowsiness or dizziness, and occasional visual blurring. Flecainide acetate is an effective antiarrhythmic agent for the acute termination of recent onset paroxysmal atrial and ventricular tachyarrhythmias.     

Effective termination of reentrant supraventricular tachycardia by single dose oral combination therapy with pindolol and verapamil

We evaluated the efficacy of single oral dose combining 20 mg pindolol and 120 mg verapamil in termination of paroxysmal supraventricular tachycardia (SVT) in 12 patients with recurrent symptomatic tachycardia. All had electrically inducible SVT lasting longer than 30 minutes. Patients were administered placebo or crushed pindolol and verapamil on 2 consecutive days after tachycardia was electrically induced and allowed to sustain for 30 minutes. With placebo, SVT lasted 186 +/- 18 minutes (mean +/- SEM); five patients converted spontaneously within 121 to 180 minutes. With pindolol and verapamil, 9 of 12 patients (responders) converted to sinus rhythm within 8 to 74 minutes. The mean duration of SVT in the nine responders was 28 +/- 8 minutes compared with 168 +/- 20 minutes on placebo (p less than 0.001). Before termination, tachycardia rate on pindolol and verapamil slowed significantly from 182 +/- 5 to 164 +/- 7/min (p less than 0.05) compared with no significant change in the rate of SVT on placebo. The mean systolic blood pressure during tachycardia was 97 +/- 5 mm Hg with placebo and 101 +/- 7 mm Hg with pindolol and verapamil. Serum levels of pindolol and verapamil obtained in seven patients at time of spontaneous termination of tachycardia were 66 +/- 13 and 56 +/- 14 ng/ml, respectively. The side effects with pindolol and verapamil included lightheadedness in one patient and symptoms of rapid palpitations in three. A single oral dose of pindolol and verapamil is safe and effective in termination of acute paroxysmal SVT and may be the initial therapy of choice in selected patients.     

Combination of procainamide and quinidine for better tolerance and additive effects for ventricular arrhythmias

The efficacy and tolerance of quinidine and procainamide used individually and in combination were studied in 19 patients with frequent ventricular premature complexes (VPCs). During single-drug treatment, the maximum tolerated dose of quinidine without extracardiac dose-related side effects was 1.6 +/- 0.21 g/day and that of procainamide was 4.1 +/- 1.05 g/day. During combination therapy with smaller doses (p less than 0.05) of quinidine (1.16 +/- 0.26 g/day) and procainamide (2.80 +/- 0.98 g/day), no patient had side effects. Before treatment, all patients had frequent (more than 60 per hour) VPCs and 17 had ventricular tachycardia on Holter monitoring. The frequency of VPCs was reduced to 22 +/- 19% with quinidine, 47 +/- 40% with procainamide and 9 +/- 11% with combination therapy (p less than 0.05, combination vs procainamide or quinidine alone). Individually, an effective regimen (more than 83% reduction of VPCs and abolition of ventricular tachycardia) was found in 5 patients (26%) receiving quinidine alone at maximal tolerated dose, in 4 (21%) receiving procainamide alone at maximal tolerated dose, and in 14 (74%) receiving combination therapy (p less than 0.01 vs quinidine or procainamide). Thus, the antiarrhythmic effects of quinidine and procainamide are additive. When quinidine or procainamide are additive. When quinidine or procainamide is ineffective because dose-related extracardiac side effects limit the maximal tolerated dose, combination therapy in smaller and tolerable doses avoids side effects and is more effective than either drug alone at the maximal tolerated dose.     

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.     

A randomized trial of circumferential pulmonary vein ablation versus antiarrhythmic drug therapy in paroxysmal atrial fibrillation: the APAF Study.

OBJECTIVES: We compared ablation strategy with antiarrhythmic drug therapy (ADT) in patients with paroxysmal atrial fibrillation (PAF). BACKGROUND: Atrial fibrillation (AF) ablation strategy is superior to ADT in patients with an initial history of PAF, but its role in patients with a long history of AF as compared with ADT remains a challenge. METHODS: One hundred ninety-eight patients (age, 56 +/- 10 years) with PAF of 6 +/- 5 years' duration (mean AF episodes 3.4/month) who had failed ADT were randomized to AF ablation by circumferential pulmonary vein ablation (CPVA) or to the maximum tolerable doses of another ADT, which included flecainide, sotalol, and amiodarone. Crossover to CPVA was allowed after 3 months of ADT. RESULTS: By Kaplan-Meier analysis, 86% of patients in the CPVA group and 22% of those in the ADT group who did not require a second ADT were free from recurrent atrial tachyarrhythmias (AT) (p < 0.001); a repeat ablation was performed in 9% of patients in the CPVA group for recurrent AF (6%) or atrial tachycardia (3%). At 1 year, 93% and 35% of the CPVA and ADT groups, respectively, were AT-free. Ejection fraction, hypertension, and age independently predicted AF recurrences in the ADT group. Circumferential pulmonary vein ablation was associated with fewer cardiovascular hospitalizations (p < 0.01). One transient ischemic attack and 1 pericardial effusion occurred in the CPVA group; side effects of ADT were observed in 23 patients. CONCLUSIONS: Circumferential pulmonary vein ablation is more successful than ADT for prevention of PAF with few complications. Atrial fibrillation ablation warrants consideration in selected patients in whom ADT had already failed and maintenance of sinus rhythm is desired. (A Controlled Randomized Trial of CPVA Versus Antiarrhythmic Drug Therapy in for Paroxysmal AF: APAF/01; http://clinicaltrials.gov/ct/show; NCT00340314).     

AMIODARONE THERAPY FOR LIFE THREATENING OR REFRACTORY CARDIAC ARRHYTHMIAS

Amiodarone was used in 40 patients with life-threatening or refractory tachyarrhythmias. Eighteen patients had recurrent ventricular tachycardia of whom 13 had suffered a cardiac arrest. Control has been excellent or good in 17 of these 18 patients during an average follow-up period of 10 months. A further 22 patients had supraventricular arrhythmias, including three with Wolff-Parkinson-White syndrome and paroxysmal atrial fibrillation. In 20 of these control has been excellent or good. The mean daily maintenance dose of amiodarone was 300 mg for patients with ventricular tachyarrhythmias and 200 mg for those with supraventricular tachyarrhythmias. Side-effects were common and included corneal microdeposits, skin rash and discolouration, alteration in thyroid function, and symptomatic bradycardia. Serious adverse effects were uncommon however and necessitated discontinuation of the drug in only two patients. Amiodarone did not appear to precipitate or exacerbate cardiac failure in any patient although many had severe left ventricular dysfunction. We conclude that amiodarone is effective in the therapy of life-threatening or refractory cardiac arrhythmias.     

Clinical experience with sotalol in patients with drug-refractory ventricular arrhythmias

Sixty-five patients with symptomatic, drug-refractory, sustained ventricular tachycardia or fibrillation were treated with oral sotalol (80 to 480 mg twice daily). Sotalol was withdrawn in 11 patients because of continued inducibility of ventricular tachycardia at the time of follow-up electrophysiologic study. Therefore, the clinical effectiveness of sotalol could be evaluated in 54 patients followed up for 11.5 +/- 6 months (range 0.2 to 25). The actuarial incidence of successful sotalol therapy was 54 +/- 13% at 6 months and 47 +/- 13% at 12 months. In 39 patients who underwent electrophysiologic testing while receiving oral sotalol, the drug prevented the reinduction of ventricular tachycardia/fibrillation in 8 (20%). During follow-up study, arrhythmia recurred in 1 (17%) of 6 patients whose ventricular tachycardia was noninducible with oral sotalol and in 8 (44%) of 18 with inducible tachycardia but who were continued on oral sotalol therapy. Adverse effects were noted in 28 patients (42%), requiring drug withdrawal in 13 (22%) and dose reduction after hospital discharge in 10 (15%). Exacerbation of ventricular arrhythmia occurred in six patients (9%), one of whom had associated hypokalemia. Sotalol is frequently useful in the control of intractable, life-threatening ventricular arrhythmias, and its efficacy appears to be predicted by programmed stimulation. However, there is a high rate of limiting side effects, which precludes its use in a large number of patients, and a substantial risk of arrhythmia exacerbation.     

High incidence of clinical and subclinical toxicity associated with amiodarone treatment of refractory tachyarrhythmias

Amiodarone has been hailed as the most effective single antiarrhythmic drug for treatment of refractory supraventricular and ventricular arrhythmias. However, questions continue to arise about its long-term potential toxicity and true efficacy rates. We, therefore, reviewed our experience with 78 patients, mean age 59 +/- 14 years, with drug refractory tachyarrhythmias treated with amiodarone. Sixty-two patients were treated for recurrent ventricular tachycardia or ventricular fibrillation, 4 for complex ventricular ectopy and 12 for supraventricular tachyarrhythmias. Patients have been treated for a mean of 9.9 months (range, 1 day to 39.1 months); 34(55%) continued to be successfully treated for ventricular tachycardia/ventricular fibrillation, 2 (50%) for complex ventricular ectopy and 5 (42%) for supraventricular tachyarrhythmias. Amiodarone toxicity was frequent, occurring in 57/72 patients (79%) who were treated for more than one week. Adverse effects led to drug discontinuation in 15 (21%), 3 because of pulmonary toxicity (1 in combination with neuropathy and another with drug-induced hepatitis); 2 because of chemical hepatitis; 1, confusion; 6, neuropathy; 2, arrhythmia exacerbation; 2, symptomatic bradycardia; and 1 because of impotence. Of the 62 ventricular tachycardia/ventricular fibrillation patients who were treated with amiodarone, 8 (13%) expired: 4 died suddenly and 4 from documented ventricular tachycardia during treatment. In contrast, of 16 patients who had discontinued amiodarone because of initial adverse effects or drug failure and were treated with alternative antiarrhythmic medications, 5 (31%) died suddenly. In conclusion, amiodarone appears to be fairly effective in high risk patients with refractory cardiac tachyarrhythmias but results in a rather high incidence of adverse effects in long-term follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effectiveness of Rapid Atrial Pacing for Termination of Drug Refractory Atrial Fibrillation: Results of a Dual Chamber Implantable Cardioverter Defibrillator Trial

There is increasing interest in the use of an implantable cardioverter defibrillator (ICD) to manage atrial tachyarrhythmias. Although device-based shock therapy is highly effective in terminating persistent atrial tachyarrhythmias, atrial overdrive pacing may also be useful, particularly when this therapy is applied early after the onset of an arrhythmia. A dual-chamber ICD (Medtronic 7250 Jewel AF(R)) has been studied in 267 patients with drug-refractory symptomatic AF. The patients were enrolled as part of multicenter clinical trial to evaluate the safety and efficacy of the device to manage atrial tachyarrhythmias in the absence of a standard ventricular ICD indication. The device discriminates atrial tachycardia (AT) from atrial fibrillation (AF) based on cycle length and regularity, and employs multiple methods of atrial overdrive pacing as well as shocks to terminate tachyarrhythmia episodes. Patients were followed for an average of 15.8 +/- 9.3 months. A majority (63%) of patients presented with a history of persistent AF and 34% presented with a history of paroxysmal AF. The pacing therapies terminated 54% of AT episodes and 27% of AF episodes. In patients with persistent AF, 75% of the AT/AF episodes that were successfully terminated by pacing lasted 相似文献