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 and safety of short intravenous amiodarone in supraventricular tachyarrhythmias.

The safety and efficacy of short intravenous therapy with amiodarone were evaluated in 44 patients (24 males, 20 females), aged 21-84 years, with supraventricular tachyarrhythmias newly arisen in less than 24 hours. The study group consisted of 15 patients with paroxysmal supraventricular tachycardia, 8 patients with atrial flutter and 21 patients with atrial fibrillation. They were treated with a single infusion of amiodarone up to 2 hours after the restoration of a stable sinus rhythm, or up to a maximum dose of 2400 mg in 24 hours. Our study shows that 88.6% of all supraventricular tachyarrhythmias reverts to sinus rhythm in less than 24 hours: 100% of paroxysmal supraventricular tachycardia, 75% of atrial flutter, and 85.7% of atrial fibrillation. Intravenously administered amiodarone proves to take effect rapidly (0.5 to 22 hours). The plasma amiodarone concentrations at sinus rhythm restoration showed a wide range (405-3800 ng/ml). Piecewise analysis suggested that the probability of sinus rhythm was 14.4-fold greater in paroxysmal supraventricular tachycardia. No linear statistical relationship was detectable between the log-dose-body mass index and log-QTc. Total amiodarone dose and left atrial volume are inversely correlated with a statistically significant difference. The toxicity in our short intravenous course with amiodarone was not relevant. We conclude that short high-dose intravenous amiodarone shows efficacy and safety in all newly occurring supraventricular tachyarrhythmias.     

Intravenous Flecainide in the Management of Acute Supraventricular Tachyarrhythmias*

Intravenous flecainide (1.5 mg/kg) was given to 30 patients with acute supraventricular tachyarrhythmias: atrial fibrillation (12 patients), atrial flutter (7 patients), and reciprocating tachycardia due to reentry through an accessory pathway (5 patients). The total rate of conversion to sinus rhythm was 18 out of 30 patients (60%), 11 out of 11 patients (100%) with reciprocating tachycardia and 7 out of 19 patients (37%) with atrial flutter or fibrillation. In those patients not converted to sinus rhythm, the mean ventricular rate significantly (P < 0.1) slowed from 140 ± 15 beats/min with slowing of ventricular rate below 100 beats/min in 2 patients. Tolerable side effects occurred in 5 patients (17%) and included transient moderate hypotension (1 patient), blurred vision (1 patient), and transient conduction defects (3 patients). We conclude that intravenous flecainide is a safe and effective antiarrhythmic agent for the termination of acute reciprocating tachycardias and moderately useful for the management of atrial flutter or fibrillation.     

Evaluation of the anti-arrhythmia effect of intravenous flecainide in supraventricular tachyarrhythmias

We studied the effects of intravenous flecainide acetate, given as a single dose of 2 mg/kg in no less than 15 minutes, on 31 patients with supraventricular tachyarrhythmias. Fourteen (87%) of the 16 patients with paroxysmal atrial fibrillation converted to sinus node rhythm. All 7 (100%) of the patients with paroxysmal supraventricular tachycardia converted to sinus node rhythm. Five (60%) of the 8 patients with paroxysmal atrial flutter converted to sinus node rhythm. The average time of conversion, after completion of drug administration, was 15 +/- 20 minutes. The QRS was prolonged an average of 82 to 91 milliseconds; in those cases who converted, the PR interval duration was 180 milliseconds average; QT was prolonged an average of 425-450 milliseconds. There were no changes in the JT interval, and we observed no hemodynamic untoward effects.     

Effects of intravenous verapamil on cardiac arrhythmias and on the electrocardiogram.

The effects of intravenous verapamil on the electrocardiogram in 15 patients with heart disease in sinus rhythm and in 44 patients with supraventricular and ventricular tachyarrhythmias were evaluated. Verapamil prolonged the P-R interval without effect on the QRS duration or the Q-Tc interval. In patients with atrial flutter and fibrillation, A-V block was increased, with slowing of the ventricular rate, in almost all cases but sinus rhythm was restored in only 1 of 12 patients in atrial fibrillation and in 2 of the 11 patients with flutter. Verapamil had no effect in 3 patients with atrial fibrillation complicating WPW syndrome; in 1 of 5 patients with ventricular tachycardia it caused reversion to sinus rhythm. Sinus rhythm was restored promptly by verapamil in 13 of 17 patients with paroxysmal supraventricular tachycardias; in 2 others, sinus rhythm became established 1 to 2 hours after administration of the drug. Transient hypotension, not requiring treatment, was the only side effect noted but not in the patients with supraventricular tachycardias, in whom blood pressure generally increased after reversion to sinus rhythm by verapamil.     

Intravenous diltiazem for termination of reentrant supraventricular tachycardia: a placebo-controlled, randomized, double-blind, multicenter study

To assess the efficacy and safety of intravenous diltiazem, 54 patients with inducible sustained supraventricular tachycardia received diltiazem, 0.25 mg/kg or 0.25 mg/kg, followed by 0.35 mg/kg body weight, or placebo in a double-blind, randomized study. Twenty patients had atrioventricular (AV) node reentrant tachycardia, whereas 34 had orthodromic AV reciprocating tachycardia associated with the Wolff-Parkinson-White syndrome. Supraventricular tachycardia was terminated in 24 (86%) of 28 patients given intravenous diltiazem compared with 5 (19%) of 26 given placebo (p = 0.0000014). Nineteen (95%) of 20 patients initially given placebo had termination of supraventricular tachycardia after receiving diltiazem. Overall, 43 (90%) of 48 patients receiving intravenous diltiazem had conversion of supraventricular tachycardia to sinus rhythm; the median time to tachycardia termination was 2 min after initiation of a 2 min diltiazem infusion. All 20 patients (100%) with AV node reentrant tachycardia treated with diltiazem had conversion of tachycardia to sinus rhythm as did 26 (81%) of 30 patients with AV reciprocating tachycardia treated with diltiazem. Diltiazem prolonged refractoriness and slowed conduction of the AV node and thereby provided antiarrhythmic action to cause tachycardia termination. Diltiazem had no effect on the electrophysiologic properties of accessory AV connections. Adverse effects were seen in 3 (6%) of the 48 patients given diltiazem. For paroxysmal supraventricular tachycardia initiated in the electrophysiology laboratory, it is concluded that intravenous diltiazem is safe and very effective for acute tachycardia termination when the AV node is part of the reentrant circuit.     

Flecainide acetate for conversion of acute supraventricular tachycardia to sinus rhythm

The efficacy of intravenous flecainide acetate (maximum 2 mg/kg or 150 mg given at a rate of 15 mg/min) was assessed in patients with acute supraventricular tachycardia (SVT) (within 24 hours). Fifty patients were studied, 46 with spontaneous SVT and 4 with induced SVT at electrophysiologic assessment. Conversion to sinus rhythm was achieved within 45 minutes in 76%: in 25 patients with atrial fibrillation (76% conversion), 15 with atrioventricular (AV) nodal or AV reentrant tachycardia (100% conversion) and 10 with atrial flutter or atrial reentrant tachycardia (40% conversion). Adverse effects were noted in 21 patients (42%): paresthesia in 9, drowsiness in 8, nausea in 2, accelerated ventricular rate in 5, ventricular tachycardia in 1, sinus bradycardia in 1 and hypotension in 5. Adverse effects were associated with larger dosage and atrial flutter or atrial reentrant tachycardia. Thus, flecainide acetate is effective in converting to sinus rhythm acute atrial fibrillation and AV nodal and AV reentrant tachycardias, but not atrial flutter or atrial reentrant tachycardia.     

Efficacy, safety, and tolerance of d-sotalol in patients with refractory supraventricular tachyarrhythmias

The efficacy, safety, and electrophysiologic effects of intravenous and oral d-sotalol, an investigational class III antiarrhythmic agent, are not yet well characterized. We evaluated the electrophysiologic, antiarrhythmic, and hemodynamic effects of d-sotalol infusion (1.5 to 2.75 mg/kg) and of chronic oral therapy (200 to 400 mg bid) in 10 patients with chronic, paroxysmal supraventricular tachyarrhythmias refractory to 5 +/- 2 standard agents. Four patients had paroxysmal supraventricular tachycardia (PSVT), four had paroxysmal atrial fibrillation, two had atrial flutter, and one had nonparoxysmal reciprocating junctional tachycardia (NPRJT). PSVT was inducible or spontaneously present in 4 of 4 before d-sotalol. After intravenous d-sotalol PSVT was noninducible in three patients and slowed by 40% in one. Atrial fibrillation was inducible or spontaneously present in 4 of 4 before therapy. After intravenous d-sotalol, one became noninducible, and three achieved rate-slowing (the mean falling from 69 to 61 bpm). In one patient, atrial flutter became noninducible; in another, d-sotalol slowed the rate of atrial flutter by 28%. D-sotalol restored sinus rhythm in the patient with NPRJT. Intravenous d-sotalol increased the sinus cycle length; the QTc, PR, and AH intervals; and the AV nodal functional refractory period, the AV nodal effective refractory period; and the right ventricular effective refractory period significantly. The atrial effective refractory period, sinoatrial conduction time, and corrected sinus recovery time tended to increase, but did not reach statistical significance. The QRS, PA, and HV intervals did not change. Mean BP fell 13.4 +/- 9.2% after intravenous d-sotalol, but no adverse symptoms developed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Diagnostic and therapeutic use of adenosine in patients with supraventricular tachyarrhythmias

Adenosine has been shown to affect both sinus node automaticity and atrioventricular (AV) nodal conduction. The effects of increasing doses of intravenous adenosine were assessed in 46 patients with supraventricular tachyarrhythmias. Adenosine reliably terminated episodes of supraventricular tachycardia in all 16 patients with AV reciprocating tachycardia, in 13 of 13 patients with AV nodal reentrant tachycardia and in 1 of 2 patients with junctional tachycardia with long RP intervals. Adenosine produced transient high grade AV block without any effect on atrial activity in six patients with intraatrial reentrant tachycardia, four patients with atrial flutter, three patients with atrial fibrillation and in single patients with either sinus node reentry or an automatic atrial tachycardia. The dose of adenosine required to terminate episodes of supraventricular tachycardia was variable (range 2 to 23 mg). Side effects were minor and of short duration. These results demonstrate that adenosine is useful for the acute therapy of supraventricular tachycardia whenever reentry through the AV node is involved. When arrhythmia termination is not affected, atrial activity may be more readily analyzed during adenosine-induced transient AV block.     

One to one atrioventricular conduction during atrial pacing at rates of 300/minute in absence of wolff-parkinson-white syndrome

One to one atrioventricular (A-V) or atrio-His bundle (A-H) conduction occurred during right atrial pacing at rates of 300/min in two patients with short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias. Patient 1 had episodes of reciprocating A-V tachycardia and of atrial fibrillation with very fast rates (270 to 290/min) that were slowed to 100 to 135/min after administration of intravenous verapamil. Enhanced A-V (A-H) conduction was exposed only during stimulation from the high right atrium, but not from the low lateral right atrium or coronary sinus. Patient 2 had episodes of atrial flutter with 1:1 A-V conduction and rates of 290/min. The H-V interval was short (25 ms) during sinus rhythm and atrial pacing presumably because conduction occurred through an atrio-“distal” His bundle (atriofascicular) tract. In contrast, the H-V interval was normal (40 ms) in echo beats or when the “proximal” His bundle was stimulated.In these two patients, having as “common denominators” short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias, enhanced A-V (A-H) conduction was (1) possibly due to different electrogenetic mechanisms; (2) pacing-site dependent; (3) manifested, during atrial fibrillation and atrial flutter, by extremely fast ventricular rates; and (4) unrelated to the rate of reciprocating A-V tachycardias because the latter was predominantly a function of anterograde conduction through the “slow” nodal pathway.     

Holter monitoring in patients with mitral stenosis and sinus rhythm

To determine the type and frequency of supraventricular arrhythmias in patients with mitral stenosis and sinus rhythm we studied 63 such patients, mean (sd) age 48.8 (8.2) years, by 24 hour ambulatory ECG monitoring. Thirty-five patients (55.6%) had supraventricular tachyarrhythmias. Twenty-five (39.7%) had paroxysmal atrial tachycardia, 14 (22.2%) atrial fibrillation, 8 (12.7%) multifocal atrial tachycardia and 5 atrial flutter. Ninety-five per cent (101) of episodes were asymptomatic and 96% non-sustained. Supraventricular premature beats occurred in 59 patients with couplets and triplets in 40 (63.5%) and 28 (44.4%), respectively. Frequent supraventricular premature beats, couplets, triplets and episodes of paroxysmal arrhythmias were commoner in patients greater than 50 years. Ectopic atrial rhythms with varying P wave morphology occurred in 12 patients (19%). Nine patients (14.3%) had suffered systemic embolic episodes. We conclude that supraventricular ectopic and tachyarrhythmias occur frequently in patients with mitral stenosis and sinus rhythm and that most paroxysms are non-sustained and asymptomatic.     

Intravenous amiodarone in the therapy of paroxysmal supraventricular tachycardias

The Authors evaluated the effectiveness and the tolerance of intravenous Amiodarone in 50 cases of recent onset paroxysmal supraventricular tachyarrhythmias. Fifty consecutive patients, aged 17 to 84 (mean 52 years), presenting with paroxysmal supraventricular tachycardia (PSVT, 33 cases) or atrial flutter (11 cases) or atrial fibrillation (6 cases), were given 300 mg of Amiodarone intravenously within 2 min, followed in 4 patients by 150 mg after 15 min. All patients were monitored for 1 hour; ECG and blood pressure were recorded at fixed times. Within 15 min sinus rhythm was restored in 88% of PSVT, in 27% of atrial flutter and in 17% of atrial fibrillation cases; the other cases of atrial flutter and fibrillation always showed a 48-81% reduction of the average heart rate within 15 min. We have evidenced neither significant modifications of blood pressure and ECG parameters (P-Q, QRS and Q-T duration) nor particular side effects, except for 2 cases in which brief hot flushes were reported. The Authors believe Amiodarone to be an effective and well tolerated drug for the above mentioned arrhythmias, particularly promptly acting in PSVT cases, in whom sinus rhythm was restored within 15 min in 88% and within 1 hour in 100% of the cases.     

三磷酸腺苷静脉注射诱发快速性心律失常

本研究选择79例阵发性室上性心动过速患者,在窦性心律或诱发的室上性心动过速发作时分级递增静脉注射三磷酸腺苷332次,诱发出窦性心动过速194例次(58.43%)、房性反复搏动34例次(10.24%)、室上性心动过速13例次(3.92%)、偶发房性早搏8例次(2.41%)、阵发性心房颤动3例次(0.9%)和偶发室性早搏2例次(0.6%)。除室上性心动过速外,均为一过性。未引起血液动力学障碍。     

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.     

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.     

Short-term control of supraventricular tachycardia with verapamil infusion and calcium pretreatment

Nineteen consecutive patients with atrial fibrillation/flutter or other types of supraventricular tachycardia were given intravenous (IV) calcium salts (1 g) followed by verapamil infusion at a rate of 1 mg/min. Successful treatment was defined as control of ventricular response to less than or equal to 100 beats per minute (bpm) or conversion to sinus mechanism in patients with atrial arrhythmias: 11 patients had atrial fibrillation; three had atrial flutter; four had reentrant supraventricular tachycardias (SVT); and one had paroxysmal SVT. Therapy was successful in all patients. The mean dose of verapamil required to achieve desired outcome was 20 mg. Heart rate showed no significant change as a result of calcium pretreatment (160 bpm v 151 bpm). However, heart rate was significantly decreased, to 95 bpm, after treatment with verapamil. Blood pressure showed no change from baseline with either calcium or verapamil therapy. Verapamil infusion following IV calcium successfully treats atrial fibrillation/flutter or SVTs without depressing systemic blood pressure.     

Clinical pharmacology of the new beta-adrenergic blocking drugs. Part 5. Pindolol (LB-46) therapy for supraventricular arrhythmia: a viable alternative to propranolol in patients with bronchospasm.

Pindolol (LB-46) is a new beta-adrenoceptor blocking agent with intrinsic sympathomimetic activity. In order to evaluate the efficacy of pindolol in the treatment of patients with supraventricular arrhythmias and propranolol-induced bronchospasm, 18 patients with paroxysmal supraventricular tachycardia, atrial fibrillation, atrial flutter, multifocal atrial tachycardia or junctional tachycardia, were treated with placebo followed by pindolol in intravenous and then oral form. Following a no-response placebo period (in all patients), intravenous pindolol converted six out of seven patients with paroxysmal supraventricular tachycardia to normal sinus rhythm. In six patients with atrial fibrillation, three reverted to normal sinus rhythm, and three remained in atrial fibrillation but with a slower ventricular response (less than 100 beats/minute). Of two patients with atrial flutter, one converted to normal sinus rhythm, while the other patient failed to respond. Both patients with junctional tachycardia and one with multifocal atrial tachycardia converted to normal sinus rhythm. Long-term oral pindolol therapy sustained these responses in most patients, as documented by serial Holter ECG studies. There was no deterioration in indices of airway resistance ($\text{FEV}{}_{\mathrm{1·0}}\text{VC}$) in patients treated with pindolol (both intravenously and orally), in contrast to a marked deterioration in $\text{FEV}{}_{\mathrm{1·0}}\text{VC}$ in the same patients treated with propranolol. Pindolol appears to be a reasonable substitute for propranolol in patients with bronchospastic illness who require beta-blockade for control of supraventricular arrhythmias.     

Usefulness of invasive and non-invasive electrophysiologic studies in the selection of antiarrhythmic drugs for the patients with paroxysmal supraventricular tachyarrhythmia

A comparison of the effects of several antiarrhythmic agents was made in a study of 70 patients - 15 with manifest Wolff-Parkinson-White (WPW) syndrome, 17 with concealed WPW syndrome, 18 with AV nodal re-entrant tachycardia, 14 with paroxysmal atrial fibrillation and 6 with paroxysmal atrial flutter - employing intracardiac stimulation and esophageal pacing. For the termination of paroxysmal supraventricular tachycardia, intravenous administration of verapamil or aprindine was more effective than that of disopyramide or procainamide. In AV nodal re-entrant tachycardia, verapamil was the most effective for termination. In the manifest WPW syndrome, disopyramide or aprindine was indicated especially for patients with the accessory pathways of the short antegrade refractory period, because these drugs lengthened the refractory period of the accessory pathways. For the purpose of converting atrial fibrillation or flutter to the sinus rhythm, type IA drugs such as disopyramide were indicated. However, verapamil was effective for slowing down the ventricular rate in atrial fibrillation or flutter except in cases of manifest WPW syndrome. A 6-month follow-up study showed that oral administration of verapamil was also useful for putting a stop to the attacks in 24 out of 32 patients with paroxysmal supraventricular tachycardia, while oral disopyramide prevented the recurrence of atrial fibrillation in only 4 of 10 patients.     

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.     

Pacing therapy for atrial tachyarrhythmias

The use of pacing techniques for the treatment of atrial tachyarrhythmias has been advocated for more than 30 years. Although it has played a beneficial role in the management of paroxysmal supraventricular tachycardia (PSVT) in drug-refractory patients, tachycardia acceleration and development of atrial fibrillation has been the major drawback. With the availability of radiofrequency catheter ablation therapy, the use of implantable antitachycardia devices for PSVT is currently negligible. From retrospective and small control studies it has been shown that atrial or dual-chamber pacing in patients with sick sinus syndrome has been associated with a lower incidence of paroxysmal atrial flutter or fibrillation than in those who received a ventricular pacemaker. Furthermore, recent studies have reported the potential benefit of reducing frequency of paroxysmal atrial flutter and fibrillation with multisite atrial pacing. As a result, there is a resurgence of research interest in antitachycardia pacing for prevention of atrial tachyarrhythmias. This paper briefly describes the basic aspects of antitachycardia pacing, reviews the data on the use of implantable antitachycardia devices for PSVT and the selection of patients, and assesses the current status of research on atrial pacing for prevention of paroxysmal atrial flutter and fibrillation.