Atrial premature beats coupling interval determines lone paroxysmal atrial fibrillation onset.

In 20 patients with recurrent episodes of lone paroxysmal atrial fibrillation we assessed the onset pattern of each episode of either atrial fibrillation or of atrial flutter during a 24-h Holter monitoring. We evaluated 24 twenty-four-hour Holter tape recordings and our data are related to 168 episodes of paroxysmal atrial fibrillation and 27 episodes of paroxysmal atrial flutter. Eighty-five percent of atrial fibrillations and 67% of atrial flutters were of short duration (less than 5 min). The majority of patients (80%) had either nocturnal or daily episodes of arrhythmia and PP intervals immediately before onset of arrhythmia did not show significant variations in 77% of cases. The coupling interval of the supraventricular premature beats eliciting atrial fibrillation was significantly shorter than the coupling intervals of the spontaneous isolated supraventricular premature beats (p less than 0.0001); again, in 6 patients with either atrial fibrillation or flutter, the coupling interval at onset of fibrillation was significantly shorter in comparison to flutter (p less than 0.0001). In conclusion, vagal or sympathetic prevalence does not seem to influence significantly the beginning of the arrhythmia, while the coupling interval of the atrial premature beats plays a critical role in the inducibility of atrial flutter or fibrillation.     

Akuttherapie lebensbedrohlicher tachykarder Rhythmusstörungen

Life-threatening supraventricular tachyarrhythmias include atrial fibrillation, atrial flutter, AV-nodal reentrant tachycardia with rapid ventricular response and preexcitation syndromes combined with atrial fibrillation. Ventricular tachyarrhythmias still remain one of the leading causes of death; these arrhythmias include monomorphic and polymorphic ventricular tachycardia, torsade de pointes tachycardia, ventricular fibrillation and ventricular flutter. In all patients with tachycardias, an attempt should be made to differentiate between narrow (QRS duration < 0.12 s) or wide QRS complex (QRS duration ≥ 0.12 s) tachycardias. In the assessment of patients (pts) with supraventricular/ventricular tachyarrhythmias, attention should be given to identify whether the tachycardia is associated with worsening angina or low cardiac output. In pts with narrow QRS complex tachycardias or pts with atrial fibrillation and preexcitation syndromes immediate synchronized cardioversion should be performed if signs or symptoms of instability (hypotension, evidence of end-organ dysfunction, worsening angina) exist. In pts with a stable hemodynamic situation, vagal maneuvers, adenosine or calcium channel blockers can be used. Management of atrial flutter usually centers on cardioversion or rapid atrial pacing to normal sinus rhythm. In the treatment of patients with deemed unstable ventricular tachycardia (VT), electrical cardioversion is the treatment of choice. In more stable patients, ajmaline is the preferred agent after myocardial infarction and lidocaine if myocardial ischemia is present. In pts with torsade de pointes tachycardias aggressive steps must be taken to prevent degeneration of this rhythm to ventricular fibrillation (VF). Magnesium sulfate has recently been demonstrated efficacious and is currently considered first-line drug therapy. Transcutaneous overdrive pacing should be attempted if magnesium is unsuccessful. The pt with pulseless VT or VF demands early electrical countershock.     

Spectrum of regular tachycardias with wide QRS complexes in patients with accessory atrioventricular pathways

Reciprocating tachycardia and atrial flutter or fibrillation are the rhythm disorders most frequently documented in patients with accessory atrioventricular (A-V) pathways. Reciprocating tachycardia typically results in a regular tachycardia (140 to 250/min) with a normal QRS pattern, although on occasion bundle branch block aberration occurs. Atrial flutter or fibrillation may result in an irregular ventricular response, with the QRS configuration being normal or exhibiting bundle branch block or various degrees of ventricular preexcitation, or both. Although much less common than either reciprocating tachycardia or atrial flutter/fibrillation, regular tachycardias with a wide QRS complex suggestive of ventricular preexcitation are observed in patients with accessory pathways. Excluding functional or preexisting bundle branch block, several arrhythmias may cause these electrocardiographic findings which may mimic those of ventricular tachycardia.In the present study a variety of arrhythmias that resulted in tachycardias with a wide QRS complex were examined in 163 patients with accessory pathways who underwent clinical electrophysiologic study for evaluation of recurrent tachyarrhythmias. Twenty-six patients (15 percent) manifested a regular tachycardia with a wide QRS complex suggesting ventricular preexcitation. Atrial flutter with 1:1 anterograde conduction over an accessory pathway (15 of 26 patients, 58 percent) was the most frequent arrhythmia and was usually associated with a heart rate of 240/min or greater (12 of 15 patients). Reciprocating tachycardia with conduction in the anterograde direction over an accessory pathway (antidromic reciprocating tachycardia) occurred in 7 of 26 patients (27 percent), and resulted in a slower ventricular rate than atrial flutter (217 ± 22 versus 262 ± 42, P < 0.01). Other arrhythmias included reciprocating tachycardia with reentry utilizing a fasciculoventricular or nodoventricular connection (two patients, 8 percent), reciprocating tachycardia with reentry in the atrium or A-V node and anterograde accessory pathway conduction (one patient, 4 percent) and ventricular tachycardia (one patient, 4 percent).In this study the clinical electrophysiologic diagnostic features of several arrhythmias which cause tachycardias with a wide QRS compex suggesting ventricular preexcitation are outlined. It is apparent that definitive arrhythmia diagnosis during these tachycardias is often complex and usually requires careful study using intracardiac electrode catheter techniques.     

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.     

Wide Complex Tachycardia in the Presence of Class I Antiarrhythmic Agents: A Diagnostic Challenge

We present two patients with paroxysmal atrial fibrillation on class 1C antiarrhythmic drugs without concomitant atrioventricular (AV) nodal blocking agents who developed atrial flutter with 1:1 AV conduction. Their electrocardiogram revealed wide complex tachycardia with rates >200/minute. Atrial flutter with 1:1 conduction in the presence of class IC antiarrhythmic drugs may present a diagnostic challenge. These cases illustrate the importance of coadministering an AV nodal blocking agent with class IC antiarrhythmic agents in patients with atrial fibrillation. The differential diagnosis of wide complex tachycardia in patients taking class IC agents should include atrial flutter with 1:1 AV conduction.     

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.     

The use of atrial pacing to induce atrial fibrillation and flutter

We studied the clinical and electrophysiological significance of induction of atrial fibrillation or atrial flutter by atrial electrical stimulation. Our atrial fibrillation/flutter induction protocol included incremental atrial pacing up to a rate of 200 beats/min, ramp up to 250 and 300 beats/min, and bursts up to 600 beats/min. The end point was sustained atrial fibrillation/flutter induction (30 sec). We performed a provocative study on 72 subjects previously divided into three groups: the first was the control group; the second comprised patients with spontaneous paroxysmal atrial fibrillation/flutter; the third comprised patients without spontaneous atrial fibrillation/flutter, but with pathologies assumed to put them at risk for atrial fibrillation/flutter. We were unable to induce sustained atrial fibrillation/flutter in the control group, but were able to induce these arrhythmias in 95% of the subjects with spontaneous atrial fibrillation/flutter. Thus the methods have a sensitivity of 95% and a specificity of 100%. We were also able to induce atrial fibrillation/flutter in 57% of patients at risk for atrial fibrillation/flutter, that is a lower incidence than patients with spontaneous episodes. When sustained atrial fibrillation/flutter could be induced, it was well tolerated and stopped spontaneously in less than 24 hours without treatment. The technique thus involves no risk and demonstrates that antiarrhythmic therapy is usually superfluous in interrupting induced atrial fibrillation/flutter.     

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.     

起源于肺静脉的房性心律失常体表心电图和心内电生理特点

目的:分析起源于肺静脉的房性心律失常体表心电图和心内电生理特点,识别触发心房纤颤(房颤)的房性期前收缩(房早)和房性心动过速(房速)。方法:回顾性分析房性心律失常并阵发性房颤84例体表心电图(房颤组),非房颤组84例体表心电图为频发房早(800次/24 h)。房颤组结合心内电生理检查及Lasso环状电极标测,行导管射频消融(RFCA)肺静脉隔离(PVI)。结果:房颤组电隔离肺静脉286支,均达即刻成功标准,无并发症发生。房颤组体表心电图呈房早、房速、心房扑动(房扑)和阵发性房颤(房颤)频繁发作和交替转换,并常伴长间歇,房早联律间期470～280(420±57)ms明显短于非房颤组的房早联律间期660～350(610±86)ms,P0.05,房颤多由短联律间期房早触发。心内电生理改变为Lasso环状电极标测到起源于肺静脉的连续、快速、有序或无序的较P波提前,时限短、峰锐利的尖峰电位(Spike电位),同步心电图显示该Spike电位常是阵发性房颤的触发因素。经导管射频消融消除肺静脉内电位或隔离肺静脉与心房间的电或组织连接,可终止房性心律失常,维持窦性心律。结论:起源于肺静脉的房性心律失常的特点是短联律间期房早,也是阵发性房颤的触发因素。     

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.     

Enlarged effects of adenosine in a septic patient with multiple myeloma and atrial flutter

We report the history of a 60-year-old patient with a multiple myeloma and Staphylococcus aureus associated sepsis to whom adenosine in a dose of 6 mg was administered, when a regular, narrow QRS complex tachycardia at a heart rate of 120 beats/minute started. Adenosine led to a complete AV-block and revealed atrial flutter. Atrial flutter waves persisted for about 15 seconds and were followed by atrial and ventricular asystole for about 20 seconds. Repeated nonsustained polymorphic ventricular tachycardias followed and after about 90 seconds sinus rhythm was restored.     

Radiofrequency ablation of atrial flutter due to administration of class IC antiarrhythmic drugs for atrial fibrillation

In selected patients, atrial fibrillation (AF) converts to atrial flutter (AFI) due to treatment with class IC antiarrhythmic drugs. In this study, we prospectively investigated the effects of AFI ablation and continuation of drug therapy in patients with AF who developed AFI due to long-term administration of class IC antiarrhythmic drugs. The study population consisted of 187 patients from an AF registry with paroxysmal AF who were orally treated with flecainide (n = 96) or propafenone (n = 91). Twenty-four patients (12.8%) developed AFI during the course of treatment. In 20 of these patients (10.7%), electrophysiologic study revealed typical AFI. These patients underwent radiofrequency ablation of AFI. Ablation failed in 1 patient. All patients continued preexisting drug treatment. Recurrence of AF was assessed by ambulatory Holter monitoring and serial questionnaires. During a mean follow-up of 11 +/- 4 months, the incidence of AF episodes was significantly lower in patients with a combined therapy (2.7 +/- 3.6 per year) than in control subjects with a sole drug treatment (7.8 +/- 9.2 per year, p <0.05) and than before therapy (10.2 +/- 5.4 per year, p <0.001). Subgroup analysis revealed that 7 patients (36.8%) remained symptom free with no evidence of atrial tachyarrhythmia. Eight additional patients (42.1%) had ongoing paroxysmal AF, however, with a significantly lower incidence of AF episodes than before therapy (2.3 +/- 1.6 per year vs 11.5 +/- 5.0 per year, p <0.001). In the remaining 4 patients (14.7%), no beneficial effect of AFI ablation was found. It is concluded that in patients with AF who develop typical AFI due to administration of class IC antiarrhythmic agents, a combined therapy with catheter ablation of AFI and continuation of drug treatment is highly effective in reducing occurrence and duration of atrial tachyarrhythmias.     

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.     

Autodecremental pacing for the interruption of ventricular tachycardia and atrial flutter

The efficacy and safety of autodecremental pacing (ADP) to interrupt ventricular tachycardia (VT) and atrial flutter was examined. Once tachycardia was recognized, ADP was initiated using a short train of stimuli with gradual shortening (3%) of the interstimulus interval. ADP was applied to 13 consecutive patients during 75 episodes of VT (mostly following induction by ventricular stimulation). Successful interruption of VT occurred in 88% of the episodes. In 6 episodes (8%), ADP resulted in ventricular fibrillation and in 3 episodes VT was unaffected by ADP. The only significant discriminator between the failure or success of ADP was the rate of VT. ADP was also applied to 17 consecutive patients with an atrial flutter that was resistant to conventional antiarrhythmic agents. Successful conversion of atrial flutter to sinus was seen in only 8 patients (47%). A temporary acceleration to atrial fibrillation appeared in 3 patients (18%), and in 6 patients atrial flutter was unaffected by ADP. ADP was successful in 70% (7/10) of patients with type 1 (< 300 beats/min) atrial flutter. The authors conclude that ADP is beneficial in the interruption of VT and atrial flutter in a selected group of patients, especially with a slower rate of tachyarrhythmia (atrial rate during atrial flutter < 300 beats/min and ventricular tachycardia < 180 beats/min).     

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.     

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

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

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.     

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.     

Efficacy and safety of timolol for prevention of supraventricular tachyarrhythmias after coronary artery bypass surgery

Forty-one patients undergoing coronary artery bypass grafting were randomly assigned to receive prophylactic timolol or placebo, given in a double-blind fashion. beta-Adrenoceptor-blocking therapy was stopped at least one half-life before surgery. Three to 7 hr after surgery (304 +/- 56 min), 0.5 mg of timolol or placebo was given intravenously twice daily in a double-blind manner. When oral medications were resumed postoperatively, 10 mg of timolol twice daily or placebo was continued orally. Continuous electrocardiograms were recorded for 24 hr before and for 7 days after surgery with a standard cassette recorder. No patient received digoxin. Both groups were comparable for frequency of preoperative supraventricular arrhythmias, left ventricular ejection fraction, duration of cardiopulmonary bypass, aortic cross-clamp time, number of bypass grafts, and total duration of monitoring. Analysis of arrhythmias was done by hand counts, and supraventricular arrhythmias were divided into supraventricular tachycardia and atrial fibrillation and/or flutter. Timolol decreased the frequency of supraventricular tachycardia (581 episodes placebo vs 84 timolol; p less than .05) and of atrial fibrillation and/or flutter (291 episodes placebo vs five timolol; p less than .05). Timolol decreased the number of patients with severe (heart rate greater than 200 beats/min, duration greater than 50 beats) episodes of supraventricular tachycardia (four placebo vs 0 timolol; p less than .05) and also decreased the number of episodes of severe (heart rate greater than 200 beats/min, duration greater than 5 min) atrial fibrillation and/or flutter (16 placebo vs one timolol; p less than .005). There were differences in the durations of supraventricular arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.