Efficacy of rapid atrial pacing for conversion of atrial flutter in medically treated patients

To determine factors affecting the success rate of rapid atrial pacing in converting atrial flutter to sinus rhythm in medically treated patients, we prospectively used this technique for 120 consecutive episodes in a total of 110 patients (94 male, 16 female, mean age 63 ± 14 years). Structural heart disease was present in 77%, and all patients were receiving antiarrhythmic drugs at the time of the procedure. Atrial flutter type I was present in 92 of 110 patients (84%), and atrial flutter type II in 18 of 110 (16%). Primary success rate (return to sinus rhythm either immediately or after < 10 min of atrial fibrillation) was 70% (71/102) for flutter type I, and 6% ( 1/18) for flutter type II (p < 0.001). Delayed success (conversion to sinus rhythm in > 10 min but < 24 h) was observed in 15 additional episodes of flutter type I (15%) and in 1 additional episode of flutter type II (6%). The only clinical factors predicting primary success were (a) characteristics of flutter waves on the 12-lead surface electrocardiogram, (b) duration of flutter (primary success rate of 81 % if flutter < 1 month vs. 57% if > 1 month, p< 0.05), and (c) flutter rate (primary success rate of 78% if < 260/min vs. 56% if > 260/min, p< 0.05). In 6/71 episodes of flutter type I (8%), prolonged sinus pauses or severe bradyarrhythmias occurred after conversion to sinus rhythm. It was concluded that overdrive atrial pacing is an effective procedure to convert atrial flutter type I in sinus rhythm in medically treated patients; the primary success rate of the procedure depends on flutter type, duration, and rate. Because severe bradyarrhythmias are not uncommon at the time of conversion and because it does not require general anesthesia, this technique can be considered as a first-step therapy in this particular population.     

Pre-implant determinants of adequate long-term function of single lead VDD pacemakers.

AIMS: An inherent limitation of single lead VDD pacing is the inability to stimulate the atria. Reprogramming and upgrading the pacemaker system may be required when sinus node dysfunction, atrial undersensing, or atrial fibrillation develop. We evaluated whether routine clinical information is sufficient to select patients to benefit in long-term from VDD pacing. METHODS AND RESULTS: We collected data on 12-lead and monitored electrocardiograms and routine clinical information at implantation of a VDD pacing system in 350 consecutive patients with grade II or III atrioventricular conduction block. The age at implantation was 74.5 +/- 8.0 years, and the follow-up lasted 1.5 +/- 1.5 years. The cumulative maintenance of VDD pacing mode was 91.%. Loss of VDD mode was due to permanent atrial fibrillation in 16 (4.6%), sinus node dysfunction in six (1.7%). atrial undersensing in 11 (3.1%). Chronic atrial fibrillation developed in 23% of patients who had heart enlargement in chest x-ray and a history of paroxysmal atrial fibrillation or flutter. A criterion of normal sinus rate at implantation sufficiently predicted adequate sinus node function. Poor atrial sensing was not predicted by pre-implant characteristics. CONCLUSIONS: According to our data, adequate sinus-driven atrial rate and no history of paroxysmal atrial fibrillation and cardiac enlargement predict maintenance of the VDD pacing mode in elderly patients treated for heart block. Routine information available at implantation is sufficient to guide acceptance of single lead VDD pacing therapy.     

Short-term rapid atrial pacing produces electrical remodeling of sinus node function in humans

INTRODUCTION: Depression of sinus node function occurs in dogs and in patients after cessation of atrial flutter and fibrillation. We tested whether transient atrial pacing might produce similar changes in humans. METHODS AND RESULTS: We studied the impact of short-term rapid atrial pacing, simulating atrial tachyarrhythmias, on sinoatrial conduction time (SACT) and corrected sinus node recovery time (CS-NRT) in 10 patients undergoing electrophysiologic study. None had recognizable structural heart disease, history of atrial fibrillation or flutter, autonomic dysfunction, or any tachycardia for at least 24 hours before study. All cardiac drugs were discontinued >5 half-lives prior to study. No patient had significant hypotension during atrial stimulation. SACT and CSNRT were measured at baseline, and sinus node reset zone was determined. Right atrial pacing was performed for 10 to 15 minutes, after which SACT and CSNRT were measured again. Both parameters increased significantly, from 423+/-208 msec to 491+/-214 msec and from 80+/-50 msec to 96+/-53 msec, respectively (P = 0.02 and P < 0.001, respectively). CONCLUSION: Rapid atrial pacing for only 10 to 15 minutes, simulating transient atrial tachyarrhythmias, alters sinus node function in humans. Additional studies are needed to evaluate the mechanism, but the clinical implication is that even transient episodes of atrial tachyarrhythmias can cause sinus node remodeling in patients.     

Direct conversion of atrial flutter to sinus rhythm with low-output,short-duration transesophageal atrial pacing

Background and hypothesis: Transesophageal atrial pacing (TAP) is useful for terminating paroxysmal non-selfterminating atrial flutter (RAF); however, high output pacing of long stimulus duration causes severe symptoms such as chest pain. The objective of this study was to investigate the effect of low-output, short-duration TAP on the conversion of PAF. Methods: We applied low-output (within 15 mA with a pulse duration of 10 ms), short-duration (within 4 s) TAP in 31 patients (50±19 years) with PAF. Transesophageal pacing was delivered with 10 pulses of burst pacing at intervals that were 20 ms shorter than those of the flutter wave length. When the conversion was unsuccessful, we delivered 20 pulses of burst pacing. Results: Sixteen patients (52%) were converted directly to sinus rhythm and 12 (38%) to atrial fibrillation. Transesophageal pacing was ineffective in 3 (10%) patients. The duration of atrial flutter, maximum flutter wave amplitude, effective pacing intervals, underlying heart diseases, and cardiac function were not different between patients who had direct conversion to sinus rhythm and those converted to atrial fibrillation. The patients who had direct conversion to sinus rhythm had longer flutter wave cycle lengths than those converted to atrial fibrillation (248 vs. 221 ms, p<0.005). No patient had complications and complained of any symptoms. Conclusion: Low-output, short-duration TAP was useful to convert PAF directly to sinus rhythm without side effects.     

Conduction abnormalities detected by electrophysiologic testing following repair of ostium primum atrioventricular septal defect

Since 1983 we have performed electrophysiologic studies in 6 patients who had previously undergone repair of an ostium primum atrioventricular septal defect. Information obtained during electrophysiologic studies was crucial in guiding appropriate pacemaker therapy in these patients. As judged from the resting electrocardiogram, sinus or junctional bradycardia was present in 3/6, atrial flutter / fibrillation in 2/6, and paced rhythm in 2 patients who had had ventricular pacemakers implanted for complete atrioventricular block. During maximal exercise testing 4 patients had reduced heart rates; 2 had sudden drops in heart rate at 1 min postexercise; 1 patient had exercise induced ventricular bigeminy; and 1 patient with atrial flutter and 2: 1-4: 1 block at rest developed 1: 1 conduction during Stage II with an effective ventricular rate of 220/min. During electrophysiologic studies, the maximum corrected sinus node recovery time was abnormal in five of the six, ranging from 410 to 5630 msec. There was no spontaneous atrial rhythm in the other patient. Complete atrioventricular block was present in 2 patients while the atrioventricular Wenckebach phenomenon occurred abnormally at atrial pacing cycle lengths greater than 450 msec in 2 others. Supraventricular tachycardia or atrial flutter/fibrillation, was either spontaneous or induced in 2/6 patients, while ventricular tachycardia was induced in 1/3 patients who underwent programmed ventricular stimulation. Electrophysiologic studies were important in unmasking severe sinus node disease in 3 patients and atrioventricular node disease in 2. We therefore recommend that electrophysiologic studies be strongly considered as part of the evaluation of conduction abnormalities following repair of ostium primum atrioventricular septal defect.     

The effectiveness and safety of d,l-sotalol in the ambulatory treatment of atrial fibrillation and flutter]

Data on short and long term efficacy and safety of d,l sotalol in patients with atrial fibrillation or atrial flutter is limited. The aims of this study were to (1) assess the antiarrhythmic efficacy of d,l sotalol maintaining normal sinus rhythm in patients with refractory atrial fibrillation or flutter, (2) evaluate the efficacy of d,l sotalol in preventing recurrences of paroxysmal atrial fibrillation or flutter, (3) evaluate the control of ventricular rate in patients with paroxysmal or refractory atrial fibrillation or flutter unsuccessfully treated with other antiarrhythmic agents, (4) determine predictors of efficacy (5) assess the safety of d,l sotalol in this setting. Two hundred patients with chronic or paroxysmal atrial fibrillation or atrial flutter or both, who had failed one to six previous antiarrhythmic drug trials were treated with d,l sotalol 80 to 440 mg/day orally. Fifty four percent was female, age 47 +/- 16 years (range 7-79), follow up period 7 +/- 7 months (range 1 to 14 months), 79% of patients had the arrhythmia for more than one year. The atrial fibrillation in 37.5% of patients was chronic and paroxysmal in 23.5. The atrial flutter was chronic in 31% of patients and paroxysmal in 8%. Eighty two percent of patients was in functional class I (NYHA) and 82% had cardiac heart disease: left atrial (LA) size 44 +/- 10 mm, right atrial (RA) size 37 +/- 7 mm and left ventricular ejection fraction (LVEF) 58 +/- 8%. Total success was achieved in 58% of patients (atrial fibrillation 40% and 18% in atrial flutter), partial success in 38% (atrial fibrillation in 18% and 20% in atrial flutter) and 4% of patients failure. It was p < 0.07 when compared total success vs partial success among atrial fibrillation and atrial flutter groups. Patients with cardiac heart disease responded worst (p = 0.10) to the drug than those without it, specially if the heart was dilated. We concluded that d,l sotalol has moderate efficacy to convert and maintain normal sinus rhythm, as well as it acts controlling paroxysmal relapses and ventricular heart rate.     

Remodeling of sinus node function after catheter ablation of right atrial flutter

INTRODUCTION: The purpose of this study was to investigate the effect of ablation of right atrial flutter upon sinus node function in humans. METHODS AND RESULTS: This study enrolled 35 patients. Twenty-four patients (16 men and 8 women; age 68 +/- 11 years) were referred for ablation of persistent atrial flutter (duration 8 +/- 11 months). After ablation, there was abnormal sinus node function defined as a corrected sinus node recovery time (CSNRT) > or = 550 msec. The control group consisted of 11 patients who were undergoing pacemaker implantation for sinus node disease but did not have a history of atrial dysrhythmias or ablation. Within 24 hours of ablation or pacemaker implantation, baseline maximal CSNRT was measured through a permanent pacemaker by AAI pacing at six cycle lengths: 600, 550, 500, 450, 400, and 350 msec. CSNRT then was measured in the same manner at 48 hours, 14 days, and 3 months after ablation/pacemaker implantation. P wave amplitude and duration, and percent atrial sensing also were assessed at the same intervals. For patients undergoing atrial flutter ablation, there was progressive temporal recovery of CSNRT (1,204 +/- 671 msec at baseline vs 834 +/- 380 msec at 3 months; P < 0.001) and a significant increase in the percent atrial sensing and P wave amplitude at 3 months compared with baseline (P < 0.001). In control subjects, there was no change in the CSNRT, percent atrial pacing, or P wave amplitude. CONCLUSION: After ablation of persistent atrial flutter, there is temporal recovery of CSNRT and increase in spontaneous atrial activity. These findings suggest that atrial flutter induces reversible changes in sinus node function.     

Electrophysiologic determinants of recurrent atrial flutter after successful termination by overdrive pacing

The potential ability of electrophysiologic abnormalities to predict recurrence of atrial flutter was evaluated. Twenty-five patients with chronic atrial flutter resistant to combined digitalis and quinidine therapy were studied electrophysiologically after restoration of sinus rhythm by overdrive pacing or by eventual direct current cardioversion. Recurrence of atrial flutter was observed in 12 patients during a mean follow-up period of 17 months (range 3 to 50). Electrophysiologic testing included programmed high right atrial stimulation at a paced drive cycle length of 600 ms and incremental pacing up to 200-ms paced intervals. When coupling intervals of 90% of the drive cycle length were compared to coupling intervals of 48% of the drive cycle length, the increase in S1A1 interval, defined as the interval between the stimulus artifact and the atrial activation near the atrioventricular junction, was greater in patients with subsequent recurrence of atrial flutter (47 +/- 11 vs 21 +/- 18 ms). Stepwise logistic regression analysis identified the S1A1 increase to be the sole independent predictor of recurrence (p = 0.0082) while previous episodes of atrial flutter or the presence of organic heart disease were identified as dependent variables. Reclassification showed a 91% sensitivity and a 92% specificity. Correct classification was achieved in 92% of patients. The initiation of atrial dysrhythmia had no predictive value. The assessment of the S1A1 interval by programmed atrial stimulation appears helpful in delineating the patient risk of recurrent atrial flutter after termination by overdrive pacing.     

Dispersion of atrial refractoriness in patients with sinus node dysfunction.

Abnormal atrial refractoriness was examined as a cause of atrial fibrillation/flutter (AFF) in patients with bradycardia. Refractory periods at three disparate right atrial sites were compared in 17 patients with sinus node dysfunction (SND) and 16 controls. Atrial pacing shortened refractory periods, but failed to decrease dispersion of refractoriness significantly. During sinus rhythm, duration and dispersion of refractoriness were greater in SND patients than in controls. These differences persisted with atrial pacing. For example, at the paced rate, dispersion of effective refractory periods in SND patients was greater than in controls (62.9 +/- 34 vs 36.6 +/- 21 msec, p less than 0.01). Six SND patients had AFF, but they did not have greater dispersion than other SND patients, or unusually short or long refractory periods. Thus, prolonged and nonuniform refractoriness were features of SND. Abnormal refractoriness in SND reflected atrial disease and persisted with pacing. These abnormalities were not unique to patients with AFF.     

Atrial pacing for cardioversion of atrial flutter in digitalized patients

To test the safety and reliability of atrial pacing as a conversion technique in patients with atrial flutter who are receiving digitalis therapy, atrial pacing conversion was attempted for 49 episodes of atrial flutter in 32 consecutive patients. All patients except one were receiving digitalis. To control ventricular rates most patients had received larger than usual therapeutic doses of digitalis glycoside before pacing. Fourteen of the 25 patients whose serum levels were measured had glycoside concentrations greater than 2 ng/ml. Before atrial pacing the mean atrial and ventricular rates were, respectively, 290 +/- 20.6 and 134 +/- 27.9/min (mean +/- standard deviation). Successful rhythm conversion was achieved on 48 occasions (98%) in 31 patients. One patient required transthoracic direct current synchronized countershock cardioversion. With atrial pacing, the atrial flutter rhythm reverted immediately to sinus mechanism in 23 instances, and there were 25 episodes of atrial fibrillation. Among those who experienced atrial fibrillation, the rhythm spontaneously reverted to sinus mechanism within 24 hours on 14 occasions; on 11 occasions; the rhythm reverted to atrial flutter and repeat pacing was required. Sinus mechanism was eventually established in all 31 patients.     

Natural history of sinus node disease treated with atrial pacing in 213 patients: implications for selection of stimulation mode.

OBJECTIVES. This study was designed to analyze the incidence and determinants of complications and long-term survival in sinus node disease treated with atrial pacing. BACKGROUND. Knowledge of the natural history of sinus node disease treated with different pacing modes is imperfect, and controversy exists regarding the optimal pacemaker therapy. METHODS. A consecutive series of 213 patients with sinus node disease initially treated with atrial pacing was studied for a median follow-up period of 60 months. The end points studied were permanent atrial fibrillation, high grade atrioventricular (AV) block, P wave undersensing, pacing mode change, reoperation and death. Several prognostic factors were evaluated statistically and the survival rate was compared with that of a matched general population. RESULTS. The incidence rate of permanent atrial fibrillation during follow-up was 7% (1.4%/year). The risk of this arrhythmia increased substantially with age greater than or equal to 70 years at pacemaker implantation. Only 2 of the 15 patients who developed permanent atrial fibrillation required ventricular pacing. High grade AV block occurred in 8.5% (1.8%/year) and its incidence was much greater in patients with complete bundle branch block or bifascicular block (35%) than in patients without such conduction disturbances (6%). A change to ventricular or dual-chamber stimulation was necessary in 14% of all patients, primarily because of early lead dislodgment or high grade AV block. Surgical intervention with maintenance of atrial pacing was required in 7% of patients. The survival rates of 97% at 1 year, 89% at 5 years and 72% at 10 years did not differ significantly from those of a matched general population. CONCLUSIONS. In sinus node disease, atrial pacing can be successfully applied during long-term follow-up. Patients with complete bundle branch or bifascicular block in addition to sinus node disease should initially receive a dual-chamber pacemaker, but routine application of dual-chamber stimulation does not appear to be warranted.     

迷宫手术对二尖瓣病合并的慢性心房颤动电生理的影响

对21例二尖瓣疾患伴心房颤动（简称房颤）施行了迷宫手术和二尖辩手术的患者，采用12导联心电图、心内电生理、动态心电图、踏车运动试验方法进行检查，探讨迷宫手术对慢性房颤患者心脏围手术期和远期电生理的影响。平均随访17．9±7．9个月。结果如下：①术后3个月90％（18／20）恢复窦性心律，随访1年以上者（14例）房颤均未见复发。②术后除1例窦房结恢复时间延长外余均正常，无窦性起搏或房室给传导功能障碍。③术后都有正常的心房激动和房室同步激动顺序。④术后在各标测部位猝发刺激和程控刺激均不能诱发心房扑动和颤动，心房各部位有效不应期均显著长于高位右房有效不应期。⑤动态心电图和运动试验证明有良好的心率变时性反应和运动耐力。⑥1例术后4个半月死于急性坏死性肝炎。以上表明通过电生理检查手段证实了迷宫手术治疗房颤能达到：①消除房颤恢复窦性心律，②重建和（或）维持房室同步活动，③恢复心房传输功能。提出对二尖瓣疾患合并的慢性房颤病人在施行二尖瓣手术时应作迷宫手术。     

Cardiac rhythm disturbances early after orthotopic heart transplantation: prevalence and clinical importance of the observed abnormalities

To precisely define the incidence, type and consequences of cardiac arrhythmias early after heart transplantation, 25 cardiac transplant recipients were monitored continuously for 728 days from the day of surgery to discharge or death. A subset of 15 patients had sinus node function studies with overdrive suppression performed weekly at the time of endomyocardial biopsy. Results revealed sinus bradycardia in 10 patients (40%) and junctional bradycardia in 6 (24%). Supraventricular tachycardia in the form of atrial tachycardia, atrial fibrillation and atrial flutter occurred in 11 patients (44%). Ventricular tachycardia occurred in 15 patients (60%) and was nonsustained in all. Cardiac pacing for 1,403 h was used in nine patients with a pulse rate less than 50 beats/min; seven recovered and permanent pacing was instituted in two. In the subgroup that had sinus node function studies, seven patients were identified with clinical bradyarrhythmia; each had abnormal sinus node recovery time (greater than 1,400 ms) and abnormal corrected sinus node recovery time (greater than 525 ms) in at least one study. These seven patients also had a significantly prolonged ischemic time (236 +/- 26 versus 159 +/- 68 min, p less than 0.01). In conclusion, cardiac arrhythmias, particularly ventricular tachycardia and bradyarrhythmia, occur more commonly early after orthotopic heart transplantation than has previously been reported. Sinus node dysfunction due to prolonged organ ischemic time, antiarrhythmic drug use or surgical trauma, alone or in combination, may contribute to these arrhythmias.     

Use of procainamide with rapid atrial pacing for successful conversion of atrial flutter to sinus rhythm

Rapid atrial pacing is a useful technique and often the therapy of choice to terminate atrial flutter in patients. However, interruption of atrial flutter by rapid atrial pacing may not always produce sinus rhythm, but rather may result in atrial fibrillation. Twelve patients with spontaneous atrial flutter that had been present for greater than 24 h were studied to assess the efficacy of atrial pacing, alone and in combination with procainamide, to convert atrial flutter to normal sinus rhythm. Rapid atrial pacing for greater than or equal to 15 s from selected atrial sites at selected pacing rates were performed during atrial flutter. The initial pacing rate was always at a cycle length 10 ms shorter than the atrial flutter cycle length. If atrial flutter persisted after cessation of pacing, it was repeated at progressively shorter cycle lengths until either a rate of 400 beats/min was achieved or atrial fibrillation was induced. In two patients, atrial flutter was converted to sinus rhythm with pacing alone. Three patients developed sustained atrial fibrillation as a result of the rapid atrial pacing, this rhythm ultimately reverting back to atrial flutter in two. Ten patients received procainamide and 9 of the 10 had lengthening of the atrial flutter cycle length by a mean of 68 ms (1 patient continued to have atrial fibrillation). Then, using the same atrial pacing protocol, high right atrial pacing alone at a mean cycle length of 227 ms interrupted atrial flutter in all these patients, returning their rhythm to sinus rhythm. It is concluded that intravenous procainamide effectively augments the efficacy of rapid atrial pacing to convert atrial flutter to sinus rhythm.     

Inter- and intraatrial dissociation during spontaneous atrial flutter: Evidence for a focal origin of the arrhythmia

Programmed electrical stimulation of the heart was performed in 2 patients with spontaneous atrial flutter. Patient 1 was a young man with paroxysmal atrial flutter that had proved resistant to drug therapy and who was studied during an episode of sustained flutter. In this patient rapid atrial pacing from the coronary sinus at a critical rate faster than the intrinsic flutter rate provoked local atrial fibrillation in the mid and low right atrium which persisted after termination of pacing. In spite of persistent local fibrillation in these regions, atrial flutter continued in the left atrium and the high right atrium. A second burst of pacing resulted in restoration of sinus rhythm. Patient 2 was an elderly woman with probable sick sinus syndrome who developed spontaneous atrial flutter during the course of an electrophysiologic investigation. During flutter intracavitary recordings from multiple sites in the atria revealed a pattern of 3:2 Wenckebach conduction between the left atrium and the high right atrium, with block of every third atrial depolarization at the latter site. These results indicate that atrial flutter may exist at some sites in the atria which are functionally dissociated from the remainder of the atrial tissue, thus supporting the hypothesis that flutter in some patients may be focal in origin.     

Long term management of atrial arrhythmias in young patients with sick sinus syndrome undergoing early operation to correct congenital heart disease.

AIMS: The objective of our study was to evaluate the clinical outcome of patients with operated congenital heart disease (CHD), post-operative sinus node dysfunction and atrial tachyarrhythmias (AT) who had a new generation of DDDRP pacemakers (Model AT501, Medtronic Inc., MN, USA) able to deliver preventive atrial pacing and antitachycardia pacing (ATP) therapies. METHODS AND RESULTS: Fifteen CHD patients (mean age 17+/-9 years, eight after Mustard operation, five after extracardiac Fontan operation and two after atrial septum repair) received a dual-chamber pacemaker with transvenous (eight patients) or epicardial leads (seven patients). In the year before implantation, all patients had symptomatic AT (palpitations), eight patients required hospitalization and five required electrical cardioversion. Pacing prevention algorithms were enabled in all patients, and ATP therapies in six patients. During a mean follow-up of 30 months (range 24-44), three patients (two Fontan, one Mustard) died of CHF, whereas AT required hospitalization in three patients (two Fontan, one atrial septum repair). Only seven patients had symptomatic AT. One hundred and twenty-five AT episodes were treated by ATP in three patients, with an overall termination efficacy of 43.2%. In one patient, atrial lead noise induced inappropriate AT detection that resulted in ATP delivery. Several AT episodes were not treated owing to their very short duration, atrial undersensing, or 1:1 atrioventricular conduction. CONCLUSIONS: Our experience with antitachycardia pacemakers in CHD patients with post-operative sick sinus syndrome after biventricular correction or palliation shows that these devices are safe and that atrial pacing may play a role in AT prevention and treatment.     

A comparison of transoesophageal atrial pacing and direct current cardioversion for the termination of atrial flutter: a prospective, randomised clinical trial.

OBJECTIVE--To compare the safety and efficacy of transoesophageal atrial pacing (TAP) with an easily swallowed pill electrode and direct current cardioversion (DCC) in patients with atrial flutter that was refractory to appropriate medical treatment. DESIGN--Prospective, randomised clinical trial. SETTING--Community based United States naval hospital. SUBJECTS--Twenty one consecutive patients with refractory atrial flutter selected consecutively from the inpatient cardiology consultation service. All patients were haemodynamically stable and medical treatment with a class IA or IC antiarrhythmic agent had failed. Eleven patients were treated with TAP and 10 patients were treated with DCC. INTERVENTIONS--Digoxin was given to all patients to control the ventricular rate to < 100/minute. MAIN OUTCOME MEASURE--Conversion to normal sinus rhythm and arrhythmias after cardioversion. RESULTS--Conversion to normal sinus rhythm was similar in both groups (TAP 8/11, DCC 9/10, p = 0.31). Arrhythmias after cardioversion including third degree heart block and non-sustained ventricular tachycardia were more frequent in the DCC group (TAP 0/11, DCC 6/10, p = 0.02). CONCLUSION--Transoesophageal atrial pacing with an easily swallowed pill electrode is safe, well tolerated, and is as efficacious as DCC for refractory atrial flutter.     

Comparison of atrial overdrive pacing with and without extrastimuli for termination of atrial flutter.

Atrial overdrive pacing has been successfully used to terminate atrial flutter. This study compared the efficacy of atrial extrastimuli following a rapid pacing train to overdrive pacing without atrial extrastimuli for the termination of atrial flutter. Patients were randomized to treatments of short or long burst atrial overdrive pacing or atrial overdrive pacing followed by atrial extrastimuli in a crossover study design. A total of 22 patients (73%) had successful conversion of atrial flutter to sinus rhythm. The success rates in patients exposed to each therapy, including crossover therapies, were 62% with the atrial extrastimuli method, 8% with the short burst pacing method, and 8% with the long burst pacing method (p less than 0.001). Transient atrial fibrillation developed in 15 patients and in 9 of these this arrhythmia preceded conversion to sinus rhythm. Sustained atrial fibrillation was induced in 3 additional patients but never with the atrial extrastimuli method. In conclusion, the method of delivering atrial extrastimuli after a rapid pacing train is highly efficacious for the termination of atrial flutter. Furthermore, this method is more effective than atrial overdrive pacing methods delivered at the same pacing cycle length. These observations have important implications for the programming of antitachycardia pacemakers.     

双房同步起搏技术的临床应用

双房同步起搏是恢复双房电活动同步化的一种新的起搏技术,可防治快速房性心律紊乱。笔者对１７例房内、房间传导阻滞并快速房性心律失常患者进行双房同步起搏治疗,１４例行三腔起搏（ＤＤＤ）、３例行双房起搏（ＡＡＩ）,冠状静脉窦电极均经左锁骨下静脉途径放置。起搏器及电极导线均顺利植入,未发现脱位、穿孔等并发症。冠状静脉窦电极导线顶端电极测定的Ｐ波振幅为５．６９±２．６３（２．４～９．６）ｍＶ、起搏阻抗６５５±１９４．１１（５２０～９６０）Ω、单极起搏阈值０．９２±０．６８（０．４～２．２）Ｖ。冠状静脉窦电极位置较深,则测得起搏阈值较低。随访８．６（３～１５）个月,１例猝死、１６例健在;其预防心房扑动、颤动的显效率达６２．５％、有效率达８１．２５％。结论：双房同步起搏技术是房间传导阻滞合并房性心动过速,心房扑动、颤动的有效治疗和预防方法。     

Determinants of recurrent atrial flutter after cardioversion.

Eighteen male patients (mean age 59 years) who were electrically cardioverted for pure atrial flutter were retrospectively studied to determine those factors influencing the maintenance of regular sinus rhythm or reversion to atrial flutter. Six months after successful cardioversion, 10 patients (55%) had recurrent atrial flutter and eight patients (45%) were still in sinus rhythm. The two groups were not significantly different with respect to age, symptomatology, abnormalities on the 12 lead electrocardiogram (during sinus rhythm), or the administration of digoxin and a class Ia antiarrhythmic agent (after cardioversion). There was a trend for those patients with recurrent atrial flutter to have a higher incidence of underlying heart disease and previous episodes of atrial flutter than the non-recurrent group. There were statistically significant differences between the recurrent and non-recurrent groups with respect to echocardiographically determined left atrial size and left ventricular ejection fraction. Patients with a left atrial size greater than 45 mm or with an ejection fraction less than 45% were all at high risk for recurrent atrial flutter after successful cardioversion.