The effects of class IA antiarrhythmic drug on the common type of atrial flutter in combination with pacing therapy

In 11 patients with common type of atrial flutter (common AF), rapid atrial pacing from the high right atrium was performed before and/or after class Ia antiarrhythmic drug administration, confirming transient entrainment by decreasing the pacing cycle length by 10 ms. In 10 patients before the drug administration, common AF was not interrupted although the pacing cycle length was decreased to 200 ms in 5 patients, accelerated atrial flutter or atrial fibrillation was induced in 4 patients, and common AF was converted into sinus rhythm in only 1 patient. After the drug administration common AF was converted into sinus rhythm in 5 out of 6 patients. The class Ia antiarrhythmic drug prolonged the common AF cycle length (255 +/- 12 ms vs. 298 +/- 37 ms, p less than 0.005) and widened the entrainment zone (64 +/- 7 ms vs. 90 +/- 20 ms, p less than 0.05). The widening of the entrainment zone and the prolongation of the common AF cycle length facilitate the successful conversion of common AF at a longer pacing cycle length, which would not precipitate atrial fibrillation or accelerated atrial flutter. The combination therapy of rapid atrial pacing and the class Ia antiarrhythmic drug is thought to be useful in the therapy of common AF.     

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.     

Facilitating influence of procainamide on conversion of atrial flutter by rapid atrial pacing

In a prospective, double-blind, randomized, placebocontrolledstudy we investigated the facilitating influence of intravenousprocainamide on conversion of atrial flutter by rapid atrialpacing. Fifty consecutive patients with spontaneous sustained atrialflutter were 1:1 randomized into two homogenous groups: groupA received 10 mg. kg^–1 procainamide intravenously, groupB placebo. After infusion there was a significant (P<0·01)lengthening of the flutter cycle with respect to baseline ingroup A, exceeding the flutter cycle length of the control group(P<0·05). The overall success rate of rapid atrialpacing in restoring sinus rhythm was significantly higher afterpre-treatment with procainamide compared to placebo (100% vs76% P<0·05): 20 patients of group A reverted immediatelyafter pacing to sinus rhythm, the remaining five after a briefepisode of atrial fibrillation. In the placebo group, 16 patientsshowed a prompt conversion to sinus rhythm and three after transientatrial fibrillation. In the remaining six patients, due to sustainedpacing-induced atrial fibrillation, direct current cardioversionwas necessary. After administration of procainamide a less aggressivestimulation protocol with significantly (P<0·01) longerpaced cycles to interrupt atrial flutter was achievable. In conclusion, intravenous procainamide augments the efficacyof atrial pacing to convert atrial flutter to sinus rhythm.     

Haemodynamics of induced atrial fibrillation: a comparative assessment with sinus rhythm, atrial and ventricular pacing

The haemodynamics and myocardial lactate consumption during induced atrial fibrillation (AF) were studied in 10 patients with paroxysmal AF. Their mean age (+/- SD) was 61 +/- 5 years and none had clinical evidence of ischaemic or rheumatic heart disease. Compared with sinus rhythm, the onset of AF was associated with a reduction in systolic blood pressure (152 +/- 13 mmHg) in AF vs 169 +/- 23 mmHg in sinus rhythm, P less than 0.01). There was no consistent change in cardiac output at the onset of AF compared with sinus rhythm, but the cardiac output was lower compared with regular atrial pacing at rates similar to those of induced AF (3.85 +/- 0.76 vs 4.38 +/- 0.89 l min-1, P less than 0.02). Compared with sinus rhythm or rate-matched atrial pacing, AF was associated with an elevated pulmonary arterial pressure (24.2 +/- 5.6 mmHg in AF vs 17.9 +/- 14.4 mmHg in sinus rhythm, P less than 0.01) and pulmonary arterial wedge pressure (18.6 +/- 5.6 vs 9.7 +/- 3.9 mmHg, P less than 0.01). The haemodynamic changes during AF were similar to those seen during regular ventricular pacing at an equivalent rate, although the latter was associated with a lower systolic blood pressure (152 +/- 13 mmHg in AF vs 136 +/- 25 mmHg in ventricular pacing, P less than 0.05) and higher right atrial pressure (8.2 +/- 4.4 vs 11.5 +/- 7.5 mmHg respectively, P less than 0.05), presumably due to the deleterious effects of cannon 'a' waves.(ABSTRACT TRUNCATED AT 250 WORDS)     

Predictors of failure of transoesophageal cardioversion of common atrial flutter.

BACKGROUND: Common atrial flutter is due to a re-entry circuit in the right atrium. It is possible to entrain and interrupt this arrhythmia with transoesophageal pacing (TEAP) in a substantial percentage of patients. The aim of this study is to evaluate factors associated with failure of transoesophageal cardioversion of common atrial flutter. METHODS: One hundred consecutive patients underwent an attempted transoesophageal cardioversion of their common atrial flutter. In order to detect factors associated with failure of this procedure, the following were considered: (a) age and gender; (b) underlying heart disease; (c) time of onset of the arrhythmia; (d) antiarrhythmic treatment at the time of cardioversion; (e) flutter cycle length, (f) A/V deflection ratio at the site of transoesophageal pacing; and (g) longitudinal and transverse diameters of right and left atrium on the echocardiogram. RESULTS: In 84 of 100 patients, TEAP modified the atrial flutter circuit: in 23 of these, sinus rhythm was restored; in 31 patients, flutter was converted into atrial fibrillation which spontaneously reverted to sinus rhythm; and in remaining 30 patients, persistent atrial fibrillation was obtained. In 16 cases, no modification in atrial flutter circuit was obtained by TEAP (Group 2). Using univariate analysis, this group of patients showed no significant difference in flutter cycle length, a smaller A/V ratio at the site of TEAP, a longer transverse diameter of left atrium and a shorter transverse diameter of right atrium. Analysis of the therapy at cardioversion shows that no Group 2 patients was on intravenous amiodarone, while a greater percentage of patients of the former group was on chronic amiodarone treatment. A logistic regression model applied to the data showed that flutter cycle length, transverse diameter of left atrium and A/V deflection ratio at the site of TEAP were independent variables with influence on the failure rate. CONCLUSION: Transoesophageal pacing is able to modify the circuit of common atrial flutter in a large percentage of patients, and can convert this arrhythmia to sinus rhythm in more than 50% of cases. Failure of this procedure is associated with electrophysiological parameters (flutter cycle length, A/V ratio at the site of TEAP), anatomical factors (left and right atrial diameters) and treatment in use at the time of TEAP.     

递进式消融法治疗持续性心房颤动的初步体会

目的评价一种递进式消融法治疗持续性心房颤动（房颤）的疗效。方法34例持续性房颤患者,年龄（54．8±11．4）岁,病程（36．5±9．8）个月。按以下顺序进行递进式消融：环肺静脉前庭消融达肺静脉电学隔离,左心房顶部和二尖瓣环峡部线性消融,心房碎裂电位消融,针对房颤转变的心房扑动（房扑）／房性心动过速（房速）行Carto激动标测结合拖带技术以明确其机制,并力求通过消融终止。结果递进式消融法使88．2％患者房颤节律发生变化（直接终止或转变为房扑／房速）,61．8％直接通过消融恢复窦性心律。随访（12．6±6．2）个月,82．4％患者维持窦性心律（其中42．9％服用胺碘酮）。结论递进式消融是治疗持续性房颤的一种有效方案。     

Novel electrophysiologic parameter of dispersion of atrial repolarization: comparison of different atrial pacing methods

INTRODUCTION: Heterogeneity of ventricular repolarization plays a major role in reentrant tachyarrhythmias in cardiac tissue. However, the role of atrial repolarization added activation time (AT) to refractoriness in atrial vulnerability has not been investigated in detail. METHODS AND RESULTS: The study population consisted of 34 patients: 18 with atrial fibrillation (AF) and 16 without AF (control group). The effective refractory periods (ERPs) in the right atrial appendage, low lateral right atrium, high right septum, and distal coronary sinus, and ATs from P wave onset to each electrogram during sinus rhythm and right atrial appendage, low lateral right atrial, high right septal, distal coronary sinus, and biatrial pacing were measured. Atrial recovery time, defined as the sum of AT and ERP, and its dispersions during sinus rhythm, right atrial appendage, low lateral right atrial, high right septal, distal coronary sinus, and biatrial pacing were calculated. Both ERP dispersion and atrial recovery time dispersion during sinus rhythm were significantly greater in the AF group than in the control group. Atrial recovery time dispersion during distal coronary sinus, high right septal, or biatrial pacing was significantly smaller than that during right atrial appendage or low lateral right atrial pacing in each group. In particular, atrial recovery time dispersion during distal coronary sinus pacing was the smallest of the five pacing methods in the AF group. P wave duration during biatrial or high right septal pacing was significantly shorter than during right atrial appendage, low lateral right atrial, or distal coronary sinus pacing in each group. CONCLUSION: Atrial recovery time dispersion is suitable as an electrophysiologic parameter of atrial vulnerability. Distal coronary sinus pacing may prevent AF by increasing homogeneity of atrial repolarization, whereas biatrial and high right septal pacing contribute not only homogeneity of atrial repolarization but also improvement of atrial depolarization.     

肺静脉在犬持续性心房颤动维持中的作用

目的探讨快速起搏肺静脉建立持续性心房颤动(简称房颤)犬模型的电生理特性以及射频消融隔离肺静脉对其影响。方法选杂种犬15只,以20Hz的固定频率行肺静脉持续起搏,建立持续时间>24h的房颤的动物模型。对该模型的左、右房游离壁,左上、下肺静脉,右上、下肺静脉进行心外膜标测,测量各标测部位的有效不应期(ERP)和平均房颤波周长(AFCL)。对肺静脉电隔离,观察电隔离前后房颤的诱发以及各部位ERP和AFCL的变化。结果11只犬完成实验,在28.2±3.0d内诱发出持续超过24h的房颤。肺静脉电隔离前,ERP和AFCL分布呈明显的梯度分布,自短至长依次为:肺静脉,左、右房游离壁;肺静脉隔离后,8只犬转变为窦性心律,3只犬先转变为房性心律失常后,在60min内转变为窦性心律,再进行快速心房起搏刺激仅能诱发出小于60s的阵发性房颤,各部位ERP和AFCL也明显延长(P<0.05)。结论肺静脉的快速电活动可能在持续性房颤的维持中起关键作用。     

Stepwise linear approach to catheter ablation of atrial fibrillation

BACKGROUND: This study attempted to convert atrial fibrillation (AF) to sinus rhythm using a stepwise linear catheter ablation approach. METHODS: One hundred and ninety-six patients (43 with persistent AF) were enrolled in the study. A multiple electrode array was used for anatomical navigation and activation mapping. Continuously incremental stimulation was used to induce AF if spontaneous AF was not present. Stepwise linear ablation was applied until AF was converted to sinus rhythm or atypical atrial flutter (AAFL) or atrial tachycardia (AT). The stepwise approach initially utilized a figure-7 lesion line between the right and left superior pulmonary vein on the roof of the left atrium and then extended along the ridge between the left appendage and the left pulmonary veins until the mitral valve annulus, as the primary lesions. If AF still persisted, high-frequency potentials in the inferior left atrium, coronary sinus, or right atrium were targeted. Noninducibility of AF was used as the end point. RESULTS: AF was converted to sinus rhythm in 81.6% of patients (90.8% of paroxysmal and 51.1% of persistent AF, P<.01). The remainders of patients were converted to AAFL or AT. AF was terminated after ablation in right atrium in 7 patients. During an 18.2+/-7.3 month follow-up, 88.3% of patients were free of atrial tachyarrhythmias without medication, 9.7% of patients had refractory AAFL/AT, and only 2.1% of patients had paroxysmal AF. CONCLUSION: Stepwise linear ablation is effective in converting AF to sinus rhythm and the figure-7 lesion line should be the basic lesion. Right atrium ablation is necessary in some patients.     

单纯碎裂电位指导心房颤动消融的初步临床观察

目的探讨碎裂电位指导心房颤动（房颤）射频导管消融的可行性。方法22例药物治疗无效有症状的房颤患者（阵发性16例,持续性6例）,在自发或诱发房颤时,用Carto构建左心房或左、右心房的三维模型并标测、消融碎裂电位,终点是消除标测到所有碎裂电位或转复窦性心律。结果碎裂电位消融后,13例（59％）转复为窦性心律（直接转复7例,先转为房性心动过速（房速）／心房扑动（房扑）然后转复6例）,9例消融未转复窦性心律患者行电复律或药物复律成功。6例复发（5例房速／房扑,1例阵发性房颤）再次消融,5例成功,随访3—18（10．9±4．8）个月,共有16例（73％）无快速房性心律失常事件,碎裂电位主要分布于左侧房间隔、肺静脉周围、左心房顶部。碎裂电位消融后房颤终止前房颤周期与碎裂电位消融前相比明显延长[（157±18）ms vs （211±32）ms,P〈0．05]。除一例发生心脏压塞且心包穿刺成功引流外,无消融术相关的并发症和后遗症。结论碎裂电位指导房颤导管射频消融安全有效可行。     

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.     

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.     

Failure of rapid atrial pacing in the conversion of atrial flutter

Rapid atrial pacing, at rates of 150 to 600/min with stimulus strength up to 15 ma, was attempted in 15 patients with atrial flutter. In 13 of the patients, atrial capture was achieved with changes in both atrial and ventricular rates. In 7 of these, flutter resumed upon cessation of pacing. In the other 6, rapid atrial pacing produced atrial fibrillation which persisted until cardioversion. In 2 patients, atrial capture could not be obtained because of increased atrial refractoriness secondary to flutter. Thus, rapid atrial pacing was ineffective in converting atrial flutter to normal sinus rhythm in all 15 patients. This was in contrast to direct-current cardioversion which was successful in 12 of the patients, in all of whom stable sinus rhythm developed. The 3 patients who did not undergo cardioversion subsequently experienced spontaneous conversion to sinus rhythm. These results suggest that rapid atrial pacing has little place in the management of atrial flutter.     

Atrial pacing for conversion of atrial flutter

Fifty-seven episodes of atrial flutter in 46 consecutive medically treated patients (aged 60 +/- 17 years) were treated by rapid atrial pacing. Thirty-three patients (72%) had structural heart disease. Most pacing trials were conducted in patients receiving digoxin (88%) and antiarrhythmic drugs (77%). In 51 of 57 trials (89%), patients were successfully converted to normal sinus rhythm. Multivariate analysis revealed that patients who had congestive heart failure and who were older were more likely to be refractory to pacing. Left atrial size did not influence outcome. Confirmation of local atrial capture with a bipolar atrial electrogram and use of multiple atrial pacing sites enhanced the success rate. Eight patients (17%) demonstrated sinus node suppression after atrial pacing; sinus node disease was previously unsuspected in 4 of these patients. These bradyarrhythmias were easily managed because a pacing catheter was already in place. The only significant complication was femoral vein thrombosis in 1 patient. It is concluded that atrial pacing is an effective, safe and convenient method for the elective conversion of atrial flutter in the general population of medically treated patients. This technique is an attractive alternative to transthoracic cardioversion, and may be preferable in many patients.     

Linear lesions provide protection from atrial fibrillation induction with rapid atrial pacing

INTRODUCTION: In the animal model, segmentation of the atria with radiofrequency-generated linear lesions (LL) using the loop catheter has been shown to be highly effective in terminating chronic atrial fibrillation (AF). This study addresses the question whether the same lesion set also would prevent reinduction and sustainability of AF. METHODS AND RESULTS: We studied two groups of dogs. The AF group included eight dogs in which the atria were paced until chronic AF was present. After 6 months of sustained AF, the dogs were converted to normal sinus rhythm (NSR) by the creation of LL in both atria. Rapid atrial pacing was restarted 6 months later and continued for 4 weeks. In the NSR group, there were nine dogs in NSR without inducible AF at baseline. LL were created, and after 6 months rapid atrial pacing was applied for 4 weeks. Rhythm status was monitored weekly. Transthoracic echocardiography was performed at baseline, before linear lesion placement, and before pacing/repacing. At the conclusion of the study, the hearts were excised and examined. The lesions were stained, and their quality was assessed. AF was induced in a much shorter interval in the dogs in which AF had previously been present than in NSR dogs (8 +/- 5 days vs 25 +/- 13 days; P < 0.05). LL prevented sustainability of AF induced via rapid pacing once the pacing stimulus was stopped. Incomplete lesions were associated with increased inducibility of atrial tachycardia and AF. CONCLUSION: In this animal model of AF, LL are not only capable of terminating chronic AF, but also lead to self-termination of AF once the rapid pacing is stopped. Self-termination of AF after induction with rapid pacing was not observed in this AF model in the absence of LL. In the dogs with 6 months of AF, the presence of AF led to increased atrial susceptibility to AF induction by rapid pacing, even with LL and after 6 months of recovery. Incomplete LL allows induction of atrial tachycardia and AF.     

Ablation of atrial fibrillation in the rapid pacing canine model using a multi-electrode loop catheter

OBJECTIVES: This investigation details our experience using a loop catheter to ablate atrial fibrillation (AF) in dogs. BACKGROUND: Atrial fibrillation is the most common arrhythmia and has significant morbidity. Maintenance of normal sinus rhythm (NSR) after conversion in many patients is still a challenge. METHODS: A multi-electrode loop catheter was used to create linear atrial lesions to ablate AF in a rapid atrial pacing model in 29 dogs. Rhythm status was assessed over a six-month recovery period, after which tissue analysis was performed. RESULTS: Acute conversion to NSR or atrial tachycardia (AT) was achieved in 90% of cases. Six of 26 conversions occurred after only left atrial (LA) lesions, and two after just right atrial lesions. Sixteen (62%) of 26 lesions that resulted in AF conversion were in the LA, and 11 of these 16 conversions occurred during a lesion connecting the mitral ring to the pulmonary veins. Acute conversion rate was similar with ring and coil electrodes, but AT was more frequent with coil electrodes (63% vs. 31%). At six months 80% of dogs were in NSR, 14% were in AT, and 7% remained in AF. There was an average reduction in P-wave amplitude of 64 +/- 26% after power application. Tissue analysis revealed transmural contiguous lesions when final outcome was NSR, and nontransmural/noncontiguous lesions where AF persisted. CONCLUSIONS: Multi-electrode loop catheters can create contiguous transmural lesions in either atrium to safely and effectively ablate AF and provide a stable long-term rhythm outcome in this dog model. The left atrium appears to be the dominant chamber that sustains AF. Atrial tachycardia is a frequent acute outcome with coil electrodes.     

Effect of Bachmann's bundle pacing on atrial fibrillation: electrophysiologic assessment

BACKGROUND: It has recently been reported that simultaneous multisite atrial pacing, Bachmann's bundle (BB) pacing, and coronary sinus (CS) pacing are useful for preventing the induction of atrial fibrillation (AF). HYPOTHESIS: We investigated whether a simple pacing approach via BB could reduce the induction of AF by extrastimuli (S2) from the right atrial appendage (RAA). METHODS: Programmed electrical stimulation was performed from the RAA and the area of BB at the superior aspect of the atrial septum, and bipolar recordings were obtained from the RAA, BB, and CS in 14 patients. RESULTS: In five patients, AF was induced with critically timed RAA-S2 delivered during RAA pacing. However, AF was not induced in any patient when RAA-S2 was delivered during BB pacing. The duration of the P wave during BB pacing was significantly shorter than that during RAA pacing and sinus rhythm (BB 80 +/- 16 ms vs. RAA 106 +/- 36 ms vs. sinus rhythm 100 +/- 24 ms, p < 0.05). The intra-atrial conduction time to the distal coronary sinus (CSd) caused by early S2 at the RAA was significantly reduced by BB pacing (BB 114 +/- 22 ms vs. RAA 157 +/- 35 ms, p < 0.001). CONCLUSION: Bachmann's bundle pacing reduces atrial conduction time caused by RAA-S2 and may be useful for preventing the induction of AF.     

Intravenous flecainide versus verapamil for acute conversion of paroxysmal atrial fibrillation or flutter to sinus rhythm

In a single-blind randomized study, the efficacy of intravenous flecainide (2 mg/kg/10 minutes) versus verapamil (10 mg/1 minute) was assessed in 40 patients with paroxysmal atrial fibrillation (AF) or atrial flutter (AFI). The treatment was considered successful if sinus rhythm occurred within 1 hour. Of 20 patients receiving flecainide, 14 of 17 (82%) with AF converted to sinus rhythm, but in 3 patients with AFI flecainide failed. All patients treated with verapamil (17 AF, 3 AFI) showed lower ventricular rates after 1 hour; however, only 1 (6%) with AF converted to sinus rhythm and 1 (6%) converted to AFI. Patients who did not convert to sinus rhythm after treatment with verapamil were treated with flecainide and observed for another hour. After the change to flecainide, 9 of 15 patients (60%) with AF still converted. Thus, 23 of 32 patients (72%) with AF and none of 7 with AFI converted to sinus rhythm after treatment with flecainide. Conversion to sinus rhythm was achieved in 19 of 22 patients (86%) when AF lasted less than 24 hours and in 4 of 10 (40%) when the arrhythmia lasted greater than 24 hours. Transient adverse effects were noted in 10 patients (26%) after flecainide. In summary, flecainide is an effective and safe drug for conversion of paroxysmal AF to sinus rhythm, but ineffective for AFI. Verapamil appears to be of no use for conversion of AF or AFI to sinus rhythm.     

递进式个体化心房基质消融治疗心房颤动

目的 以肺静脉电学隔离为终点的心房颤动（房颤）消融术式的疗效难以令人满意。本研究旨在探索规范化的递进式个体化心房基质改良消融术治疗房颤的方法。方法 124例患者（男性96例,女性28例）,年龄27-76（53．6±8．7）岁。其中92例为阵发性房颤,32例为持续性／永久性房颤。若无自发房颤则在心房进行持续递增的快速刺激（频率200—600次／min）诱发房颤。均在非接触式标测观察房颤时心房激动情况,将最常激动部位做为房颤基质进行改良消融,并根据消融后重复等电位标测的结果作出递进式调整,直至房颤被终止不再被诱发。结果 在既不隔离肺静脉也不寻求碎裂电位的情况下,87．1％（108／124）的房颤消融转复为窦性心律,其余被转为非典型心房扑动（房扑）或房性心动过速（房速）。可将消融灶分为3种类型,其中以7字形的A型线性消融最关键,71．6％的阵发性房颤可被A型消融终止且不再被诱发,而68．8％的持续性／永久性房颤则需通过B型消融终止。随访（21．6±5．3）个月,90．3％（112／124）的患者不服药亦无房颤发生。其余9．7％（12／124）的患者有顽固性非典型房扑／房速,其中仅1．6％（2／124）的患者伴有阵发性房颤。结论 递进式的心房基质消融术可以将房颤有效地转复为窦性心律,并有满意的远期疗效。此种术式简单易行有望在NavX和Carto标测下复制。     

Electrical remodeling in fibrillating canine atrium: action potential alternans during rapid atrial pacing and late phase 3 early afterdepolarization after cessation of rapid atrial pacing

Sustained atrial fibrillation (AF) was induced by atrial burst pacing, and monophasic action potentials (MAPs) were recorded. MAP alternans was observed at a cycle length (CL) of 167.5 ± 28.2 msec before burst pacing and 201.3 ± 40.2 msec after burst pacing. AF > 5 minutes duration was induced in 1 dog in the control condition but in all 8 dogs after burst pacing. The difference in RA MAPD(80) of the first spontaneous beat and steady-state sinus rhythm was significantly larger after atrial burst pacing than before atrial burst pacing (31.5 ± 15.9 msec versus 8.2 ± 9.0 msec) In 4 dogs, late phase 3 early after depolarization was observed after rapid atrial pacing. Rapid atrial pacing-induced electrical remodeling includes APD alternans during rapid atrial pacing and also causes an increase in the MAPD of the initial several beats and the development of late phase 3 early afterdepolarizations after a sudden increase in CL.