射频消融心房扑动拖带刺激的电生理特征

探讨射频消融心房扑动 (简称房扑 )拖带刺激的电生理特征 ,更好的理解房扑机制 ,以期提高消融成功率、减少复发率。 5例阵发性典型房扑患者 ,诱发房扑后 ,在高位、低位右房 ,冠状窦口 (CSO)及右房下部的峡部分别进行拖带刺激 ,分析心房激动顺序 ,然后进行三尖瓣环至下腔静脉之间的线性消融。 5例房扑折返环均为逆钟向旋转 ,峡部 ,高位、低位右房及CSO呈现隐匿拖带 ,左房和卵圆窝呈现显性拖带 ,平均放电 9± 6次 ,均达到右房峡部双向阻滞。CSO起搏时体表心电图Ⅱ、Ⅲ、aVF导联P波形态发生改变。结论 :隐匿、显性拖带对判断峡部依赖性逆钟向房扑有较高价值 ,CSO起搏时心内电图激动顺序和体表心电图P波改变可做为判断峡部消融达到双向阻滞的标志     

非接触球囊导管标测系统指导心房扑动消融的初步经验

目的　评价非接触球囊导管标测系统在心房扑动 (房扑 )标测和射频消融中的临床应用。方法　 7例房扑患者 ,年龄 (6 0± 10 )岁 ,男 4例 ,女 3例。其中 1例为房间隔缺损修补术后 ,2例为采用常规方法消融典型房扑后复发患者。应用非接触球囊导管标测系统构建右房三维几何模型 ,标测心动过速的折返激动顺序和关键峡部 ,并利用其导航系统指导峡部的线性消融。消融后分别于峡部两侧起搏判断峡部阻滞情况。结果　 6例患者诱发出房扑 ,心动过速周长 (2 16± 2 2 )ms。6例房扑均为峡部依赖型 ,2例呈逆钟向传导 ,4例呈顺钟向传导 ;4例房扑呈双环折返激动 ;7例消融均成功 ,房扑不再诱发 ,峡部呈完全双向传导阻滞 ;手术时间 (30 0± 12 9)min ,X线曝光时间 (2 5 0± 6 5 )min ,放电次数 (2 5 7± 12 1)次。无手术并发症。随访 3～ 14个月无复发病例。结论　在房扑标测和消融中应用非接触球囊导管标测系统是安全有效的 ,不仅能确定折返环路 (特别是双环折返激动 )的顺序和关键峡部 ,而且能准确判断线性损伤的连续性 ,同时可减少X线曝光时间。     

射频消融治疗典型心房扑动不同消融终点的评价

评价导管射频消融治疗峡部依赖性心房扑动 (AFL)中 ,心房激动顺序的变化与双电位标测这两种消融终点的判断方法 ,以期提高成功率 ,减少复发率。选取 1997年 11月至 2 0 0 2年 9月连续收治的 4 3例典型AFL病人。按照消融终点不同 ,以及收治时间顺序分为心房特征性激动顺序变化组 (AC组 ) ,双电位组 (DP组 )。于右房三尖瓣环与下腔静脉之间的峡部进行线性消融。AC组以出现右房特征性激动顺序的变化 (即低侧位右房刺激时呈逆钟向阻滞 ,冠状静脉窦刺激时呈顺钟向阻滞 )为依据判定为峡部双向阻滞。DP组在AC组消融结果基础上 ,以消融线上标测到宽间期双电位 (>10 0ms)为依据判定为峡部双向阻滞。随访复发率。结果 :4 3例患者 ,所有患者均达到相应的射频消融终点。DP组所有患者消融成功后双电位为 116 .6± 12 .5ms。随访 14 .5± 5 .4个月 ,AC组的复发率高于DP组 (2 3.5 %vs 0 ,P <0 .0 5 )。结论 :作为峡部双向阻滞的指征 ,宽间期双电位比心房特征性激动顺序变化更准确 ,手术成功率更高。     

欧氏瓣对老年人Ⅰ型心房扑动射频消融的影响

目的探讨欧氏瓣对Ⅰ型心房扑动(简称房扑)导管射频消融即刻效果的影响。方法28例老年Ⅰ型房扑患者(呈逆钟向折返18例,顺钟向折返10例)在透视解剖标志和Halo电极三尖瓣环标测电图指引下,在房扑发作或冠状窦口起搏时以温控方式消融位于三尖瓣口和下腔静脉口之间的后峡部,消融方向从三尖瓣叶右室侧到下腔静脉开口。预设温度70℃,每点消融30s,每次移动消融电极3～5mm。观察下列指标:①房扑终止和后峡部阻滞时消融电极在消融线上所处的位置;②房扑终止后峡部残存传导间隙在消融线上所处的位置;③房扑终止后继续消融致后峡部完全阻滞的最终消融部位。结果根据右前斜位30°透视影像测得后峡部平均弧长(即消融线)为38.6±9.7mm。28例全部达到后峡部完全阻滞的消融终点,无并发症。与欧氏瓣有关的房扑终止率为100%(17/17),与欧氏瓣有关的后峡部完全阻滞发生率为92.9%(26/28)。结论欧氏瓣是Ⅰ型房扑后峡部消融线终点的重要标志,线性消融时欧氏瓣心室侧易残存传导间隙,消融该部位的残存传导间隙是Ⅰ型房扑后峡部消融的重要环节。     

温控自动监测和阻抗上限监测消融老年人Ⅰ型心房扑动效果比较

目的　比较采用温控和阻抗监测消融法电隔离右心房后峡部治疗老年人Ⅰ型房扑的效率和优缺点。方法　在透视解剖标志的指引下 ,在Halo电极三尖瓣环标测电图监测下 ,在房扑发作或冠状窦口起搏时 ,随机选择温控监测和阻抗监测射频消融法电隔离位于三尖瓣口和下腔静脉口之间的后峡部 ,消融方向从右心室到下腔静脉。采用温控监测消融时 ,预设温度 70℃ ;采用阻抗监测消融时 ,能量选择 2 0W ,预设阻抗 15 0 。消融方法都是每点放电 30s,每次移动消融电极 5mm。消融终点是后峡部完全阻滞。比较下列指标 :(1)放电次数 ;(2 )放电时间 ;(3)消融操作时间 ;(4 )消融能量 ;(5 )高阻抗报警次数 ;(6 )病人胸痛反应。结果　 37例老年Ⅰ型房扑病人平均年龄 (6 9.2± 3.7)岁 ,男 /女为 2 6 / 11,合并高血压病 13例 ,糖尿病 5例 ,冠心病 3例 ,卵圆孔未闭 1例。房扑心室率(12 8.4± 2 7.5 )次 /min ,呈逆钟向折返 2 5例 ,顺钟向折返 12例。温控监测消融 19例 ,非温控监测消融 18例 ,两组病人在性别、年龄、基础心脏病、房扑心室率和折返方式方面无显著差异 (P >0 .0 5 )。 37例病人全部达到后峡部完全阻滞的消融终点 ,无并发症。温控监测和阻抗监测消融观察指标比较 :(1)放电次数为 6 .4± 3.5比 11.3± 5 .8(P <0 .0 5 )。     

非接触标测对于典型心房扑动的标测、消融和电生理机制的新认识

目的介绍非接触标测对于典型心房扑动(简称房扑,AFL)的标测、消融和电生理机制的新认识.方法 9例典型AFL,男性7例,女性2例.使用非接触标测对窦律时峡部的双向传导、AFL时的折返激动序列进行详细标测,在导航系统指导下完成后位峡部线性消融,然后验证峡部双向传导阻滞.结果 (1)1例为顺钟向AFL,7均为逆钟向AFL,1例未能诱发AFL,所有AFL平均心房心动周期(215±36)ms;(2)非接触标测三维显示AFL在右房内的整个折返环及其与解剖结构的三维关系;(3)激动可以穿过界嵴上部并且传导相对缓慢,提示右心房平滑部是折返环的一部分;(4)非接触标测可直观显示复发病例的消融线缺口,并直接导航消融;(5)1例术中出现心房颤动,1例因不能耐受消融所致胸痛放弃手术,其余7例即刻均达到峡部双向阻滞,随访12～36月未见复发.结论非接触标测系统可直观再现典型AFL的完整折返环及其与右房解剖结构的关系,确认折返机制,对复发病例可发现消融线裂隙并导航消融.同时发现激动可横向穿过界嵴并且速度缓慢.     

低右房电图极性改变评价典型心房扑动射频消融结果

目的　在典型心房扑动 (房扑 )射频消融中观察临近峡部的低位右房心内电图极性改变 ,来迅速判断是否形成峡部双向阻滞。方法　对 10例典型房扑患者 ,沿三尖瓣环放置Halo电极 ,Halo远端紧邻峡部消融线 ,房扑发作中消融在房扑终止后行冠状窦起搏 ,窦性心律下消融则同时行冠状窦电极起搏 ,观察紧邻消融线低右房侧的心房电极电图起始部分的主波方向 (H电位 )的极性表现 ,并与最终双向阻滞评价结果比较。结果　 8例在窦性心律下行冠状窦电极起搏时消融 ,2例在房扑发作中消融。 10例患者最终消融结果均为双向阻滞。 2例房扑发作时H电位极性均为负向 ,8例窦性心律下H电位极性均为正向 ,峡部缓慢传导时该极性仍为正向 ,形成双向阻滞后H电位极性变为负向。结论　典型心房扑动行峡部线性消融时 ,行冠状窦起搏观察到紧邻峡部消融线低右房侧H电位的极性改变可能是峡部消融成功的新指标。该指标简单、快速、可靠性高。     

典型心房扑动消融术后峡部计时间期的变化预测双向阻滞的价值

典型的心房扑动(房扑)是右心房内的大折返所致已成共识，下腔静脉、三尖瓣环峡部是折返环的一部分。因此，射频消融下腔静脉、三尖瓣环峡部并产生峡部双向阻滞，是成功消融典型房扑和减少复发的可靠标志。目前，多采用心房激动顺序或消融部位的双电位技术确定峡部双向阻滞的存在。通过比较房扑成功消融前、后右心房峡部传导时间，从而提出峡部传导时间的延长程度对峡部完全性     

非接触标测系统用于典型心房扑动的右房标测和导航消融

应用非接触标测系统实施典型心房扑动 (AFL)的右房 (RA)全心腔标测和导航射频消融。 6例典型AFL ,男 5例、女 1例 ,年龄 5 6 .2± 15 .3(35～ 76 )岁。常规放置冠状静脉窦和His束电极 ,将标测球囊置于RA中下部 ,构建RA心内膜模型 ,分别于低位RA和冠状窦口 (CSO)S1S16 0 0ms起搏观察峡部传导 ,诱发并标测AFL的激动顺序和折返路径。 1例为顺钟向AFL ,4例为逆钟向AFL ,1例未能诱发AFL。AFL周期 2 0 7± 34ms,非接触标测可显示整个折返环路、激动顺序和缓慢传导区。AFL的激动可以穿过界嵴上部并且传导相对缓慢 ,提示RA平滑部是折返环的一部分。后位峡部线性消融在导航系统指导下进行 ,无需X线透视。消融完成后重复上述起搏验证峡部双向传导阻滞。除 1例术中出现心房颤动 (AF)外 ,其余病例即刻均达到峡部双向阻滞 ,未出现其他并发症 ,随访 8.1± 6 .7(3～15 )个月未见复发。非接触标测系统可安全、有效和直观地实现典型AFL的右房全心腔标测并导航消融 ,验证峡部双向阻滞 ,减少X线曝光时间和无效放电次数。界嵴在典型AFL时具备传导功能 ,RA平滑部和粗糙部共同参与折返环的组成。     

对典型心房扑动折返环的再认识

典型心房扑动(简称房扑)心房率一般为300次/分,当典型房扑心房率减慢时可使房扑1∶1下传激动心室,导致较快的心室率,可达230～270次/分;心内电生理检查表明典型房扑患者行射频消融术前在窦性心律时以冠状窦口S1起搏时房室结前传文氏点多≤190次/分,2∶1阻滞点多≤230次/分。三尖瓣环和下腔静脉之间的峡部为典型房扑折返环的关键部位,同时峡部也是致密房室结右侧后延伸的分布区域,结合典型房扑房室传导比例和心室率的心电学特点推断至少在部分患者致密房室结及其右侧后延伸可能参与了典型房扑折返环的构成。     

导管射频消融Ⅰ型心房扑动的方法学评价

比较在心房扑动 (AFL)时、冠状静脉窦口 (CSO)或低外侧右房 (LRA)起搏下和窦性心律 (简称窦律 )下消融Ⅰ型AFL的优缺点。 48例阵发性AFL随机分为AFL消融组、起搏消融组和窦律消融组 ,对下腔静脉口和三尖瓣环之间的后峡部作线性消融 ,终点为后峡部双向传导阻滞。比较三组患者的电生理参数、急性成功率和远期效果。结果 :三组均达到后峡部双向阻滞 ,随访 2 1.8± 5 .6个月无AFL复发。AFL消融组在AFL终止后均不能达到后峡部双向阻滞 ,需继续在起搏下消融。起搏消融组的操作和曝光时间、放电能量和次数小于其他两组 (P <0 .0 5 )。三组在后峡部双向阻滞后记录局部心房双电位的阳性率为 37.5 %。结论 :①对Ⅰ型AFL采用窦律消融法、起搏消融法和AFL消融法都能取得满意的近远期疗效。②后峡部双向传导阻滞是保证近远期疗效的重要消融终点。③在消融部位标测到双电位可作为消融有效的指标 ,但不能代替后峡部双向阻滞作为消融终点。④起搏消融法的操作和曝光时间、放电能量和次数明显少于在AFL和窦律下消融 ,可作为常规方法使用     

典型心房扑动对心房颤动导管消融复发的影响

目的 评价典型心房扑动(房扑)对心房颤动(房颤)导管消融复发的影响.方法 120例药物治疗无效的阵发性房颤患者在三维电解剖标测系统和肺静脉环状标测电极导管联合指导下行环肺静脉电隔离.其中17例(14.2%)合并典型房扑(房扑组,其余作为对照组),行三尖瓣环峡部消融,三尖瓣环峡部消融终点为三尖瓣环峡部双向阻滞.房颤复发定义为导管消融3个月后发生房性快速心律失常.结果 房扑组房颤病程(9.8±10.7)年,长于对照组(5.9±6.3)年,差异有统计学意义(P=0.036).房扑组与对照组相比,年龄、性别、合并器质性心脏病、左心房直径、左心室射血分数差异无统计学意义.随访91～401(237±79)d,房扑组房颤复发率为47.1%,对照组房颤复发率为12.6%,两组间差异有统计学意义(P=0.001).经校正年龄、房颤病程、合并器质性心脏病、左心房直径等因素,Cox多因素分析发现消融术前合并房扑是房颤复发的独立危险因素(危险比3.52,95%可信区间1.32～9.34,P=0.012).结论 典型房扑可能增加房颤导管消融术后房颤的复发,房颤导管消融前应对患者是否合并典型房扑进行认真评价.     

Clinical significance of inducible atrial flutter during pulmonary vein isolation in patients with atrial fibrillation

OBJECTIVES: This study was designed to determine the prevalence and clinical significance of atrial flutter (AFL) that occurs during catheter ablation for atrial fibrillation (AF). BACKGROUND: Atrial flutter frequently occurs in patients with AF. METHODS: Pulmonary vein isolation was performed in 133 consecutive patients (age 52 +/- 11 years) for paroxysmal (n = 112) or persistent (n = 21) AF. A clinical episode of AFL was documented in 40 of the 133 patients (30%). During the ablation procedure, AFL occurred in 86 patients (65%), either spontaneously (n = 36) or by rapid atrial pacing (n = 50), with AFL being typical in the majority (80%). Cavo-tricuspid isthmus ablation was performed in 28 of the 133 patients. RESULTS: Among the 105 patients who did not undergo isthmus ablation, 25 patients (24%) were documented to have symptomatic AFL during a mean follow-up of 609 +/- 252 days. Among the clinical variables of age, gender, history of clinical AFL, ejection fraction, left atrial diameter, duration of AF, and occurrence of AFL during ablation, only a history of clinical AFL (p = 0.05) and occurrence of typical AFL during the ablation (p = 0.01) were independent predictors of symptomatic AFL during follow-up. The incidence of symptomatic AFL during follow-up was similar among patients who did and did not have long-term freedom from recurrent AF. CONCLUSIONS: In patients with AF who have either a history of AFL or an episode of typical AFL during an electrophysiologic study, symptomatic AFL is common after pulmonary vein isolation. Therefore, cavo-tricuspid isthmus ablation is appropriate during pulmonary vein isolation if AFL has been observed clinically or in the electrophysiology laboratory.     

不纯心房扑动发生机制的心内电生理探讨

目的：心内电生理检查研究体表心电图不纯心房扑动的可能发生机制。方法6例患者经体表心电图证实有不纯心房扑动,射频消融时进行了心内电生理检查,并进行峡部阻断法消融心房扑动。结果：体表心电图与心心内电图同步记录证实,6例不纯心房扑动发作时均为右心房扑动、左心房颤动的心房脱节,心房扑动射频消融均获成功。随访期中2例复发,再次消融成功。结论：不纯心房扑动的发生可能是在右心房扑动的同时,左心房发生一过性颤动的结果。     

Mechanism of propensity to atrial fibrillation in patients undergoing isthmus ablation for typical atrial flutter

Mechanism of propensity to atrial fibrillation. BACKGROUND: Patients undergoing isthmus ablation for atrial flutter (AFL) may reveal postablation atrial fibrillation (AF). The electrophysiological mechanism is unclear. In patients with idiopathic AF, enhanced spatial dispersion of right atrial refractoriness was the substrate for the initiation of AF. We hypothesize that dispersion of right atrial refractoriness in patients undergoing AFL ablation is the major cause of postablation AF. METHODS: Consecutive patients (n=42) undergoing isthmus ablation for typical AFL were included. Twelve right atrial unipolar electrograms were recorded. Inducibility of AF was assessed by a pacing protocol, starting with one extrastimulus, followed by more aggressive pacing until AF was induced. Mean fibrillatory intervals were used to assess local refractoriness of each recording site. Spatial dispersion of right atrial refractoriness was calculated as the coefficient of dispersion (CD-value: standard deviation of the mean of all local mean fibrillatory intervals as a percentage of the overall mean fibrillatory interval). A CD-value of 3.0 or less was defined as normal, whereas CD-value greater than 3.0 was considered enhanced dispersion. PES and refractoriness analysis were followed by isthmus ablation. RESULTS: Of the 42 patients, 29 had CD-value of 3.0 or less. In these 29 patients, AF was induced with 1 extrastimulus in only 1 patient, with 2 extrastimuli in 4 patients and burst pacing was required to induce AF in 24 of these 29 patients. Prior to the procedure, 5 of 29 patients had AF episodes, after ablation 6 of 29 patients. Of the 42 patients, 13 had CD-value greater than 3.0, AF was induced with a single extrastimulus in 11 patients, with 2 extrastimuli in the remaining 2 patients. Of the 13 patients, 11 had AF episodes both before and after ablation (P<0.001). CONCLUSION: Enhanced spatial dispersion of right atrial refractoriness may be the substrate for propensity to AF in patients with AFL. The substrate was associated with enhanced inducibility of atrial fibrillation.     

Effects of cavotricuspid isthmus catheter ablation on paroxysmal atrial fibrillation

It has been demonstrated that successful cavotricuspid isthmus ablation of typical atrial flutter combined with atrial fibrillation (AF) sometimes influences the preablation history of paroxysmal AF. However, the effectiveness of only isthmus ablation on AF itself is unclear. Endocardial catheter mapping during induced AF was performed around the tricuspid annulus using duodecapolar clectrode catheters in 39 patients with drug-refractory paroxysmal AF. Isthmus ablation was performed in 16 patients (41%) in whom catheter mapping during AF showed an organized activation pattern around the tricuspid annulus. During a mean follow-up of 12.3 months, isthmus ablation was successful in preventing AF in 12 (75%) patients, 8 without medication and 4 with a previously ineffective drug. This success group had a significantly higher F wave amplitude in lead V1 (0.29+/-0.10 vs 0. 15+/-0.04 mV, p < 0.01), a higher left ventricular ejection fraction (74+/-9 vs 58+/-2%, p < 0.05), and a smaller left atrial dimension (35+/-6 vs 43+/-4 mm, p < 0.05) than the failure group. Isthmus ablation may be effective in preventing paroxysmal AF with an organized activation pattern around the tricuspid annulus. F wave amplitude, left ventricular ejection fraction, and left atrial dimension were significant predictors of success.     

Use of double-potential barrier to identify functional isthmus at the cavotricuspid isthmus for facilitating catheter ablation of isthmus-dependent atrial flutter

INTRODUCTION: The aim of the study was to identify an alternative target for more effective radiofrequency catheter ablation (RFCA) of isthmus-dependent atrial flutter (AFL). METHODS AND RESULTS: We hypothesized that a functional isthmus formed by preexisting double potential barrier at the cavotricuspid isthmus (CTI) could serve as a new target site for facilitating RFCA of AFL. Forty-three consecutive patients with recurrent isthmus-dependent AFL were studied using three-dimensional navigated magnetic mapping and ablation technique. Twenty patients (47%, group A) were shown to have a narrower functional channel at the CTI (functional isthmus). The remaining 23 patients did not have this feature (53%, group B). In group A, double potentials were clustered near the border of the inferior vena cava (IVC) of the CTI and served as a functional channel along the tricuspid annulus (TA). The interspike interval of double potentials was 87 +/- 26 ms near the IVC border and 45 +/- 17 ms (P < 0.0001) near the TA border of CTI. RFCA targeting at the functional isthmus in group A resulted in interruption of bidirectional transisthmus conduction with fewer radiofrequency pulses (6.7 +/- 4.7 in group A vs 21.1 +/- 17.1 pulses in group B, P < 0.001), shorter ablation line (11.6 +/- 4.0 mm vs 37.8 +/- 7.2 mm, P < 0.0001) with no arrhythmia recurrence. These functional isthmuses were found to be located at the lateral third of CTI in 12 patients, middle third in 7, and medial third in 1. This finding is different from that obtained by the conventional method in group B (lateral in 5, middle in 16, medial in 2, P < 0.038). CONCLUSION: In our study, a functional, rather than anatomic, isthmus formed by preexisting double-potential barrier at the CTI was identified in 47% of patients with isthmus-dependent AFL. It is a useful guide to facilitate RFCA of isthmus-dependent AFL.     

Right atrial flutter due to lower loop reentry: mechanism and anatomic substrates

BACKGROUND: The mechanisms of an atrial flutter (AFL) that is more rapid and at times more irregular than typical AFL are unknown. METHODS AND RESULTS: Twenty-nine patients with AFL were studied. Atrial electrograms were recorded from a 20-pole catheter placed against the tricuspid annulus (TA), with its distal electrodes lateral to the isthmus between the TA and the eustachian ridge (ER), and from the His bundle and coronary sinus catheters. Atrial extrastimuli were delivered in the TA-ER isthmus during typical AFL. Episodes of a right atrial flutter rhythm that was different from typical AFL were induced in 3 patients and occurred spontaneously in 3 patients. This sustained AFL, designated as lower-loop reentry (LLR), involved the lower right atrium (RA), as manifested by early breakthrough in the lower RA, wave-front collision in the high lateral RA or septum, and conduction through the TA-ER isthmus. Linear ablation resulting in bidirectional conduction block in the TA-ER isthmus terminated spontaneous LLR in 3 patients and rendered LLR noninducible in all patients. The cycle length of LLR was shorter than that of typical AFL (217+/-32 versus 272+/-40 ms, P<0. 01). Alternating LLR and typical AFL in 1 patient resulted in cycle length oscillation. CONCLUSIONS: LLR is a subtype of right atrial flutter and depends on conduction through the TA-ER isthmus.     

Mechanism of conversion of atypical right atrial flutter to atrial fibrillation

The purpose of this study was to explore the mechanisms of conversion from atypical atrial flutter (AFL) to atrial fibrillation (AF), and the long-term results of cavotricuspid isthmus ablation in these patients. We retrospectively reviewed the records of 221 patients with typical AFL referred to our hospital for ablation. A total of 25 patients had atypical AFL, and cavotricuspid isthmus ablation was performed in 23 with isthmus-dependent atypical AFL, as well as in 180 patients with typical counterclockwise and/or clockwise AFL. In all, 13 spontaneous transitions from atypical AFL to AF were documented in 11 of 17 patients. Before AF, a pattern of lower loop reentry was observed in 11 of 13 patients (85%) and upper loop reentry in 3 (1 had both). Multiple early breaks along the tricuspid annulus during AFL were noted in 6 of 13 patients (46%). Among the 13 transitions, discrete atrial premature complexes before AF were found in 5 patients with lower loop reentry and in 1 with upper loop reentry (46%). In the remaining patients, a more rapid atrial rhythm was involved in the development of AF with a pulmonary venous focus in 2. In some cases, additional "breaks" in the functional line of block occurred before the development of AF. There was a significant increased incidence of AF (68%) in those with atypical AFL compared with those with typical AFL (38%) (p = 0.004). After a mean follow-up of 28 +/- 9 months for the atypical group and 18 +/- 11 months for the typical group, the AF recurrence rate was similar (57% vs 48%, p = 0.4). Discrete atrial premature complexes or atrial tachycardia may initiate AF either directly or by producing further breaks in lines of functional block. Bidirectional cavotricuspid isthmus block is associated with cure or control of AF in approximately 50% of patients with AFL.