阵发性心房颤动患者心房及肺静脉不应期离散度的变化

目的探讨阵发性房颤患者房颤相关组织的电生理特性改变情况。方法选取阵发性房颤患者10例(房颤组)和无房颤病史的左侧旁路有显性预激波患者15例(对照组)。将大头电极分别放置在两组患者左上肺静脉、左下肺静脉、右上肺静脉、右下肺静脉开口及左心房顶壁、前壁、后壁、高位右心房,分别测定各部位有效不应期(EPR)。结果①房颤组心房及肺静脉EPR离散度指数(DI)为0.117±0.028,对照组为0.074±0.029,两组比较,P<0.05。②房颤组左心房ERP为(234.00±28.72)ms,肺静脉ERP为(230.75±32.69)ms;对照组左心房ERP为(248.00±25.99)ms,肺静脉ERP为(244.33±26.78)ms,两组比较,P均<0.05。结论阵发性房颤患者DI明显增大,左心房、肺静脉ERP显著缩短。     

消融犬Marshall韧带对刺激心房左后脂肪垫所致心房颤动的影响及机制

目的探讨消融犬Marshall韧带对刺激心房左后脂肪垫所致心房颤动(简称房颤)的影响及机制。方法成年杂种犬14条,随机分为实验组8条,对照组6条。实验组首先测量左肺静脉和左心耳的有效不应期,继而刺激心房左后脂肪垫诱发房颤。消融Marshall韧带上段后和下段后重复上述步骤。对照组除不干预Marshall韧带外,其它电刺激方案与实验组相同,同时对该组犬的心脏进行迷走神经染色。结果①实验组消融Marshall韧带后,左肺静脉和左心耳的有效不应期均显著延长(P0.05)。②和消融前比较,实验组消融Marshall韧带上段后的房颤诱发率有下降趋势(70.8%vs87.5%,P0.05);消融Marshall韧带全程后房颤诱发率显著下降(33.3%,P0.001)。对照组三次电刺激所测得的不应期和房颤诱发率无差异。③Marshall韧带与左下肺静脉、心房左后脂肪垫、左心耳之间存在迷走神经的直接联系。结论消融犬Marshall韧带可显著降低刺激心房左后脂肪垫所致房颤的诱发率。     

Alterations in atrial electrophysiology associated with chronic atrial fibrillation in man.

BACKGROUND: The purpose of this study was to determine the changes in atrial electrophysiology associated with chronic persistent atrial fibrillation in man. METHODS AND RESULTS: Atrial monophasic action potential duration at 90% repolarization and the effective refractory period were measured in 13 patients with chronic persistent atrial fibrillation after low-energy endocardial cardioversion, and compared to eight controls without a history of atrial fibrillation. Measurements were made at the right atrial appendage and midlateral right atrial wall at basic, 600 ms and 400 ms drive cycle lengths. In control patients, the effective refractory periods were significantly longer at the atrial appendage than the lateral wall at 600 ms (right atrial appendage 265 ms, midlateral right atrial wall 228 ms, P<0.05), and 400 ms cycle lengths (right atrial appendage 270 ms, midlateral right atrial wall 218 ms, P<0.05), but this was not evident in patients with atrial fibrillation. The monophasic action potentials and effective refractory periods at both atrial sites were shorter in the atrial fibrillation patients compared to controls; however, only the effective refractory periods at atrial appendage at 600 ms (atrial fibrillation 210 ms, controls 265 ms, P<0.001), and 400 ms cycle lengths (atrial fibrillation 200 ms, controls 270 ms, P>0.001) reached statistical significance. Effective refractory period dispersion was significantly greater in controls than in patients with atrial fibrillation (cycle length 600 ms: controls 36, atrial fibrillation 13, P=0.01; cycle length 400 ms: controls 54, atrial fibrillation 18, P<0.01). CONCLUSIONS: In patients without a history of atrial fibrillation, the refractory period at the right atrial appendage is significantly longer than at the midlateral right atrial wall. This 'normal' pattern of atrial refractory dispersion is lost in patients with chronic persistent atrial fibrillation, with marked shortening of the effective refractory period at the right atrial appendage. This may explain the high risk of recurrence of atrial fibrillation following successful electrical cardioversion.     

Distribution of atrial electrogram types during atrial fibrillation: Effect of rapid atrial pacing and intercaval junction ablation

Objectives. This study examined the anatomic distribution types and possible determinant of atrial electrogram types during atrial fibrillation.

Background. Different types of atrial electrograms during atrial fibrillation have been observed and classified, but their anatomic distribution patterns, determinants and potential usefulness in guiding future catheter ablation are unknown.

Methods. Two animal models of atrial fibrillation were used: the sterile pericarditis model (n = 10) and the rapid atrial pacing model (400 beats/min for 6 weeks, N = 6). The atrial electrogram of atrial fibrillation and the atrial effective refractory period were obtained from multiple sites of the right and left atrium. In addition, decremental rapid atrial stimulation was applied to the site of shortest and longest atrial effective refractory periods until atrial fibrillation induction in a subgroup of nine dogs. Ablation of the intereaval junction was performed using the radiofrequency catheter technique in dogs with atrial fibrillation duration > 1 min.

Results. In both models, organized atrial electrograms (type I) were predominantly observed at the left atrial sites and the right atrial appendage, whereas disorganized atrial electrograms (type III) were mainly observed at the right posterolateral atrium. The distribution of the atrial electrogram types closely followed that of the atrial effective refractory period, with the shortest atrial effective refractory period corresponding to organized atrial electrograms (type I) and the longest atrial effective refractory period corresponding to disorganized atrial electrograms (type III). The correlation of atrial electrogram type with the atrial effective refractory period was further demonstrated by the effect of rapid atrial stimulation. When rapid atrial stimulation was applied to the site with the shortest atrial effective refractory period, disorganized atrial electrograms were observed at sites with the longest atrial effective refractory period, whereas 1:1 atrial capture was still present at the stimulation site. Ablation of the intercaval junction made atrial fibrillation noninducible or tended to shorten the atrial fibrillation duration (from 26.4 ± 24.2 to 8.8 ± 22.6 min in the pericarditis group, P = 0.02, and from 33.7 ± 29.2 to 12.1 ± 23.8 min in the rapid pacing group, P = 0.09) bud did not change the atrial electrogram types during atrial fibrillation.

Conclusions. Various types of atrial electrograms are present at different locations during atrial fibrillation. The atrial electrogram characteristics of atrial fibrillation at a specific location are related to the atrial effective refractory period, with short effective refractory periods associated with organized atrial electrograms and long effective refractory periods associated with disorganized electrograms.     

Regional endocardial left atrial voltage and electrogram fractionation in patients with atrial fibrillation

Introduction: Heterogeneities in electrophysiological properties may contribute to the development of atrial fibrillation, and regional disparities in endocardial voltage in the left atrium have been related to arrhythmogenic mechanisms. This study aimed at investigating endocardial voltage in different regions of the left atrium in patients with atrial fibrillation (AF). Methods and Results: Thirty‐six patients (aged 56 ± 7 years, 10 female) scheduled for circumferential ablation for paroxysmal AF were studied. Voltage measurements were performed during AF and with constant right ventricular pacing in the anterior, posterior, superior and inferior walls outside the antrum of the left (LPV), and right (RPV) pulmonary veins, by means of electroanatomical mapping. There was a high agreement among measurements performed in the endocardium of the posterior atrial wall (ICC > 0.70), and moderate agreement among measurements performed in the superior and inferior walls (0.50 < ICC< 0.70), outside both PV antra. The posterior left atrial wall demonstrated significantly higher voltages both outside the LPV antrum (1.29 ± 1.36 mV) and the RPV antrum (1.20 ± 0.63 mV) compared to the inferior, anterior and superior walls (0.47 ± 0.49, 0.68 ± 0.69, and 0.61 ± 0.83 mV outside the LPV antrum, and 0.39 ± 0.23, 0.65 ± 0.49, and 0.49 ± 0.24 mV outside the RPV antrum, respectively). Fractionated electrograms were mainly identified at the posterior left atrial wall, outside the right PV antrum. Conclusion: During AF, the posterior wall displays significantly higher voltage and electrogram fractionation compared with other parts of the left atrial endocardium outside the antra of both pulmonary veins in patients with paroxysmal AF.     

Bronchogenic cyst causing atrial fibrillation by impinging the right inferior pulmonary vein

Atrial fibrillation is the most common sustained cardiac arrhythmia and is usually associated with underlying structural heart disease, but may also occur in isolation--the entity of "lone" atrial fibrillation. Recently, attention has been directed to the pulmonary veins as a source of the arrhythmia through identification of rapidly firing ectopic foci within the covering myocardial sleeves. We describe a 38-year-old man who presented with treatment-resistant atrial fibrillation and a posterior mediastinal mass. Electrophysiological studies demonstrated abnormal foci of electrical activity at the entrance of the right inferior pulmonary vein into the left atrium. Surgical exploration revealed a bronchogenic cyst that distorted and stretched the right inferior pulmonary vein as it traversed the posterior mediastinum towards the left atrium. Restoration of sinus rhythm without recurrence of atrial fibrillation characterized the clinical course after surgical resection of the mass. This case demonstrates that a retro-cardiac bronchogenic cyst can cause atrial fibrillation by impinging on a pulmonary vein.     

犬肺静脉肌袖电生理随龄性改变

目的对比研究老龄和成年犬肺静脉肌袖电生理特性.方法采用经导管房间隔穿刺技术,应用程序刺激和短阵快速起搏分别对正常自然老龄和成年实验犬肺静脉、上腔静脉、左房、右房、以及冠状静脉窦的有效不应期、激动传导及心房颤动诱发阈值进行标测.结果老龄犬的左、右心房,上腔静脉,冠状静脉窦和肺静脉的有效不应期较成年犬均有不同程度的缩短,其中左心房,上腔静脉和肺静脉有效不应期的随龄性变化有统计学差异(P＜0.01).老龄犬的肺静脉不应期较其左房的不应期明显缩短,而成年犬肺静脉与左房的不应期则无显著性差异.老龄犬的肺静脉和上腔静脉内激动传导呈显著递减性传导.在多数老龄犬的肺静脉、左心房和上腔静脉,快速短阵起搏及程序刺激能诱发持续时间＞30s的房颤.结论老龄犬肺静脉肌袖有易于房颤发生的电生理变化,提示心脏老龄化可能是房颤发生的潜在基质.     

High-density mapping of left atrial endocardial activation during sinus rhythm and coronary sinus pacing in patients with paroxysmal atrial fibrillation

INTRODUCTION: This study was designed to record global high-density maps of left atrial endocardial activation during sinus rhythm and coronary sinus pacing. METHOD AND RESULTS: Noncontact mapping of the left atrium was performed in nine patients with paroxysmal atrial fibrillation undergoing pulmonary vein ablation procedures. High-density isopotential and isochronal activation maps were superimposed on three-dimensional reconstructions of left atrial geometry. Mapping was repeated during pacing from sites within the coronary sinus. Earliest left atrial endocardial activation occurred anterior to the right pulmonary veins in seven patients and on the anterosuperior septum in two patients. A line of conduction block was seen in the posterior wall and inferior septum in all patients. The direction of activation in the left atrial myocardium overlying the coronary sinus was different from the electrogram sequence in the coronary sinus catheter in 6 of 9 patients. During coronary sinus pacing, activation entered the left atrium a mean (SD) of 41 (13) ms after the pacing stimulus at a site 12 (10) mm from the endocardium overlying the pacing electrode. Lines of conduction block were present in the posterior wall and inferior septum. CONCLUSION: In patients with paroxysmal atrial fibrillation, lines of conduction block are present in the left atrium during sinus rhythm and coronary sinus pacing. Electrograms recorded in the coronary sinus infrequently correspond to the direction of activation in the overlying left atrial myocardium.     

Dual independent atrial tachycardias after ablation of chronic atrial fibrillation

We report the case of a 71-year-old man with two atrial tachycardias evolving simultaneously and independently in two dissociated regions after extensive ablation for chronic atrial fibrillation. One tachycardia was a focal tachycardia originating from the right inferior pulmonary vein and activating the posterior left atrium with a 2:1 conduction block, while the other tachycardia was an atrial flutter circulating around the tricuspid annulus, activating the right atrium and the anterior wall of the left atrium. These two atrial tachycardias were successfully ablated prior to restoration of sinus rhythm.     

心房与肺静脉电重构对比的研究

目的 探讨心房与肺静脉的电生理特性.方法 在相同条件下,测定心房和肺静脉的不应期,比较不应期缩短的幅度.结果 窦性心律下进行左、右心房及4个肺静脉不应期的测定,差异无统计学意义(P＞0.05).诱发房颤/持续电刺激12 h后测定心房及肺静脉的不应期,与自身窦性心律下的数据相比较发现,均有明显缩短(P＜0.05);左、右下肺静脉不应期的变化不明显(P＞0.05);左、右上肺静脉不应期的变化明显(P＜0.05).交叉比较发现,12 h后两上肺静脉与左、右心房相比,不应期明显缩短(P＜0.05);12 h后两下肺静脉与左、右心房相比不应期变化不明显(P＞0.05).结论 肺静脉容易发生电重构,左、右上肺静脉更易于被电重构.     

The superior vena cava as a site of ectopic foci in atrial fibrillation

Radiofrequency catheter ablation of ectopic foci that trigger atrial fibrillation has been established as a curative method for patients with symptomatic paroxysmal atrial fibrillation. Although the majority of these foci are located in and around the pulmonary veins, other less common locations have been identified. Recognition that foci can lie outside the pulmonary veins is important for ensuring therapeutic success. The most frequently reported foci of ectopic activity outside the pulmonary veins are in the superior vena cava and the posterior wall of the left atrium. Here we report our experience with the ablation of ectopic foci located in the superior vena cava in patients with symptomatic paroxysmal atrial fibrillation.     

Left atrial ablation for atrial fibrillation: creating the "box lesion" with a bipolar radiofrequency device

The maze procedure is the gold standard for the ablation of atrial fibrillation, and the "box lesion" around the pulmonary veins is the most important part of this procedure. We have created this lesion with a bipolar radiofrequency ablator, abandoning the usual use of this device (to achieve bilateral epicardial isolation of the pulmonary veins).From March 2004 through the end of May 2010, we performed surgical ablation of atrial fibrillation in 240 patients. Of this number, 205 underwent operation by a hybrid maze technique and the remaining 35 (our study cohort) underwent the creation of a box lesion around the pulmonary veins by means of a bipolar radiofrequency device. Ablation lines were created by connecting the left atriotomy to the amputated left atrial appendage, with 2 ablation lines made with a bipolar radiofrequency device above and below the pulmonary veins. Lesions were made along the transverse and oblique sinuses by epicardial and endocardial application of a bipolar device. The left atrial isthmus was ablated by bipolar radiofrequency and cryoprobe. No complications were associated with the box lesion: 90% and 89% of patients were in sinus rhythm at 3 and 6 months of follow-up, respectively.By creating a box lesion around the pulmonary veins, we expect to improve transmurality by means of epicardial and endocardial ablation of 1 rather than 2 layers of atrial wall, as in epicardial pulmonary vein isolation. Isolation of the entire posterior wall of the left atrium is better electrophysiologically and renders dissection around the pulmonary veins unnecessary.     

Vagal denervation and atrial fibrillation inducibility: Epicardial fat pad ablation does not have long-term effects

BACKGROUND: Major epicardial fat pads contain cardiac ganglionated plexi of the autonomic, predominantly vagal nerves. Vagal denervation may improve the success rate of atrial fibrillation (AF) treatment. OBJECTIVES: The purpose of this study was to elucidate the long-term effects of fat pad ablation on the electrophysiologic characteristics of the atrium and AF inducibility. METHODS: Six mongrel dogs were studied. Cervical vagal stimulation was applied to determine effects on the sinus node, AV node, atrial effective refractory period (AERP), and AF inducibility. AERP and AF inducibility were evaluated at both the right atrial and left atrial appendages and at the right atrial and left atrial free walls. Radiofrequency energy was delivered epicardially to the entire areas of two major fat pads: right pulmonary vein fat pad and inferior vena cava-left atrium fat pad. Cervical vagal stimulation then was applied to confirm the acute effects of fat pad ablation. The same evaluation was repeated 4 weeks later. RESULTS: The effects of vagal stimulation on the sinus node, AV node, and AERP were significantly eliminated immediately after fat pad ablation. However, these denervation effects disappeared after 4 weeks. At baseline, AF inducibility was increased by vagal stimulation (right atrial appendage: 72% +/- 31% vs 4.8% +/- 12%; right atrial free wall: 75% +/- 31% vs 0.0% +/- 0.0%; left atrial appendage: 60% +/- 29% vs 0.0% +/- 0.0%; left atrial free wall: 65% +/- 42% vs 0.0% +/- 0.0%). Fat pad ablation significantly reduced this vagal stimulation effect (8.3% +/- 20%, 10% +/- 22%, 17% +/- 29%, and 25% +/- 29%, respectively). However, similar to baseline, AF inducibility was strongly augmented by vagal stimulation 4 weeks after fat pad ablation (96% +/- 10%, 100% +/- 0.0%, 100% +/- 0.0%, and 95% +/- 11%, respectively). CONCLUSION: Radiofrequency fat pad ablation may not achieve long-term suppression of AF induction in this canine model.     

A clinicopathologic study of atrial infarction complicating left ventricular posterior myocardial infarction]

Among a series of 400 consecutive autopsy cases we performed a clinicopathologic study of atrial infarction in 46 autopsy-proven cases, which had acute or old left ventricular (LV) myocardial infarction. We used blocks taken from both atrial appendages, the region of the sinus-node, the lateral wall of the right atrium, the posterior wall of the right atrium, and the posterolateral wall of the left atrium. Atrial infarction was identified in 13 (28%) of 46 cases with LV posterior infarction which was caused by lesions of the right coronary artery; 10 cases were right atrial infarction and 3 were both right and left atrial infarction. Among 13 cases in which the acute phase of ventricular infarction could be followed, 3 cases exhibited transient atrial fibrillation. Of these 3 cases, 2 had atrial infarction. The mean stenotic index of the proximal right coronary artery was 4.3/5 in the 13 cases of atrial infarction, 3.2/5 in 17 cases of acute necrosis or scar and 3.1/5 in 16 cases without ischemic atrial lesions. Most of the atrial infarction was found in the right atrium; 10 in the right atrial appendage, 8 in the right atrial lateral wall, 3 in the region of the sinus node and the left atrial posterolateral wall, 2 in the right atrial posterior wall, and one in the left atrial appendage. In conclusion, the incidence of atrial infarction was unexpectedly high (28%) in LV posterior infarction caused by lesions of the proximal right coronary artery, particularly in severe stenosis or obstruction.     

Coronary sinus pacing initiates counterclockwise atrial flutter while pacing from the low lateral right atrium initiates clockwise atrial flutter: Analysis of episodes of direct initiation of atrial flutter

Introduction: Rapid atrial pacing in sinus rhythm may directly induce atrial flutter without provoking intervening atrial fibrillation, or initiate atrial flutter indirectly, by a conversion from an episode of transient atrial fibrillation provoked by rapid atrial pacing. The present study was performed to examine whether or not the direct induction of clockwise or counterclockwise atrial flutter was pacing-site (right or left atrium) dependent. Methods and Results: We analyzed the mode of direct induction of atrial flutter by rapid atrial pacing. In 46 patients with a history of atrial flutter, rapid atrial pacing with 3 to 20 stimuli (cycle LENGTH = 500 − 170 ms) was performed in sinus rhythm to induce atrial flutter from 3 atrial sites, including the high right atrium, the low lateral right atrium, and the proximal coronary sinus, while recording multiple intracardiac electrograms of the atria. Direct induction of atrial flutter by rapid atrial pacing was a rare phenomenon and was documented only 22 times in 15 patients: 3, 11, and 8 times during stimulation, respectively, from the high right atrium, low lateral right atrium, and the proximal coronary sinus. Counterclockwise atrial flutter (12 times) was more frequently induced with stimulation from the proximal coronary sinus than from the low lateral right atrium (8 vs 1, P = .0001); clockwise atrial flutter (10 times) was induced exclusively from the low lateral right atrium (P = .0001 for low lateral right atrium vs proximal coronary sinus, P = .011 for low lateral right atrium vs high right atrium). Conclusions: Direct induction of either counterclockwise or clockwise atrial flutter was definitively pacing-site dependent; low lateral right atrial pacing induced clockwise, while proximal coronary sinus pacing induced counterclockwise atrial flutter. Anatomic correlation between the flutter circuit and the atrial pacing site may play an important role in the inducibility of counterclockwise or clockwise atrial flutter.     

犬快速心房起搏心房颤动模型全心房心外膜标测以及静脉胺碘酮对其心电的影响

探讨快速心房起搏心房颤动(简称房颤)模型房颤发作时肺静脉、左右心房各部位激动频率的差异以及胺碘酮对其电生理特性的影响。选健康雄性杂种犬10只,以400次/分的固定频率进行右心耳起搏,建立快速心房起搏房颤模型。10周后终止起搏,行64道全心房心外膜标测。标测部位分别为左右心房游离壁、左右心房顶部、左上肺静脉、左下肺静脉、右上肺静脉和右下肺静脉。记录以上部位的心外膜电图,测量各标测部位的平均房颤波周长(AFCL),并对不同部位心外膜标测电图进行频谱分析。静脉注射胺碘酮300mg,分析胺碘酮治疗前后各部位有效不应期(ERP)和AFCL的变化。结果:8只犬完成整个实验。在所有8只犬中,最短AFCL/ERP位于Marshall韧带的有2只,位于左下肺静脉的有6只;AFCL/ERP在心房的分布呈明显的梯度分布,自短至长依次为:肺静脉或Marshall韧带、左房游离壁和左侧Bachmann束、右侧Bachmann束和右房游离壁;频谱分析结果与AFCL分析结果一致;胺碘酮虽然可延长肺静脉和心房各部位ERP和AFCL,但是不能终止房颤的发作。结论:局灶机制可能是快速心房起搏房颤模型的发生和维持机制。     

Esophageal temperature monitoring during radiofrequency ablation of atrial fibrillation

INTRODUCTION: Ablative strategies for atrial fibrillation have centered on the left atrium, in particular the pulmonary veins. An emphasis on ablating outside the ostia of the pulmonary veins appears to have reduced the risk of pulmonary vein stenosis. Unfortunately, ablation in the posterior left atrium has been reported to result in fatal atrio-esophageal fistula. METHODS AND RESULTS: We monitored esophageal temperatures in 16 consecutive patients undergoing atrial fibrillation ablation. There were 14 men and 2 women; average age 54.7 +/- 10.6 years. Eight patients had a lasso-guided pulmonary isolation procedure, eight an electroanatomically guided left-atrial circumferential approach. A commercially available esophageal temperature probe (Mallinckrodt Mon-a-therm 12F Esophageal Stethoscope with Temperature Sensor, Thermistor 400 Series) was positioned under general anesthesia. Temperature changes were noted and related to the relative location of the ablation catheter and the temperature probe during the temperature change. The esophagus was midline in three, right sided in three, and left sided in the remaining patients. Temperature rises could be recorded at the posterior aspect of any pulmonary vein. Detailed analysis of six patient maps revealed heating occurred with lesions created within 1 cm of the esophagus. CONCLUSION: The location of the esophagus relative to the back of the left atrium displays considerable variability. It is rarely midline and most often lies in close proximity to the left-sided veins. Ablation in close radiographic proximity (approximately 1 cm) to the esophagus as defined by a radio-opaque temperature probe can result in heating at the esophageal lumen.     

Anatomy of the left atrium: implications for radiofrequency ablation of atrial fibrillation

INTRODUCTION: The feasibility of treating atrial fibrillation with radiofrequency ablation has revived interest in the structure of the left atrium, a chamber that has been neglected in many textbooks of anatomy. METHODS AND RESULTS: We reviewed the gross structure of the left atrium by examining the septum, the appendage, and insertions of the pulmonary veins in normal hearts. The limited extent of the true septal component is relevant to procedures using the transseptal approach. On gross examination, the musculature of the atrial wall is composed of overlapping bundles of aligned fibers that, in the majority of hearts, are arranged in characteristic patterns with only minor individual variations. Muscular sleeves extend into the walls of the pulmonary veins to varying distances. The longest sleeves are in the left upper veins. Bachmann's bundle anteriorly, and other smaller bundles superiorly and posteriorly, bridge the septal raphe to blend with musculature of the right atrium. Tongues of left atrial musculature from the posterior wall also extend into the wall of the coronary sinus. CONCLUSION: The left atrium is more complex than usually conceived. Understanding its structure, and the arrangement of its musculature, will help in improving strategies for linear lesions when attempting to compartmentalize the chamber, or when placing focal lesions for ablating ectopic sources.     

Radiofrequency catheter ablation of atrial fibrillation initiated by spontaneous ectopic beats

Several reports have demonstrated that most paroxysmal atrial fibrillation is initiated by ectopic beats from a focal area, and radiofrequency catheter ablation can effectively cure atrial fibrillation. Although most of the ectopic beats originate from the orifices of the pulmonary veins or from the myocardial sleeves in the pulmonary veins, ectopic beats can also originate from superior vena cava, crista terminalis, coronary sinus, ligament of Marshall, or left atrial posterior free wall. Owing to the potential risk and complexity of catheter ablation, the ideal candidates should have frequent episodes and drug refractory paroxysmal atrial fibrillation.     

Mechanisms of atrial flutter following epicardial high intensity focused ultrasound left atrial ablative procedures during concomitant cardiac surgery

IntroductionIatrogenic atrial tachyarrhythmias have increased with the widespread application of left atrial ablative procedures to treat atrial fibrillation.Methods and resultsEntrainment and activation mapping were utilized to study the mechanisms of atrial flutter in two patients who presented with atypical atrial flutter after high intensity focused ultrasound (HIFU) atrial ablation for persistent atrial fibrillation during the course of concomitant cardiac surgery. Case 1: Atrial flutter with CL of 340 ms was demonstrated to be mediated by entry into and exit from the partially isolated posterior left atrium (LA) with conduction delay across at least one of the connections. The exit site was near the left superior pulmonary vein (LSPV) and the entrance site was near the right inferior pulmonary vein (RIPV) as demonstrated by activation and entrainment mapping. Case 2: Entrainment mapping was highly suggestive of inferior exit from the HIFU ablation line between the two inferior pulmonary veins. Flutter terminated during trans-septal procedure and could not be re-induced. Activation mapping of the LA during pacing revealed the inferior exit and left superior entrance site, both of which were successfully ablated, isolating the posterior LA.ConclusionsRe-entrant atrial flutter post-HIFU epicor Maze is caused by slow conduction at entry and exit sites from the otherwise isolated posterior LA wall. In both cases, gaps were found close to the LSPV and RIPV which may reflect difficulty in achieving proper contact between the HIFU device and the left atrial wall at these sites. These gaps are amenable to catheter ablation.