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。     

阵发性房颤患者心电图P波变化分析

目的分析阵发性心房颤动（PAF）患者心电图P波的变化。方法选择100例无器质性心脏病阵发性房颤患者（PAF组）,100例无房颤患者作为对照组（无PAF组）,采用体表心电图和超声心动图分别测量两组的V1导联P波时限（Pt）、V1导联P波终末负电势（Ptfv1）和左心房内径（LAD）、舒张末期左心室内径（LVD）、左心室射血分数（LVEF）等指标。结果 PAF组、无PAF组的Pt分别为（120±10）ms、（99±11）ms,Ptfv1分别为（0.051±0.023）mm·s、（0.026±0.010）mm·s,两组比较差异有统计学意义（P均〈0.01）;PAF组、无PAF组LAD分别为（33.6±3.9）mm、（32.7±4.2）mm,LVD分别为（44.6±4.1）mm、（42.7±4.3mm）,LVEF分别为（56.6±4.9）、（59.7±5.2）,两组比较差异无统计学意义（P均〉0.05）。结论阵发性房颤可引起心电图Pt及Ptfv1值增加,与左心房内径大小无相关。     

阵发性心房颤动患者心房内阻滞的评价

目的对阵发性心房颤动(房颤)患者心房内阻滞的情况进行评价.方法入选78例阵发性房颤患者和8创无阵发性房颤的射频消融患者,电生理检查时分别放置高位右心房、希氏束、冠状静脉窦电极导管作起搏和标测用,在高位右心房进行S1S2程序刺激,S1刺激固定于500ms,S2从450ms开始,-10ms扫描,记录不同刺激时心房内和心房间传导时间及心房不应期.结果S1刺激时阵发性房颤组和对照组S1-AHB间期分别为(56.7±15.4)ms和(60.8±14.2)ms;S1-ACSd间期在两组分别为(110.2±24.3)ms和(107.5±25.6)ms;差异均无显著性(P＞0.05).S2刺激时,心房内传导时间最长延长1倍以上的患者在两组分别为15/78例和11/80例,心房间传导最长延长1倍以上的患者在两组间分别为13/78例和9/80例,两组间差异无显著性(P＞0.05).心房不应期在两组分别为(218.0±28.2)ms和(216.0±24.7)ms,两者间差异无显著性(P＞0.05).结论多数阵发性房颤患者无明显的心房内阻滞和不应期改变,传导时间延长也并非特异地发生在阵发性房颤组,提示心房内阻滞和不应期缩短在阵发性房颤的发生中的作用尚不明确.     

心房颤动消融术后心房-肺静脉电位传导恢复的随访结果与影响因素

目的 环肺静脉电隔离术已成为治疗心房颤动（房颤）的一种有效手段,但是心房-肺静脉电位传导恢复是环肺静脉电隔离术需要克服的一个难关.本研究的目的 是明确环肺静脉电隔离术的效果以及影响心房-肺静脉电位传导恢复的因素,以提高消融术成功率,预防复发.方法 232例两次行房颤射频消融的阵发性房颤和持续性房颤患者,采用Lasso环状电极导管标测,明确其心房-肺静脉电位恢复部位,并在CartoTM系统指导下予以消融.并分析患者年龄、性别、房颤病史、体重指数、左心房内径、左心房舒张末内径、左心室射血分数（LVEF）及各合并症与心房-肺静脉电位传导恢复的关系.结果 232例第2次消融术病例术中标测示44例次（19.0%）无心房-肺静脉电位传导恢复,且术中心房-肺静脉电位传导恢复部位（Gap）多存在于左肺静脉前上部65例次（28%）、前下部49例次（21.1%）、右肺静脉后上部59例次（25.4%）及后下部61例次（26.3%）.年龄是房颤消融术后心房-肺静脉电位传导恢复的独立危险因素（P=0.012）,且性别、房颤病史、体重指数、左心房内径、左心房舒张末期内径、LVEF恢复组与未恢复组差异无统计学意义.结论 环肺静脉隔离术后,经长时间随访有约80%的患者心房-肺静脉电位传导恢复,并且心房-肺静脉电位传导存在易恢复区,多集中于左肺静脉前上部、前下部、右肺静脉后上部及后下部.年龄是房颤消融术后心房-肺静脉电位传导恢复的独立危险因素.     

依那普利对房颤的干预

目的：通过观察阵发性和持续性房颤患者口服依那普利前后左心房内径、P波离散度、心钠素（ANP）的变化,探讨依那普利对房颤的干预作用及其预防机制。方法：阵发性和持续性房颤患者60例,分为治疗组和对照组各30例。恢复窦性心律后均口服抗血小板药物,治疗组加用依那普利5～10mg/d;对照组不加用血管紧张素转换酶抑制剂或血管紧张素Ⅱ受体拮抗剂类药物。治疗18个月,房颤复发为终点。观察2组治疗组前后左心房内径、P波离散度、ANP的变化。结果：治疗组房颤复发率低于对照组（11.1%比35.7%,P〈0.01）;左心房内径治疗小于对照组[（39.4±5.3）mm比（44.5±5.1）mm,P〈0.01];P波离散度治疗组较对照组明显降低[（43.8±7.8）ms比（51.9±9.8）ms,P〈0.01];ANP治疗组较对照组明显降低[（128.8±33.5）pg/mL比（165.7±32.1）pg/mL,P〈0.01]。结论：长期服用依那普利能逆转左心房扩大,降低左心房压力,防止房颤复发,影响心房重构。     

52例心房晚电位与阵发性房颤的临床关联

目的 探讨心房晚电位测试对于预测阵发性房颤发生的临床关联。方法 以P波触发信号平均心电图记录技术测试52例阵发性房颤患者及40例健康对照组的心房晚电位(滤波后的P波时限、P波终末20ms、30ms、40ms的电压均方根值)并进行比较分析。结果 阵发性房颤组的滤波后P波时限为(137.52±2.92)ms,对照组为(113.05±1.20)ms,两组比较有显著性差异(P<0.001);阵发性房颤组的P波终末20ms电压均方根值为(2.65±0.25)μV,对照组为(3.72±0.19)μv,两组比较有显著性差异(P<0.001);阵发性房颤组的P波终末30ms电压均方根值为(3.69±0.32)μV,对照组为(4.71±0.28)μV,两组比较有显著性差异(P<0.02)。结论 P波触发信号平均心电图记录心房晚电位可作为预测阵发性房颇的1个快速、无创性指标。     

卡维地洛对高血压伴房颤患者P波离散度的影响

目的研究卡维地洛对高血压伴阵发性心房颤动患者P波最大时限(Pmax)和P波离散度(Pd)的影响,探讨卡维地洛对心房颤动的抗心律失常效应。方法将52例高血压伴阵发性房颤患者随机分成卡维地洛治疗组(26例)和对照组(26例),另设正常人26例为正常组。在服药前、服药3月分别测量Pmax及Pd,并观察治疗后阵发性房颤发作情况。结果高血压伴阵发性房颤者Pmax及Pd均较正常人明显延长(Pmax:128.20±8.49msvs105.20±8.21ms,p<0.05;Pd:45.89±8.92msvs29.11±8.02ms,p<0.05)。服药第3个月治疗组Pmax及Pd较治疗前明显缩短(Pmax:108.82±8.27msvs127.24±7.25ms,p<0.05;Pd:29.28±5.92msvs45.66±8.82ms,p<0.05),较对照组也明显缩短(Pmax:108.82±8.27msvs126.28±6.24ms,p<0.05;Pd:29.28±5.92msvs44.07±6.30ms,p<0.05)。治疗第3个月时,治疗组阵发性房颤发作减少12例,而对照组6例有效。结论高血压伴阵发性房颤患者Pmax、Pd较正常人增大,卡维地洛可缩短Pmax及Pd并可能减少阵发性房颤的发作。     

心房血清TNF-α及IL-6水平与非结构性心脏病房颤的相关性

目的 通过对心房颤动(房颤)患者左心房或右心房中血清肿瘤坏死因子(TNF)-α与白细胞介素(IL)-6的水平检测,探讨两种炎症因子与无结构性心脏病的患者房颤发生的关系。方法 59例首选射频消融术治疗方案的心律失常患者,59例患者心脏皆无结构性病变,其中包括房颤患者42例（阵发性房颤24例、持续性房颤18例）、预激综合征或阵发性室上性心动过速患者共17例,分别纳入房颤组及非房颤组。术前分别采集两组患者左房和右房中血液,并通过ELISA方法对血清样本的TNF-α、IL-6水平进行检测,应用心脏超声测量左心房内径（LAD）、左心室舒张末期内径（LVEDD）及左室射血分数（LVEF）等。结果 在两组比较中,房颤组LAD（36±7）mm显著高于非房颤组（31±4）mm（P<0.01）;TNF-α水平及IL-6L水平在房颤组的左、右心房的血清中含量均显著高于非房颤组,依次为P<0.01及P<0.05。在对房颤组中持续性房颤与阵发性房颤的组内亚组比较中:持续性房颤血清IL-6（17±9）pg/ml显著高于阵发性房颤组（12±5）pg/ml（P<0.05）,而持续性房颤及阵发性房颤的血清TNF-α水平均无显著差异。结论 心房血清TNF-α、IL-6水平与无结构性心脏病的房颤有相关性,持续性房颤患者心房血清IL-6 水平较阵发性房颤患者有升高趋势,可以作为房颤持续的预测因子。     

环肺静脉隔离消融术对P波离散度的急性效应

目的观察经三维电解剖标测系统指导下成功的环肺静脉隔离导管射频消融术本身对阵发性房颤患者P波离散度（Pd）的影响。方法选取在三维电解剖标测系统（Ensite或Carto）指导下行环肺静脉隔离经导管射频消融治疗阵发性房颤患者38例。分别记录研究对象术前及术后第3天窦性心律时体表心电图（ECG）及心脏彩超（同一操作者）,其中ECG各导联P波间期最大值（Pmax）与最小值（Pmin）之间的差值即Pd。结果经导管环肺静脉隔离阵发性房颤射频消融术前Pmin和Pmax分别为（57.8±15.8）、（128.9±25.8）ms,术后分别为（60.1±14.3）、（115±20.6）ms,其中Pmax手术前后比较P〈0.01。Pd手术前后分别为（71.1±17.5）、（54.7±15.6）ms,P〈0.01。进一步分析Pd和左房大小的关系表明,不仅术前Pd和术前左心房大小未见明显相关（P=0.437）,同时手术前后Pd变化亦与术前左心房大小无显著相关（P=0.208）。结论尽管阵发性房颤Pd与左心房大小无关,但成功的环肺静脉隔离导管射频消融手术本身即能显著减少Pmax和Pd,提示其对阵发性房颤患者心房内非均质性电活动具有改善作用。     

肺静脉电隔离对阵发性心房颤动患者P向量环的影响

目的探讨成功的肺静脉电隔离对心房除极的影响。方法记录接受环肺静脉电隔离术的18例阵发性心房颤动(PAF)患者术前及术后第1天窦性心律时的心向量图。测量P环的运行时间、P向量环在正交导联额面(F)、水平面(H)、左侧面(LS)的最大振幅及方向。同时记录P环从运行开始后每10ms的除极振幅。结果肺静脉隔离术后P环F最大振幅较术前降低(0.109±0.038mVvs0.128±0.040mV,P0.05)。P环运行时间,H及LS的最大振幅,F、H、LS的最大振幅方向,术前术后无差异(P0.05)。消融成功组(n=12)术后P环H最大振幅较术前降低(0.092±0.019mVvs0.122±0.030mV,P0.05),而术后复发组(n=6)则无明显变化。肺静脉隔离术后P环振幅降低发生在P环运行至40～80ms的部分,即P向量环的中部。结论PAF病人在肺静脉电隔离成功后P环最大振幅发生改变。     

Assessment of atrial electromechanical coupling and influential factors in nonrheumatic paroxysmal atrial fibrillation

BACKGROUND: Sequential analysis of atrial electromechanical coupling (P-A) by Doppler tissue imaging (DTI) might provide important insight into the mechanisms of paroxysmal atrial fibrillation (PAF). HYPOTHESIS: The purpose of this study was to evaluate P-A and the dispersion of P-A, and to analyze the influential factors of P-A. METHODS: One hundred and ten patients with PAF and 87 normal controls were enrolled. Using DTI, the time intervals from the beginning of P-wave to the onset of atrioventricular ring motion related to atrial contraction were measured. RESULTS: Atrial electromechanical coupling at the interventricular septum atrioventricular annulus (P-A1), left lateral mitral annulus (P-A2) and right lateral tricuspid annulus (P-A3) in PAF group were significantly longer than those in control (p < 0.001). The difference between P-A2 and P-A1 (T1), P-A2 and P-A3 (T3) in PAF group were greater than those in control before age correction (p < 0.05). The linear regression analysis showed that the duration of PAF episodes and age were the greatest influential factors of P-A1 (r = 0.564). Left atrial anterior-posterior dimension (LAD) and age were the greatest influential factors of P-A2 (r = 0.459). The LAD was the greatest influential factors of T1 and T3 (r = 0.408, 0.542). CONCLUSIONS: The atrial electromechanical coupling was significantly longer and the dispersion of P-A at left lateral mitral annulus was greater in PAF patients. The prolongation of P-A may be related to left atrial enlargement, long episodes of PAF and aging and the dispersion of P-A at left lateral mitral annulus to LAD.     

The effects of aging on atrial endocardial electrograms in patients with paroxysmal atrial fibrillation

BACKGROUND: The prevalence of atrial fibrillation (AF) has been reported to increase with advancing age. Histologic studies in AF have demonstrated that the percentage of fibrosis and degenerative changes in the atrial muscle increase significantly with age. HYPOTHESIS: This study was undertaken to assess the influence of advancing age on atrial endocardial electrograms recorded during sinus rhythm in patients with paroxysmal atrial fibrillation (PAF), which had not been assessed previously. METHODS: Right atrial endocardial catheter mapping during sinus rhythm was performed in 111 patients with PAF to evaluate the influence of advancing age on atrial endocardial electrograms. The bipolar electrograms were recorded at 12 sites in the right atrium, and an abnormal atrial electrogram was defined as lasting > or = 100 ms, and/or showing eight or more fragmented deflections. RESULTS: In all, 1,332 right atrial endocardial electrograms were assessed and measured quantitatively. The number of abnormal atrial electrograms in patients with PAF showed a significantly positive correlation with age (r = 0.34; p < 0.0005). Patients aged > 60 years had a significantly greater mean number of abnormal electrograms (2.58 +/- 2.05) than those aged < 60 years (1.43 +/- 2.03; p < 0.004). The longest duration (r = 0.35; p < 0.0005) and the maximal number of fragmented deflections (r = 0.29; p < 0.005) of atrial electrograms among the 12 right atrial sites also showed a significantly positive correlation with age. CONCLUSIONS: Aging alters the electrophysiologic properties of the atrial muscle in patients with PAF. Elderly patients have a significantly greater abnormality of atrial endocardial electrograms than do younger ones. There is a progressive increment in the extension of altered atrial muscle with advancing age in patients with PAF.     

Electroanatomic characteristics of atrial premature beats triggering atrial fibrillation in patients with persistent versus paroxysmal atrial fibrillation

APBs in Persistent Versus Paroxysmal AF. BACKGROUND: Although the electrical disconnection between the left atrium (LA) and pulmonary veins (PVs) by radiofrequency catheter ablation has been proven to be effective in controlling atrial fibrillation (AF), the recurrence rate is higher in patients with persistent AF (PeAF) than with paroxysmal AF (PAF). We hypothesized that the origin of the atrial premature beats (APBs) that trigger AF and the pattern of their breakthrough into the LA differ between PAF and PeAF. METHODS: We mapped 75 APBs (53 APBs triggering AF, 22 isolated APBs) from the LA and PVs in 26 patients with AF (age: 49.5 +/- 9.6, males: 23, PAF = 17, PeAF = 9), using a noncontact endocardial mapping (NCM) system. The location of the preferential conduction (PC) sites and their conduction velocity (CV) were compared. RESULTS: In patients with PeAF, the earliest activation (EA) site and exit of the PC were more frequently located on the LA side of the LA-PV junction as compared with PAF (P < 0.001). Eighty-one percent of the PCs were located in the area between the left and right superior PVs. The incidence of PCs was similar between the PeAF and PAF patients (P = NS). PCs were more commonly found with APBs inducing AF (63.3%) than with those not inducing AF (35.2%, P = 0.01). The CV of the PC was slower for PeAF than PAF (P < 0.001). The CV in the LA during sinus rhythm was also slower for PeAF than PAF (P < 0.01). CONCLUSION: PeAF was more frequently triggered by APBs from the LA side of the LA-PV junction than PAF and resulted in slower conduction than did PAF. These findings may help explain the higher potential for recurrence after electrical PV isolation in patients with PeAF.     

Conduction delay within the coronary sinus in humans: implications for atrial arrhythmias

INTRODUCTION: Striated myocardial connections between the venous wall of the coronary sinus (CS) and the left atrium have been described in humans. This aim of this study was to investigate the conduction properties and potential arrhythmogenicity of CS and left atrial myocardial connections in patients with and patients without paroxysmal atrial fibrillation (PAF). METHODS AND RESULTS: Thirty-eight patients with PAF, 52 patients with other arrhythmias, and 44 patients without arrhythmia underwent catheter mapping of the CS from the distal superoposterior part to the ostium. Catheterization of the superoposterior CS was feasible in 21, 32, and 25 subjects in the three groups, respectively (P = 0.82). Discrete double potentials or fractionated electrograms were recorded during proximal CS or right atrial pacing in 14 (66.7%), 11 (34.4%), and 5 (20.0%) patients, respectively (P = 0.004). In 29 patients, double or fractionated potentials were recorded at the distal superoposterior CS, in 3 at the mid-CS, and in 4 at the ostium. Spontaneous or induced atrial ectopy and/or tachyarrhythmias were recorded in 18 (85.7%), 12 (37.5%), and 2 (8.0%) patients in the three groups, respectively (P < 0.001) and originated from the CS in 6, 3, and 0 patients, respectively (P = 0.010). CONCLUSION: Recording of double potentials is possible within the CS, particularly at its distal superoposterior part, near the left superior pulmonary vein. Their prevalence is higher in patients with PAF than in subjects with other or no arrhythmias, and their presence denotes possible sources or substrate for atrial arrhythmia.     

Extended distribution of prolonged and fractionated right atrial electrograms predicts development of chronic atrial fibrillation in patients with idiopathic paroxysmal atrial fibrillation

INTRODUCTION: This study evaluates whether electrophysiologic abnormalities in patients with idiopathic paroxysmal atrial fibrillation (PAF) predict the transition to chronic atrial fibrillation (CAF). METHODS AND RESULTS: Ninety-six patients with idiopathic PAF underwent electrophysiologic study and were followed up. During electrophysiologic study, endocardial mapping was performed at 12 sites in the right atrium (four aspects of the high, middle, and low right atrium). During follow-up of 60 to 130 months, conversion from PAF to CAF was observed in 17 patients (CAF group). The remaining 79 patients remained in sinus rhythm (PAF group). Although a high frequency of abnormal atrial electrograms was observed in the high right atrium in both groups, the frequency of those recorded from the middle right atrium was significantly higher in the CAF group than in the PAF group (70.6% vs 13.9%, P < 0.0005). Kaplan-Meier analysis showed that >50% of the patients with abnormal atrial electrograms in the middle right atrium developed CAF after 10 years, whereas only 7% of patients without those developed CAF (P < 0.0001). CONCLUSION: Our data suggest that extended distribution of abnormal atrial electrograms from the high to middle right atrium is predictive of the development of CAF in patients with idiopathic PAF.     

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.     

三维超声心动图及斑点追踪成像评价左心房不同构型阵发性房颤患者左心房功能的临床研究

目的应用实时三维超声心动图(3D-RTE)及二维斑点追踪成像(2D-STI)评价左心房不同构型的阵发性房颤患者(PAF)左心房结构和功能。方法入选2017年1月至2018年12月于解放军总医院第七医学中心收治的阵发性房颤患者98例。根据二维超声左心房容积指数(LAVI-2D)将房颤患者分为左心房容积正常组(LAN组,LAVI<34 ml/m^2,50例)和左心房容积扩大组(LAE组,LAVI≥34 ml/m^2,48例)。选择同期38例临床资料匹配者为对照组。实时三维超声心动图测定左心房最大容积(LAVmax),左心房最小容积(LAVmin),左心房容积指数(LAVI-3D)和左心房总排空分数(LATEF)。斑点追踪显像获取左心房纵向时间-应变曲线,记录收缩期平均应变(SSL)和各时相平均应变率(mSRs、mSRe、mSRa)。结果PAF患者LAVI平均水平高于对照组,且LAE组LAVI水平高于LAN组,LAVI-3D测量值较LAVI-2D测量值高(P均<0.05)。PAF患者LATEF平均水平低于对照组,且LAE组LATEF水平小于LAN组(P均<0.05)。与对照组比较,PAF患者mSSL、mSRs、mSRe和mSRa水平均降低,LAE组mSSL、mSRs、mSRe和mSRa水平小于LAN组,差异有统计学意义(P均<0.05)。结论三维超声心动图较二维测量左心房容积大,能更准确评估左心房容积。左心房容积无明显增大房颤患者,已出现左心房功能减低。左心房扩大者应变指标进一步下降,左心房功能减低明显。三维超声心动图及斑点追踪成像能早期评价房颤患者左心房功能异常。     

An electrocardiogram marker to detect paroxysmal atrial fibrillation

An electrocardiogram marker to detect patients who have paroxysmal atrial fibrillation (PAF) is reported. The data set of ECG records made available by PhysioNet for Cardiology Challenge 2001 was used. The method uses a filtered time series with a frequency range between 3 and 9 Hz obtained from the electrocardiogram record. Typically, frequencies observed when a patient is in atrial fibrillation and atrial flutter is within this frequency range. Filtering was done using wavelets. Thereafter, the temporal properties of this filtered time series are studied. The temporal properties studied are the standard deviation, standard deviation of successive differences, and the length of the ellipse in the Poincare plot. The results indicate that these temporal properties of patients with PAF are depressed compared to the healthy group. A marker based on these temporal properties shows promise in detecting PAF when patients are in normal sinus rhythm. Results also show that the values for these temporal properties for a patient with PAF show little variation with time, and its measure is not dependent on the time of occurrence of a PAF episode.     

Mechanisms for the genesis of paroxysmal atrial fibrillation in the Wolff--Parkinson--White syndrome: intrinsic atrial muscle vulnerability vs. electrophysiological properties of the accessory pathway

Background: Paroxysmal atrial fibrillation (PAF) develops in up to one-thirdof patients with the Wolff Parkinson–White syndrome (WPW).The reason for this high incidence of PAF in the WPW syndromeis not yet clearly understood. When PAF appears in patientswith WPW syndrome who have anterograde conduction via the accessorypathway (AP), it may be life-threatening if an extremely rapidventricular response develops degenerating into ventricularfibrillation. Methods and results: Several mechanisms responsible for the genesis of PAF in WPWpatients were hypothesized, namely, spontaneous degenerationof atrioventricular reciprocating tachycardia into atrial fibrillation(AF), electrical properties of the APs, effects of APs on atrialarchitecture, and intrinsic atrial muscle vulnerability. Focalactivity, multiple reentrant wavelets, and macroreentry haveall been implicated in AF, perhaps under the further influenceof the autonomic nervous system. AF can also be initiated byectopic beats originating from the pulmonary veins, and elsewhere.Several studies demonstrated a decrease incidence of PAF aftersuccessful elimination of the AP, suggesting that the AP itselfmay play an important role in the initiation of PAF. However,PAF still occurs in some patients with the WPW syndrome evenafter successful elimination of the AP. There is an importantevidence of an underlying atrial disease in patients with theWPW syndrome. Conclusions: Atrial vulnerability has been studied performing an atrial endocardialcatheter mapping and analysing abnormal atrial electrograms.Other studies evaluated atrial refractoriness and intraatrialconduction times, suggesting an intrinsic atrial vulnerabilityas the mechanism of PAF and considering the AP as an innocentbystander. It is our intention to analyse the available dataon this particular and interesting topic since AF has a singularprognostic significance in patients with the WPW syndrome, andits incidence is unusually high in the absence of any clinicalevidence of cardiac organic disease.     

Mechanisms for atrial fibrillation in patients with Wolff-Parkinson-White syndrome

INTRODUCTION: Paroxysmal atrial fibrillation (PAF) frequently occurs in patients with Wolff-Parkinson-White (WPW) syndrome. To elucidate the mechanisms for PAF, we performed electrophysiologic studies (EPS) before and after ablation of accessory pathways (APs). METHODS AND RESULTS: We investigated 24 patients with WPW syndrome who had AV reciprocating tachycardia and prior PAF and had undergone successful ablation of APs. Patients in whom atrial fibrillation (AF) was induced by EPS at day 7 after ablation were considered the inducible AF group (n = 14), and patients in whom AF was not induced by EPS at day 7 after ablation were considered the noninducible AF group (n = 10). Fifteen patients with AV nodal reentrant tachycardia (AVNRT) but without PAF who underwent ablation of the slow AV nodal pathways served as the control group (AVNRT group). Maximal atrial conduction delay and conduction delay zone, which are indices of atrial vulnerability, were measured before and after ablation. Before ablation, maximal atrial conduction delay and conduction delay zone were significantly greater (P < 0.0001 and P < 0.0001, respectively) in the two WPW syndrome groups than in the AVNRT group, indicating increased atrial vulnerability in WPW syndrome with PAF. After ablation, these parameters did not change in the inducible AF group, whereas they were significantly (P < 0.0001) decreased in the noninducible AF group and were not different from those in the AVNRT group, indicating normalized atrial vulnerability in the noninducible AF group after ablation. The prospective study demonstrated that PAF recurred only in the inducible AF group during long-term follow-up (17+/-7 months). CONCLUSION: The findings of this study suggest that there are two mechanisms of PAF in patients with WPW syndrome: one mechanism is reversible and AP-dependent atrial vulnerability, and the other is intrinsic and AP-independent atrial vulnerability.