The Spatial Dispersion of Atrial Refractoriness and Atrial Fibrillation Vulnerability

The local dispersion of conduction and refractoriness has been considered essential for induction of atrial arrhythmias. This study sought to determine whether a difference of refractoriness and vulnerability for induction of atrial fibrillation between trabeculated and smooth as well as high and low right atrium may contribute to initiation of atrial fibrillation in dogs.In 14 healthy mongrel dogs weighing 22.4 ± 1 kg, closed-chest endocardial programmed stimulation was performed from four distinct right atrial sites. Atrial refractory periods and vulnerability for induction of atrial fibrillation or premature atrial complexes were determined during a basic cycle length of 400 and 300 ms and an increasing pacing current strength.For a pacing cycle length of 300ms, atrial refractory periods were longer on the smooth, as compared to the trabeculated right atrium (102 ± 25 vs. 97 ± 17ms, p < 0.05), whereas for a pacing cycle length of 400ms, there was no significant difference. The duration of the vulnerability zone for induction of atrial fibrillation was longer on the smooth right atrium, for a cycle length of both 400 ms (40 ± 30 vs. 31 ± 22 ms; p < 0.05) and 300 ms (33 ± 25 vs. 23 ± 21 ms; p < 0.01). When comparing high and low right atrium, refractory periods were longer on the the low right atrium, for a cycle length of both 400 ms (111 ± 23 vs. 94 ± 24ms; p < 0.01) and 300 ms (104 ± 20 vs. 96 ± 23ms; p < 0.01). For a pacing cycle length of 300 ms, the duration of the atrial fibrillation vulnerability zone was longer for the high, as compared to the low right atrium (34 ± 22 vs. 22 ± 22, p < 0.01). Seven dogs with easily inducible episodes of atrial fibrillation demonstrated significantly shorter refractory periods as compared to 7 non-vulnerable dogs, regardless of pacing site and current strength.In conclusion, significant differences in refractoriness and vulnerability for induction of atrial fibrillation can be observed in the area of the crista terminalis in healthy dogs. Thus, local anatomic factors may play a role in the initiation of atrial fibrillation.     

Evaluation of Atrial Refractoriness and Atrial Fibrillation Inducibility Immediately after Internal Cardioversion in Patients with Chronic Persistent Atrial Fibrillation

Summary. Objective: To prospectively evaluate right atrial refractoriness and sustained atrial fibrillation (AF) inducibility at programmed electrical stimulation in two groups of patient: a series of patients with chronic persistent AF, studied immediately after successful low energy internal atrial cardioversion, and a group of control patients without history of supraventricular arrhythmias.Patients: Nineteen patients with chronic persistent AF (mean AF duration 11 ± 10 months, range 2–61 months) submitted to successful internal low energy atrial cardioversion in fully conscious state and 11 control patients without history of supraventricular arrhythmias.Methods: An electrophysiological evaluation was performed to measure atrial refractoriness and AF inducibility, by delivering single atrial extrastimuli in high right atrium, at decremental coupling, during spontaneous sinus rhythm and after 8 beats at 600, 500, 400 and 330 ms cycle length. If sustained AF was induced the protocol was terminated.Results: During programmed atrial stimulation sustained AF was induced in 8 out 19 (42%) of the AF patients but in none of the control group. Atrial effective refractory period was significantly shorter in AF patients compared to controls both at basic cycle length, at 600 ms, 500 ms and 400 ms cycle length, meanwhile no statistically significant differences were found at 330 ms cycle length. An altered relationship between atrial effective refractory period and cycle length was found in AF patients compared to controls: the slope of linear correlation slope was significantly lower in AF group than in controls (0.04 ± 0.07 vs 0.17 ± 0.10, p < 0.002).Conclusions: Marked abnormalities of atrial refractoriness and of its heart rate relationship are observed after internal cardioversion of chronic persistent AF in humans and these abnormalities are associated with an high vulnerability to AF. These observations may explain the high risk of AF recurrences in the early phases following successful cardioversion. In this scenario antiarrhythmic drug therapy seems to be mandatory for reducing arrhythmia relapses.     

Focal Atrial Fibrillation in Dextrocardia

A 49‐year‐old woman with dextrocardia and situs inversus underwent catheter ablation of paroxysmal atrial fibrillation (AF). During the electrophysiologic study, AF triggered by frequent premature atrial contractions (PACs) with a short coupling interval exhibiting a “P on T” pattern occurred. Pulmonary vein mapping revealed that those PACs originated from right‐sided (anatomic left) or left‐sided (anatomic right) pulmonary veins. In this case with mirror‐image dextrocardia, the P‐wave morphologies in leads I and aVL and the II/III ratio of the P‐wave amplitude were helpful for predicting a right‐ or left‐sided pulmonary vein origin.     

阵发性心房颤动的动态心电图特征研究

目的 探讨阵发性心房颤动发生的动态心电图特征. 方法 对38例阵发性心房颤动患者和24例非阵发性心房颤动患者的动态心电图进行分析,测定和计算房性期前收缩偶联间期和房性期前收缩指数. 结果 阵发性心房颤动共发作291次,其中221次由房性期前收缩诱发（75.95%）.诱发心房颤动的房性期前收缩与未诱发心房颤动的房性期前收缩比较,偶联间期较短,期前收缩指数较小,差异有统计学意义（P〈0.05）.心房颤动发作前1h房性期前收缩和短阵房性心动过速频率增加.35.75%阵发性心房颤动发生时出现明显的长短周期现象. 结论 房性期前收缩是阵发性心房颤动发生的主要因素,长短周期现象是阵发性心房颤动发生的重要电生理机制.     

P波离散度预测阵发性心房颤动的研究

目的观察阵发性心房颤动（PAF）病人的体表心电图P波离散度（Pd）、最大P波时限（Pmax）的变化.研究Pd与Pmax对PAF的预测价值.方法观察和测量80例PAF病人（观察组）的Pd和Pmax.并与70名健康者（对照组）对照分析.结果 PAF组与对照组比较,Pd与Pmax均有统计学意义（P＜0.001）.结论 Pd是一种新的预测PAF的体表心电图指标.     

Nonpharmacologic Approaches to the Treatment of Atrial Fibrillation and Atrial Flutter

Nonpharmacologic Approaches to Atrial Fibrillation and Flutter. The high prevalence of atrial fibrillation, the associated morbidity and mortality, the absence of safe and effective drug therapy, and an increased understanding of the pathophysiologic basis of atrial fibrillation and flutter have collectively led to the development of novel nonpharmacologic treatments for the management of these arrhythmias, including the CORRIDOR and MAZE surgical procedures, catheter-based ablation and modification of AV conduction, catheter-based ablation of atrial flutter and fibrillation, and internal atrial defibrillation. These surgical and catheter-based techniques offer potentially curative therapy while sparing the long-term risks of antiarrhythmic drug therapy. For patients with typical atrial flutter, catheter ablation affords cure rates in excess of 70%. As technological innovations further facilitate identification and ablation of the critical isthmus in the floor of the right atrium, success rates should improve substantially. For patients with atrial fibrillation, AV junction ablation with implantation of a rate-responsive ventricular pacemaker should be considered palliative therapy, as should modification of AV junction conduction. The MAZE procedure offers very high cure rates, but because it currently involves open heart surgery, patient selection is critical. Catheter-based procedures emulating aspects of the MAZE procedure may one day offer cure rates comparable to those of the surgery itself, but additional research and technological development are necessary to further define and refine the minimal effective procedure, and then to facilitate the placement of contiguous, full-thickness lesions in precise three-dimensional configurations. In the interim, the implantable automatic atrial defibrillator may offer a means for rapidly restoring sinus rhythm without the risks of long-term antiarrhythmic drug therapy.     

P‐Wave Dispersion: A Novel Predictor of Paroxysmal Atrial Fibrillation

Background: The prolongation of intraatrial and interatrial conduction time and the inhomogeneous propagation of sinus impulses are well known electrophysiologic characteristics in patients with paroxysmal atrial fibrillation (AF). Previous studies have demonstrated that individuals with a clinical history of paroxysmal AF show a significantly increased P‐wave duration in 12‐lead surface electrocardiograms (ECG) and signal‐averaged ECG recordings. Methods: The inhomogeneous and discontinuous atrial conduction in patients with paroxysmal AF has recently been studied with a new ECG index, P‐wave dispersion. P‐wave dispersion is defined as the difference between the longest and the shortest P‐wave duration recorded from multiple different surface ECG leads. Up to now the most extensive clinical evaluation of P‐wave dispersion has been performed in the assessment of the risk for AF in patients without apparent heart disease, in hypertensives, in patients with coronary artery disease and in patients undergoing coronary artery bypass surgery. P‐wave dispersion has proven to be a sensitive and specific ECG predictor of AF in the various clinical settings. However, no electrophysiologic study has proven up to now the suspected relationship between the dispersion in the atrial conduction times and P‐wave dispersion. The methodology used for the calculation of P‐wave dispersion is not standardized and more efforts to improve the reliability and reproducibility of P‐wave dispersion measurements are needed. Conclusions: P‐wave dispersion constitutes a recent contribution to the field of noninvasive electrocardiology and seems to be quite promising in the field of AF prediction. A.N.E. 2001;6(2):159–165     

心房颤动患者心房纤维化研究进展

心房颤动的发生和维持与心房重构有关。心房纤维化是心房颤动患者心房结构重构最突出的表现,目前被认为是发生心房颤动的结构基础,是心房颤动发生、维持的一个重要因素。现综述心房颤动患者心房纤维化及其发生机制。通过对心房颤动患者心房纤维化结构改变及肾素-血管紧张素系统、转化生长因子、基质金属蛋白酶等在心房纤维化的发生和心房颤动发生、维持中的作用等的全面阐述,,探讨了心房颤动患者心房纤维化的研究进展。防治心房颤动新的策略取决于对心房纤维化机制更好的理解。     

Effect of Atrial Pressure Increase on Effective Refractory Period and Vulnerability to Atrial Fibrillation in Patients with Lone Atrial Fibrillation

Background: There is evidence suggesting that atrial fibrillation (AF) may be induced by acute increase of atrial pressure. The aim of the present study was to investigate the effect of alterations in atrial pressure, induced by varying the atrioventricular (AV) interval, on atrial refractoriness, and on the frequency of induction of (AF), in patients with a history of lone atrial fibrillation (LAF).Methods and Results: Twenty-five patients were included in this study. The patients were divided in two groups: the LAF group, and the control group. None of the patients in either group had organic heart disease. Effective refractory period (ERP) and duration of atrial extrastimulus electrogram (A₂) were measured at two right atrial sites (high lateral wall, atrial appendage) during AV pacing (cycle length: 500 msec) with different AV intervals. Peak, minimal and mean atrial pressure increased from 8.57 ± 2.37 to 18.14 ± 4.74 mm Hg, 2 ± 2.23 to 5.14 ± 2.60 mm Hg (p = 0.0001) and from 4.28 ± 1.6 mm Hg to 9.77 ± 2.9 mm Hg (p = 0.001), respectively during AV interval modification. During lateral and atrial appendage pacing, with a progressive decrease of AV interval to 160, 100, 80, 40, 0 msec, the ERP, the dispersion of ERP, functional refractory period (FRP), A2 and latency period (LP) did not change significantly, in both groups. The frequency of induction of AF was not statistically different in both lateral atrial wall and appendage, during pacing in different AV intervals.Conclusions: This study demonstrates that alterations in the intraatrial pressure does not have important effects on atrial refractoriness and does not increase vulnerability to AF in patients with a history of LAF.     

The Role of Atrial Electrical Remodeling in the Progression of Focal Atrial Ectopy to Persistent Atrial Fibrillation

Although atrial fibrillation- (AF) induced changes in atrial refractoriness (atrial electrical remodeling) have been demonstrated in a number of different animal models, the clinical significance of this process is unknown. We describe a patient in whom there has been documented progression of atrial ectopy to persistent AF accompanied by evidence of atrial electrical remodeling, with reversal of remodeling following successful ablation of the focal source of AF. A second patient with focal AF, but with a "nonfocal" appearance on the ECG, is also described. These cases illustrate: (1) the possibility that a significant proportion of younger patients with idiopathic persistent AF may well have a focal source as the underlying abnormality; and (2) atrial electrical remodeling reverses following ablation of the underlying source.     

Effects of High-Frequency Atrial Pacing in Atypical Atrial Flutter and Atrial Fibrillation

Atypical atrial flutter has, hitherto, been relatively refractory totermination by rapid atrial pacing. High-frequency pacing (HFP) in theatrium, for termination of atrial flutter or atrial fibrillation (AF), andthe electrophysiologic effects related to it have not been examined. Weexamined the clinical efficacy, safety, and electrophysiologic mechanisms ofHFP using 50-Hz bursts at 10 mA applied at the high right atrium in patientswith atypical atrial flutter (group 1) or AF (group 2), using a prospectiverandomized study protocol. Four burst durations (500, 1000, 2000, and 4000ms) were applied at the high right atrium repetitively in random sequence in22 patients with spontaneous atrial flutter or AF. Local and distant rightand left atrial electrogram recordings were analyzed during and after HFP.HFP resulted in local and distant right and left atrial electrogramacceleration in 8 of 10 patients (80%) in group 1 but caused lessfrequent local atrial electrogram acceleration (6 of 12 patients) and nodistant atrial electrogram effects in group 2 (p < .05 versus group 1).The HFP protocol was effective in arrhythmia termination in 6 of 10patients in group 1 but in no patient in group 2 (p < .05 versus group1). Standard HFP protocol applied at the high right atrium can frequentlyalter atrial activation in both atria and can terminate atypical atrialflutter. Efficacy in AF is limited, probably due to limitedelectrophysiologic actions beyond the local pacing site.     

阵发性心房颤动P波最大时间及P波离散度的相关分析

目的 探讨P波最大时间（Pmax）和P波离散度（Pd）与阵发性心房颤动的关系.方法 测定72例阵发性心房颤动患者的Pd值、Pmax值、心房颤动时间和左心房内径（LAD）,并作相关性分析.结果 Pd≥40ms者心房颤动时间显著大于Pd〈40ms者（P〈0.05）;Pmaxt〉110ms者LAD大于Pmax〈110ms者（P〈0.05）.Pmax与心房颤动时间、LAD和年龄相关（P〈0.01或0.05）,Pd与心房颤动时间相关（P〈0.05）,Pmax与Pd之间存在相关性.结论 在预测心房颤动中,Pd特异性较高,Pmax敏感性较高,Pd与Pmax结合可提高阳性预测值.     

Interatrial Mechanical Dyssynchrony Worsened Atrial Mechanical Function in Sinus Node Disease With or Without Paroxysmal Atrial Fibrillation

Introduction: Atrial electromechanical dysfunction might contribute to the development of atrial fibrillation (AF) in patients with sinus node disease (SND). The aim of this study was to investigate the prevalence and impact of atrial mechanical dyssynchrony on atrial function in SND patients with or without paroxysmal AF. Methods: We performed echocardiographic examination with tissue Doppler imaging in 30 SND patients with (n = 11) or without (n = 19) paroxysmal AF who received dual‐chamber pacemakers. Tissue Doppler indexes included atrial contraction velocities (Va) and timing events (Ta) were measured at midleft atrial (LA) and right atrial (RA) wall. Intraatrial synchronicity was defined by the standard deviation and maximum time delay of Ta among 6 segments of LA (septal/lateral/inferior/anterior/posterior/anterospetal). Interatrial synchronicity was defined by time delay between Ta from RA and LA free wall. Results: There were no differences in age, P‐wave duration, left ventricular ejection fraction, LA volume, and ejection fraction between with or without AF. Patients with paroxysmal AF had lower mitral inflow A velocity (70 ± 19 vs 91 ± 17 cm/s, P = 0.005), LA active empting fraction (24 ± 14 vs 36 ± 13%, P = 0.027), mean Va of LA (2.6 ± 0.9 vs 3.4 ± 0.9 cm/s, P = 0.028), and greater interatrial synchronicity (33 ± 25 vs 12 ± 19 ms, P = 0.022) than those without AF. Furthermore, a lower mitral inflow A velocity (Odd ratio [OR]= 1.12, 95% Confidence interval [CI] 1.01–1.24, P = 0.025) and prolonged interatrial dyssynchrony (OR = 1.08, 95% CI 1.01–1.16, P = 0.020) were independent predictors for the presence of AF in SND patients. Conclusion: SND patients with paroxysmal AF had reduced regional and global active LA mechanical contraction and increased interatrial dyssychrony as compared with those without AF. These findings suggest that abnormal atrial electromechanical properties are associated with AF in SND patients.     

P Wave Dispersion: A Valuable Electrocardiographic Marker for the Prediction of Paroxysmal Lone Atrial Fibrillation

Background: The prolongation of atrial conduction time and the inhomogeneous propagation of sinus impulses are well known electrophysiological characteristics in patients with paroxysmal atrial fibrillation. Methods: The aim of this study was to test the ability of a new ECG marker to discriminate between patients with a prior history of paroxysmal lone atrial fibrillation and healthy controls. Maximum P wave duration (Pmax) and the difference between the maximum and the minimum P wave duration, which was defined as P-wave dispersion (Pdisp) were calculated from the 12-lead surface ECGs of 75 patients with a history of paroxysmal lone atrial fibrillation and 50 age-matched healthy controls. Results: Pmax was in patients 122 ± 17 ms and in controls 101 ± 10 ms (t = 7.935, P > 0.001). Pdisp was in patients 48 ± 16 ms and in controls 29 ± 8 ms (t = 7.616, P > 0.001). A Pmax value of 110 ms separated patients from controls with a sensitivity 85%, a specificity 72%, and a positive predictive accuracy of 82%. A Pdisp value of 40 ms separated patients from controls with a sensitivity of 81%, a specificity of 80%, and a positive predictive accuracy of 85%. Conclusions: (1) Pmax and Pdisp values were found to be significantly higher in patients with a prior history of paroxysmal lone atrial fibrillation than in age-matched healthy controls, and (2) Pdisp is a new simple ECG marker that could be possibly used for the identification of patients with a previous history of paroxysmal lone atrial fibrillation. A.N.E. 1999;4(1):39–45     

The Effect of Exercise to P Wave Dispersion and Its Evaluation as a Predictor of Atrial Fibrillation

Aim: Prolongation of P wave time and increase of its dispersion as an independent predictor of atrial fibrillation. In patients with paroxysmal atrial fibrillation (PAF) as in healthy people, exercise augments sympathetic activity and therefore can cause the development of atrial fibrillation. The aim of this study is to evaluate the effect of exercise on P wave dispersion and to predict the development of atrial fibrillation. Methods: One hundred and ninety‐eight patients (93 women, 105 men, mean age: 59.05 ± 11.01 years ) having the diagnosis of PAF were included in the study. The left atrial diameter of all these patients was more than 4.0 cm. One hundred and fifty‐five patients (72 females, 83 males, mean age: 58.41 ± 10.79 years ), with left atrial diameter more than 4.0 cm and without PAF were taken as control group. Symptom limited exercise test with modified Bruce protocol was performed on all patients. Rest, maximum exercise and recovery, and first, third, and fifth‐minute 12‐derivation ECG was taken in all patients. The velocity of ECG was adjusted to 50 mm/s; shortest and largest P wave durations were measured and P wave dispersion was calculated. Results: The mean left atrial diameter was 4.41 ± 0.58 cm in PAF patients and 4.38 ± 0.48 cm in control group. No differences were found between PAF patients with the controls in exercise time (10.38 ± 2.93 vs 10.81 ± 2.75 minutes ); METs (6.98 ± 1.72 vs 7.28 ± 1.75 minutes ); resting heart rate (79.13 ± 14.86 vs 79.69 ± 10.43 bpm ); peak heart rate (146.83 ± 23.21 vs 146.94 ± 16.13 bpm ). Maximum exercise P wave duration and P wave dispersion were greater than the rest measurements in PAF group (respectively P < 0.0001 and P = 0.0004 ). Conclusion: In PAF patients, P wave dispersion is significantly longer at rest, maximum exercise and recovery time than in a control group without PAF.     

消融心房脂肪垫治疗心房颤动的研究现状

近年研究表明,迷走神经过度兴奋与一部分心房颤动的发生密切相关。由于支配心房的迷走神经丛主要分布于心房外膜的脂肪垫中,因此,以心房去迷走神经化为终点的脂肪垫消融成为一项新的心房颤动治疗措施。初步研究的结果显示,该术式治疗心房颤动确实有效,但同时也存在若干弊端。现就消融心房脂肪垫治疗心房颤动的现状作一综述。     

左心耳在预测心房颤动发生脑卒中的作用

成为公共健康沉重负担的心房颤动和相关的血栓栓塞性脑卒中事件仍在以惊人的速度增长。心房颤动导致脑卒中的风险增加了5倍．．因此,预防脑卒中的心房颤动管理仍然是最关键的一方面。现在公认的重点预防措施就是规范抗凝,包括已使用很广泛的华法林和现在出现的新抗凝药如利伐沙班等。而且抗凝药的使用已有据可查。由于左心耳在心房鲡动血栓的发生中起关键作用,所以有目的性地去除或结扎左心耳来预防发生脑卒中就成了一种可替代的治疗方法,尤其是适用于那些不适合口服抗凝药的患者,,现就左心耳预测心房颤动发生脑卒中进行介绍。     

Atrioventricular Nodal Response to Retrograde Activation in Atrial Fibrillation

Atrioventricular Nodal Reset. Retrograde (ventriculoatrial) conduction that reaches the atrioventricular node simultaneous with, or just before an atrial impulse ean facilitate subsequent anterograde conduction. However, a spontaneous or programmed ventricular extrasystule during atrial nbrillation is generally followed by a compensatory pause indicating subsequent delayed anterograde transmission. This characteristic response was used as a model to study the mechanism of atrioventricular nodal behavior during atrial fibrillation. In eight medically-treated patients with chronic atrial fibrillation and a relatively slow but random ventricular response, single premature right ventricular stimuli were delivered after every eighth spontaneous R wave during at least 1 hour. A fixed coupling interval of the ex-trastimulus, considerably shorter than the shortest spontaneous RR interval, was used. The histograms of the postextrasystolic intervals were compared with those of the spontaneous noninterrupted RR intervals. The average postextrasystolic interval was 180 to 300 msec longer than the mean control RR interval, and in six of eight patients, the shape of the histogram of the postextrasystolic cycles was insignificantly different from that of the spontaneous RR intervals. This suggests that In those six patients, the retrograde impulse had reset the random timing cycle of atrioventricular nodal discharge during atrial fibrillation. This observation is compatible with the hypothesis that electrotonically-mediated propagation across a weakly coupled junctional area within the atrioventricular node, rather than decremental conduction and extinction of anterograde atrial impulses at different levels within the node, may be the mechanism of atrioventricular transmission in atrial fibrillation. (J Curdiovasc Electrophysiol, Vol. 1, pp. 437–447, October 1990)