心动过速性心房心肌病

近年来，动物实验研究表明，快速心房起搏以及由此诱发的心房纤维颤动，在完全性房室传导阻滞情况下，可单独引起心房的代谢、电、收缩及解剖重构，引起心动过速性心房心肌病。认识该病有很大临床意义。     

心房顿抑与房颤后心房重构

心房颤动(房颤)复律后左房机械功能异常,其后将房颤恢复窦性心律时出现一过性的左心房和左心耳机械功能的异常称为心房顿抑,发生率约为38%～80%。房颤持续时间越长,心房顿抑越严重、持续时间越长,更易形成心耳血栓及房颤复发。近年研究提示,造成心房顿抑的原因与房颤后的心房重构有关。房颤诱导心房发生重构包括电重构、结构重构及缝隙连接重构。缝隙连接重构与心房电重构、结构重构均有关联,参与房颤的发生与持续,可能是心房顿抑发生的原因之一。本文就心房顿抑及与房颤后心房重构的关系进行综述,并对未来的研究方向作一展望。     

心房纤颤心房重构研究进展

心房纤颤是最常见的心律失常之一 ,对其发生及维持机制的研究业已成为热点。本文就近几年来心房纤颤与心房重构的关系及心房重构可能机制的研究加以综述     

心房顿抑与房颤后心房重构

心房颤动(房颤)复律后左房机械功能异常,其后将房颤恢复窦性心律时出现一过性的左心房和左心耳机械功能的异常称为心房顿抑,发生率约为38%～80%.房颤持续时间越长,心房顿抑越严重、持续时间越长,更易形成心耳血栓及房颤复发.近年研究提示,造成心房顿抑的原因与房颤后的心房重构有关.房颤诱导心房发生重构包括电重构、结构重构及缝隙连接重构.缝隙连接重构与心房电重构、结构重构均有关联,参与房颤的发生与持续,可能是心房顿抑发生的原因之一.本文就心房顿抑及与房颤后心房重构的关系进行综述,并对未来的研究方向作一展望.     

心动过速性心房心肌病

近年来，动物实验研究表明，快速心房起搏以及由此诱发的心房纤维颤动，在完全性房室传导阻滞情况下，可单独引起心房的代谢、电、收缩及解剖重构，引起心动过速性心房心肌病。认识该病有很大临床意义。     

炎症与房颤结构重构的关系研究

心房重构,特别是结构重构是房颤发生和发展的核心环节.主要表现为心房肌肥厚、扩大、纤维化.研究表明炎症可能参与了房颤的发生.本文拟探讨炎症对心房结构重构及房颤发生的作用.     

缬沙坦对心房快速起搏犬心房电、结构和功能重构的影响

心房颤动（AF）使心房发生电、结构和功能重构，促进AF发作并持续。新近研究提示，AF时心房重构与心房肌肾素-血管紧张素系统（RAS）激活关系密切。本研究观察缬沙坦对AF犬心房重构的防治作用。     

电与结构重构在心房纤颤合并心力衰竭中的作用

心房纤颤（房颤）与慢性充血性心力衰竭（心衰）常合并存在导致心房结构和功能的改变，称之为心房重构。由于血流动力学和神经体液的影响，房颤可能是慢性心衰的结果，也可能是心衰的原因。我们回顾2者所致心房重构的实验和临床资料，对其相互关系做进一步探讨。     

肾素-血管紧张素系统与心房颤动

心房颤动(AF)是一常见的心血管疾病,心房重构是AF维持和复发的主要机制,肾素-血管紧张素-醛固酮系统(RAAS)在心房重构中起重要作用。作用于RAAS的一些药物具有抑制心房重构的作用并减少AF的发作,给AF的治疗提供了一个新的思路。本文对RAAS在心房重构中的作用,及其拮抗剂对心房重构及AF的影响作一综述。     

心房重构研究进展

心房重构是心房颤动（房颤）发生和维持的重要因素,包括电重构和结构重构。近年来心房重构机制研究逐渐深入,针对心房重构的房颤上游治疗成为研究热点。该文针对心房重构机制的研究进展和相关治疗作一综述。     

Atrial vulnerability.

The electrophysiologic substrates of atrial flutter and fibrillation (AFF) have been studied in patients with paroxysmal arrhythmias. Atrial repetitive responses to extrastimuli are a nonspecific response, even though they can precipitate AFF. AFF inducibility is rather sensitive, but not very specific, in separating patients from controls. There is no established protocol to explore vulnerability in this fashion. Atrial refractoriness is abnormal in some patients. Some authors have found a tendency toward short effective refractory periods (AERP) and others have found a poor adaptation of AERP to decreases in cycle length. Unfortunately, these abnormalities are neither sensitive nor specific enough. Atrial conduction may be abnormal basally, but subtler abnormalities are shown by premature stimulation. Early extrastimuli are conducted with increased conduction delays in patients with paroxysmal AFF in relation to controls. Again, there is not enough sensitivity and specificity in the findings to make them of diagnostic value. Electrophysiologic abnormalities are detectable in patients with AFF, but larger studies, including reproducibility and the effect of drugs on the abnormal parameters, will be necessary to develop clinical applications.     

Importance of right and left atrial dilation and linear ablation for perpetuation of sustained atrial fibrillation

INTRODUCTION: Atrial dilation associated with increasing atrial pressure plays an apparent role in the development of atrial fibrillation (AF). We characterized a new model of separate and biatrial dilation in the Langendorff-perfused rabbit heart. The aim of this study was to examine if sustained AF in this model (1) would be inducible by separate right atrial (RA) and left atrial (LA) dilation; (2) would be reproducibly inducible at the same pressure level; and (3) could be suppressed by RA, LA, or biatrial ablation. METHODS AND RESULTS: Intra-atrial pressure was increased stepwise in the RA (n = 13), LA (n = 12), or both atria (n = 25) until sustained AF could be induced or a pressure of 20 cm H2O was reached. The stimulation protocol was repeated once in RA and LA dilation (n = 9) and three times in biatrial dilation (n = 7). Then, RA orifices (superior and inferior caval veins, tricuspid valve annulus, and foramen ovale) or LA orifices (pulmonary veins, mitral valve annulus, and foramen ovale) were connected by radiofrequency (RF) lesions. Sustained AF was rendered inducible in 100% of hearts with biatrial dilation, but in only 92% of hearts with RA dilation and 67% with LA dilation. Inducibility of sustained AF was reproducible. Under biatrial dilation, not RA ablation (0/10 hearts; P = NS) but LA ablation (4/11 hearts; P < 0.05) and biatrial ablation (16/21; P < 0.01) reduced the inducibility of sustained AF. CONCLUSION: The inducibility of sustained AF due to increased intra-atrial pressure differs between the RA and LA. LA and biatrial lesions, not RA RF lesions, reduce the ability to perpetuate sustained AF.     

Implantable Atrial Defibrillator and Detection of Atrial Flutter

The implantable atrial defibrillator (IAD) is designed to detect and treat atrial fibrillation (AF) with low energy synchronized shocks. A patient with a history of persistent AF was implanted with an IAD after ineffective treatment with procainamide and sotalol. Through four months of follow-up, the IAD performed appropriate detection and treatment of AF. During the fifth month, the patient was put on flecainide in an attempt to minimize the AF recurrence rate. On flecainide the patient experienced typical atrial flutter which required IAD reprogramming for appropriate detection and therapy delivery. This case report examines the optimization of the IAD to detect atrial flutter. Six months of follow-up after optimization the IAD has shown appropriate detection of both atrial flutter and AF. During the entire follow-up period the IAD had appropriate detection of sinus rhythm (no false positive detection, i.e. sinus rhythm as AF).     

Atrial Electrograms and Activation Sequences in the Transition Between Atrial Fibrillation and Atrial Flutter

Transition Between Atrial Fibrillation and Flutter. Introduction: The eletrophysiologic mechanism of atrial fibrillation (AF) has a wide spectrum, and it seems that some atrial regions are essential for the occurrence of a particular type of AF. We focused on one type of AF: AF associated with typical atrial flutter (AFI), which was right atrial (RA) arrhythmia, and sought to investigate intra-atrial electrograms and activation sequences in the transition between AF and AFL.
Methods and Results: Intra-atrial electrograms and activation sequences in the R.A free wall and the septum were evaluated in the transition between AF and AFL in seven patients without organic heart disease (all men; mean age 57 ± 11 years). In five episodes of the conversion of AFL into AF, the AFL cycle length was shortened (from 211 ± 6 msec in stable AFL to 190 ± 15 msec before the conversion, P, 0.001). Interruption of the AFL wavefront and an abrupt activation sequential change induced by a premature atrial impulse resulted in fractionation and disorganization of the septal electrograms. During sustained AF, septal electrograms were persistently fractionated with disorganized activation sequences. However, the RA free-wall electrograms were organized, and the activation sequence was predominantly craniocaudal rather than caudocranial throughout AF. In 12 episodes of the conversion of AF into AFL, the AF cycle length measured in the RA free wall increased (from 165 ± 26 msec at the onset of AF to 180 ± 24 msec before the conversion, P, 0.001). AFL resumed when fractionated septal electrograms were separated and organized to the caudocranial direction, despite the RA free-wall electrograms remaining discrete and sharp with an isoelectric line.
Conclusion: Changes of the electrogram and activation sequence in the atrial septum played an important role in the transition between AF and AFL.     

Characterization of Atrial Activation (A‐A) Intervals During Atrial Fibrillation Due to a Single Driver: Do They Reflect Atrial Effective Refractory Periods?

Characterization of Atrial Activation Intervals During AF . Background: The mean, median, and minimum local atrial activation (A‐A) intervals have been used to determine the local atrial effective refractory period (AERP) during atrial fibrillation (AF), the underlying assumption being that AF is due to multiple reentrant wavelets. Objective: We tested the hypothesis that when AF is due to a single, rapid, stable reentrant circuit (driver), the minimum and mean local A‐A intervals will be similar at sites in the reentrant circuit, but will vary widely at sites with fibrillatory conduction, making these latter intervals unreliable indicators of AERP. Methods: During sustained AF due to a left atrial (LA) driver in 6 sterile pericarditis dogs, electrograms were recorded from 186 bipolar electrodes from both atria. A‐A intervals were measured from each recording site during 1.2 seconds of AF. Minimum A‐A intervals as well as temporal (within site) and spatial (between sites) variability were determined from all sites. Results: A‐A intervals from each site during AF demonstrated that (1) 90–100% of right atrial (RA) sites and 18–39% of LA sites showed considerable (SD > 6 ms) temporal variability; (2) RA and LA sites with fibrillatory conduction (SD > 6 ms) showed considerable (a) spatial variability (RA: 9–36 ms; LA: 5–27 ms) and (b) variability of the minimum A‐A intervals (RA: 14–35 ms; LA 11–28 ms). Conclusion: During AF due to a driver, areas with fibrillatory conduction manifested considerable variability in the mean and the minimum A‐A intervals. Therefore, it is unlikely that any of the A‐A intervals reflect AERP. (J Cardiovasc Electrophysiol, Vol. 22, pp. 310‐315, March 2011)     

Pharmacological Atrial Defibrillation via Temporarily Occluded Coronary Sinus: First clinical experience and implications for an implantable device

The aim of this paper is to report the first experience of pharmacological atrial defibrillation in humans via a temporarily occluded coronary sinus.Patients and methods: In 6 patients (3 women, 3 men; mean age 57.8y, min 31, max 71), with clinical recurrences of atrial fibrillation, an occlusive coronary venogram was carried out in order to establish the origin of the Vein of Marshall. Atrial fibrillation was then induced by atrial pacing in all the patients and after an adequate waiting period to assure that the atrial fibrillation episode was persistent and stable, a bolus of a very low dose of an antiarrhythmic drug was delivered in 3–4 seconds into the temporarily balloon occluded coronary sinus near the orifice of the vein of Marshall. For both the venogram and the pharmacological test a Baim-Turi (USCI-Bard, Billerica MA) or a Vueport (Cardima, Fremont CA) catheter was used.Results and comments: In five patients a single dose of 7mg of propafenone was immediately effective in restoring the sinus rhythm. In the remaining patient 2 doses of 7mg of propafenone failed to interrupt the arrhythmia, which was subsequently interrupted by a bolus of 0.1mg of ibutilide fumarate given after a waiting period of 20 minutes. Retroperfusion of the left atrium could account for these results; in fact the Vein of Marshall has no valvular apparatus in contrast with other coronary sinus tributary veins which are equipped with an uni- or bicuspidal valve.Conclusions: Pharmacological atrial defibrillation with a minimal dose of an antiarrhythmic drug delivered near the orifice of the Vein of Marshall via the temporarily occluded coronary sinus is feasible and effective. This new pharmacological atrial defibrillation can offer interesting opportunities in developing an implantable pharmacological atrial defibrillator.     

Conduction Barriers in Human Atrial Flutter:

Barriers in Atrial Flutter. Animal models of atrial flutter and early mapping studies of human atrial flutter have suggested the importance of barriers in this reentrant arrhythmia. The consistency of rate and morphology of typical atrial flutter suggest a common anatomic substrate for this arrhythmia. The unique endocardial architecture of the right atrium provides anatomic barriers around which reentry occurs. In typical human atrial flutter, the crista terminalis, eustachian ridge, and tricuspid annulus have been identified as barriers to conduction. The importance of conduction barriers, methodology for defining barriers, the anatomic substrate for these barriers, and the role of these barriers in other atrial arrhythmias are discussed.     

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.     

Do the Left Atrial Substrate Properties Correlate with the Left Atrial Mechanical Function? A Novel Insight from the Electromechanical Study in Patients with Atrial Fibrillation

Background: The atrial substrate is the determinant of occurrence and maintenance of atrial fibrillation (AF), which can induce remodeling of atrial function and structure. This study investigated the relationship between the left atrial (LA) substrate properties and LA mechanical function.
Methods: Forty-four consecutive patients (50.3 ± 10.7 years old, 33 men) who presented with sinus rhythm during echocardiographic study before receiving catheter ablation for AF were enrolled. The LA diameter, LA volume, ratio of early and late transmitral filling flow velocities (E/A), LA appendage flow velocity, and transmitral velocity-time integral (VTI) were measured by the echocardiography. The LA empty fraction (LAEF), which was obtained via dividing the difference between maximal and minimal LA volume by maximal LA volume, was calculated as a parameter of the global LA contractile function. The LA global contact voltage mapping (NavX system) was performed before pulmonary vein isolation.
Results: Mean LA voltage and LA low voltage zone index (LVZ index, area with voltage < 0.5 mV, divided by total LA surface area) showed significant correlation with LA diameter and volume, but only the LA LVZ index showed significant correlation with A-wave velocity, transmitral A-wave VTI, and LAEF (r =–0.340, –0.411, –0.426; P = 0.024, 0.006, 0.005, respectively). We divided the LA LVZ index into three groups (< 10%, 10–20%, > 20%). The LAEF got worse and the transmitral A-wave VTI percentage (divided by transmitral VTI) decreased as LA LVZ index increased.
Conclusions: The LA substrate properties showed close correlation with LA size, but only the LA LVZ index correlated with the LA mechanical function.