Left Atrial Voltage during Atrial Fibrillation in Paroxysmal and Persistent Atrial Fibrillation Patients

Background: Left atrial (LA) endocardial voltage characteristics assessed during atrial fibrillation (AF) have not been previously compared in different AF types. This study was aimed at investigating the LA voltages and volumes in patients with paroxysmal and persistent AF. Methods: LA electroanatomic voltage maps acquired during AF were compared between consecutive patients without major structural heart disease undergoing first catheter ablation for paroxysmal AF (n = 100) or persistent AF (n = 100). The groups were comparable in baseline clinical characteristics. Results: Patients with persistent AF presented with lower median LA voltage (median 0.41, interquartile range [IQR] 0.31–0.51 mV versus median 0.99, IQR 0.47–1.56 mV; P < 0.001), and maximum LA voltage (4.07 ± 1.76 vs 6.42 ± 2.16 mV; P < 0.001). They also had a higher proportion of the LA points exhibiting voltage <0.2 mV (30 ± 20 vs 12 ± 11%; P < 0.001) and voltage 0.2–1.0 mV (55 ± 15 vs 42 ± 19%; P < 0.001). They further displayed higher LA volume/body surface area (75 ± 16 vs 58 ± 13 mL/m²; P < 0.001). In the multivariate regression model, both LA voltage (P < 10^?9) and LA volume (P < 10^?5) were significant determinants of AF type. Conclusion: Patients with persistent AF had significantly lower LA voltage compared with patients with paroxysmal AF even after adjustment for differences in indexed LA volume. LA voltage represents an independent covariate of clinical manifestation of AF. (PACE 2010; 541–548)     

Three-Dimensional Distribution of Bipolar Atrial Electrogram Voltages in Patients with Congenital Heart Disease

DE GROOT, N.M.S., et al. : Three‐Dimensional Distribution of Bipolar Atrial Electrogram Voltages in Pa‐tients with Congenital Heart Disease. Voltage differences might be used to distinguish normal atrial tissue from abnormal atrial tissue. This study was aimed at identifying lowest voltage areas in patients with atrial tachycardia after surgical correction of congenital heart disease and to evaluate if identification of these areas in diseased hearts facilitates selection of critical conduction pathways in reentrant circuits as target sites for catheter ablation. Ten patients (four men, age 39 ± 15 years ) with normal sized atria and atrioventricular reciprocating tachycardia (control group) and ten patients (5 men, 32 ± 7 years ) with congenital heart disease and postoperative atrial tachycardia (CL 281 ± 79 ms ) referred for radiofrequency catheter ablation were studied. Mapping and ablation was guided by a three‐dimensional electroanatomic mapping system (CARTO) in all patients. In the control group, voltage maps were constructed during sinus rhythm and during tachycardia to evaluate the voltage distribution. The amplitude of bipolar signals was 1.90 ± 1.45 mV (0.11–8.12 mV, n = 660 ) during sinus rhythm and 1.45 ± 1.66 mV (0.12–5.83 mV, n = 440, P < 0.05 ) during atrioventricular reciprocating tachycardia. In the study group, the amplitude of 1,962 bipolar signals during tachycardia was 1.01 ± 1.19 mV (0.04–9.40 mV ), which differed significantly from the control group during tachycardia (P < 0.0001). No significant difference in the tachycardia cycle length was found (P < 0.05) between the control and study groups. As the lowest voltage measured in normal hearts was 0.1 mV, this value was used as the upper limit of the lowest voltage areas in the patients with congenital heart disease. These areas were identified by detailed voltage mapping and represented by a gray color. Activation and propagation maps were then used to select critical conduction pathways as target sites for ablation. These sites were characterized by fragmented signals in all patients. Ablation resulted in termination of the tachycardia in eight (80%) of ten patients. Complications were not observed. Identification of the lowest voltage areas using a cut‐off value of 0.1 mV in congenital heart disease patients with postoperative atrial reentrant tachycardia facilitated the selection of critical conduction pathways as target sites for ablation.     

Atrial Pressure and Experimental Atrial Fibrillation

SIDERIS, D.A., et al .: Atrial Pressure and Experimental Atrial Fibrillation . A possible profibrillatory effect on the atria of an elevated atrial pressure and the site of atrial stimulation was examined. In 15 anesthetized dogs, right or left atrial or biatrial pacing was applied at a high rate (300–600/min) for 5 seconds at double threshold intensity under a wide range of atrial pressures achieved by venous or arterial transfusion or bleeding. Induction of atrial fibrillation in 236 of 1,971 pacing runs was associated with a significantly higher (P < 0.001) atrial pressure (21.6 ± 12.2 mmHg, mean ± SD) than maintenance of sinus rhythm (16.8 ± 11.1 mmHg in 1,735 of 1,971 pacing runs). Stimulation of the right atrium resulted in atrial fibrillation more frequently than left atrial or biatrial stimulation, with biatrial stimulation less frequent than right or left atrial stimulation. The induction of atrial fibrillation was related to the atrial pressure and to the site of stimulation but not to the pacing rate or the prepacing heart rate. The prepacing heart rate, associated with failure to induce sustained atrial fibrillation, was higher than that associated with atrial fibrillation in 12 of 15 experiments (significantly in 6) and not significantly lower in 3 of 15. Atrial fibrillation lasting 1 minute or more was more frequently associated with simultaneous stimulation of both atria than of either atrium alone. Thus, an elevated atrial pressure may facilitate the induction of atrial fibrillation. The site of stimulation also plays an important role for both the induction and maintenance of atrial fibrillation in this model.     

Persistent Atrial Standstill with Atrial Inexcitability

Electrophysiologic studies including His bundle recording, atrial, and ventricular stimulation, were performed in three symptomatic patients with persistent atrial standstill of unknown etiology. The rhythm was junctional in two cases and ventricular in one. In two cases, evidence suggestive of associated impairment of the His bundle conduction system was found. The atria were inexcitable at multiple sites and no retrograde conduction to the right atrium could be elicited by ventricular pacing. Follow-up in the three cases, respectively for 48, 42 and 12 months after pacemaker implantation, revealed no return of spontaneous atrial electrical activity.     

Atrial and Ventricular Pressures in Atrial Flutter

The hemodynamic effects of atrial flutter (AF) are unknown. The purpose of the present study was to investigate the changes in atrial and ventricular pressures after induction of AF. In 23 patients with paroxysmal AF (age 59 ± 9 years), a hemodynamic study was performed both during sinus rhythm and after induction of the tachyarrhythmia. During AF, 13 patients showed a fixed 2:1 AV conduction and 10 patients showed variable conduction. Mean right and left atrial pressures increased (P < 0.001) and right and left ventricular end-diastolic pressures decreased (P < 0.001) after induction of AF. Roth the increase in mean atrial pressures and the decrease in ventricular end-diastolic pressures were present either in the patients with fixed 2:1 AV (heart rate: 133 ± 15 beats/min) or in those with variable conduction (heart rate 96 ± 15 beats/min), but were more marked in the former. AF produces an impairment of atrial function, as evidenced by the increase in mean atrial pressures and reduction in ventricular end-diastolic pressures in the absence of an elevated heart rate. The mechanisms responsible for the increase in mean atrial pressures are unknown; however, atrial contractions against closed AV valves seem to play an important role.     

Familial Atrial Standstill with Coexistent Atrial Flutter

A child with familial atrial staudstill and a ventricular pacemaker had syncope due to atrial flutter that was treated bv His-bundle ablation. Bradycardia protection alone may be insufficient in patients with atrial standstill.     

Atrial Septal Versus Atrial Appendage Pacing:

HERMIDA, J.-S., et al. : Atrial Septal Versus Atrial Appendage Pacing: Feasibility and Effects on Atrial Conduction, Interatrial Synchronization, and Atrioventricular Sequence. Atrial septal (Se-P) and atrial appendage pacing (Ap-P) were compared in a randomized, controlled study to assess the feasibility, the reliability, and the effects of Se-P on atrial conduction, interatrial synchronization, and the AV sequence. The main baseline characteristics of the patients were comparable in both groups. There was no difference in feasibility or reliability between the two techniques. Compared to Ap-P   (n = 28)   , Se-P   (n = 28)   decreased the P wave duration, left atrial electromechanical delay (LAEMD), and interatrial interval (−1.6% vs   +28%, P < 0.001; −3%   vs   + 30%, P < 0.001; −130%   vs   + 78%, P < 0.001   ); it induced a smaller increase of the right AEMD, a slight reversal of the timing of the atrial systoles and a shortening of the PR interval (−13% vs   + 25%, P < 0.001   ) and of the interval separating atrial systoles from ventricular activation. Finally, the shortening of the PR interval was smaller during high Se-P versus low Se-P. Se-P avoids the undesirable prolongation of the atrial, interatrial, and AV conductions observed during Ap-P. In addition, Se-P creates a slight reversal of the timing of the atrial systoles and induces a shortening of PR interval, the extent of which could depend on the height of the pacing site on the septum. (PACE 2003; 26[Pt. I]:26–35)     

Atrial Refractory Periods after Atrial Premature Beats in Patients with Paroxysmal Atrial Fibrillation

To study the effects of an atrial premature beat on atrial refractory periods, we investigated 11 patients (group A) who were the control group, 12 patients suffering from paroxysmal atrial fibrillation (group B), and 10 patients (group C) without arrhythmias but with cardiopathy or cardiomyopathy. At every eighth complex of a constant atrial electrostimulated rhythm a fixed premature extrastimulus was introduced, and effective and functional refractory periods (ERP and FRP) were measured in three different sites of the right atrium, before and after introduction of this extrastimulus. Average ERP and FRP shortened respectively in group A, from 220.28 ± 25.68 msec and 281.17 ± 28.15 msec before extrastimulation, to 190.58 ± 22.74 msec and 245.88 ± 19.86 msec after; in group B, from 219.44 ± 27.38 msec and 284 ± 30.06 msec to 191.66 ± 28.72 msec and 253.23 ± 34.01 msec; and in group C from 229.03 ± 29.65 msec and 289.67 ± 51.62 msec to 194.19 ± 24.6 msec and 237.74 ± 39.59 msec. The average dispersions of ERP and FRP in group A were, respectively: 41.81 ± 21.36 msec and 36.36 ± 18.04 msec before extrastimulation, 28.18 ± 18.14 msec and 35.45 ± 15.72 msec after. In group B: 26.66 ± 19.46 msec and 41.66 ± 16.96 msec versus 45.83 ± 23.91 msec and 45 ± 34.77 msec and in group C: 27 ±11.59 msec and 45 ± 29.15 msec versus 29 ± 18.52 and 27 ± 18.88. It is concluded that an atrial premature beat tends to shorten the dispersion of atrial refractory periods when patients are free of arrhythmias, and to lengthen them when paroxysmal atrial fibrillation are documented.     

Comparison of Arrhythmogenicity of Atrial Pacing at Several Right Atrial Pacing Sites: Evaluation of Canine Atrial Electrograms During Atrial Pacing and Arrhythmogenicity for Atrial Fibrillation

The changes in the duration of atrial electrograms and the appearance of AF during atrial pacing were compared among five atrial pacing sites in dogs to clarify the arrhythmogenicity of atrial pacing at different atrial pacing sites. In seven mongrel dogs (15–20 kg), the right atrial surface was exposed by right thoracotomy. Atrial electrograms were recorded via bipolar electrodes with an interelectrode distance of 1.2 mm at four right atrial sites: (1) the high right atrium (HRA), (2) the mid-right atrium (MRA), (3) the low right atrium (LRA), and (4) the center of the pectinate muscle (PM). The duration of the atrial electrograms at these four recording sites were measured during atrial pacing with fixed cycle lengths of 200, 150, and 120 ms delivered at five atrial sites: (1) the HRA, (2) the inferior vena cava (IVC), (3) the right atrial appendage (RAA), (4) Bachman's bundle (BB), and (5) the atrial septum (AS). In each dog, the atrial pacing with the 120-ms cycle length was performed five times at each pacing site to evaluate the in-ducibility of AF. When AF was induced, the atrial recording site which first showed a fragmented atrial electrogram was considered the initiation site of the AF. AF was induced during 9 of 35 episodes of atrial pacing at the HRA site, 11 of 35 at the IVC site, 5 of 35 at the RAA site. 3 of 35 at the BB site, and none at the AS site. The initiation site of AF was in the HRA site in 11 of 28 episodes of induced AF, in the MRA site in 9 of 28, and in the LRA site in 8 of 28. At each recording site, the shorter the paced cycle length, the longer the duration of the atrial electrogram regardless of the pacing site. During the atrial pacing with the 200-ms cycle length, the HRA pacing resulted in the shortest duration of the atrial electrogram at each recording site in comparison with the other pacing sites. However, during atrial pacing at the two shorter paced cycle lengths, the duration of the atrial electrogram was shorter during the pacing at the BB or AS sites in comparison with the other three pacing sites, i.e., the HRA, IVC, and RAA sites. These results were the same for all atrial recording sites, but the prolongation of the atrial electrogram was most prominent at the HRA and MRA recording sites, which are most likely initiation sites of the induced AF. In the canine atria, (1) the initiation sites of AF were likely to be the HRA, MRA, or LRA sites in comparison with the PM site; and (2) the atrial pacing at the BB or AS sites was considered less arrhythmogenic for AF than the pacing at the HRA, LRA, or RAA sites.     

Right Atrial Separation Procedure for Eliminating Chronic Atrial Fibrillation Associated with Atrial Septal Defect

Chronic atrial fibrillation (AF) had been documented in a patient with atrial septal defect for 7 years. A right atrial separation procedure was performed for ablation of chronic AF, concomitant with repair of the atrial septal defect, and followed by atrial electrophysiological mapping. A horizontal transectional incision extending to the borders of the atrial septum and the tricuspid annulus was made. Cryolesions of the atrial isthmus between the margin of the upper incision and the tricuspid valve annulus were created at -60†C for 2 minutes at a time. After the operation, the patient had restored normal sinus rhythm during a subsequent follow-up period of 48 months.     

Atrial fibrillation

Atrial fibrillation (AF) results from the chaotic depolarization of atrial tissue and is the most common dysrhythmia diagnosed in United States (US) emergency departments. AF affects greater than 1% of the general population, with a peak prevalence of 10% in those greater than 80 years of age. By 2050, it is estimated that nearly 16 million US patients will suffer from AF. AF has significant health effects, and places a considerable economic burden on the health care system. This article discusses recommendations that are derived from a combination of existing guidelines, additional evidence, and consensus.     

Atrial Dissociation After Atrial Compartment Operation for Chronic Atrial Fibrillation in Mitral Valve Disease

Atrial dissociation with segmental atrial arrhythmia is an interesting electrophysiological phenomenon. It was rarely reported before to be caused by anatomical exit block after cardiac surgery. We report the case of a 28-year-old patient who developed atrial dissociation after a surgical method for correcting atrial fibrillation—atrial compartment operation. The segmental atrial flutter was first found by Doppler echocardiography and proved later by detailed intracardiac mapping.     

Atrial flutter

Atrial flutter is a supraventricular tachydysrhythmia believed to arise from electrophysiologic disturbances in the atria. It tends to be an unstable rhythm and is usually associated with intrinsic cardiac or pulmonary disease or adverse extrinsic influences on the heart. It is due to either a reentry mechanism or an increased atrial automaticity. Atrial depolarization is regular at a rate of 260 to 340 beats per minute. With a normal atrioventricular (AV) node there is usually a physiologic second-degree block with resultant 2:1 conduction. Higher degrees of AV block can occur in patients with AV nodal disease, increased vagal tone, or when certain drugs are in use. One-to-one conduction may occur in patients with accessory AV nodal pathways. In this situation, serious adverse effects are often seen, including palpitations, dizziness, syncope, angina, and dyspnea. Electrical cardioversion is the safest and most reliable way of terminating atrial flutter and its use should not be delayed in an unstable patient. In the nonemergent situation a variety of medications alone or in combination can be used to convert the rhythm or slow ventricular response.