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.     

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.     

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)     

Effects of Amiodarone plus Losartan on Electrical Remodeling in Rapid Atrial Pacing in Rabbits

Objectives To investigate the electrical remodeling and the effects of amiodarone and losartan on electrical remodeling in rapid atrial pacing on rabbit model. Methods 40 normal rabbits were randomly divided into 4 groups ： the saline group （control group）, amiodarone group, losartan group, anti ＋ los group. All rabbits were raised drugs in a week. The atrial effective refractory period （AERP） was measured. Then, take a rapid atrial pacing （600 bpm） and the AERP was measured after 0.5, 1, 2, 4, 6 and 8 hours pacing and 30 minutes after the termination of rapid pacing. Results （1） In control group, after 8 hours rapid pacing, AERP200 and AERP150 were significantly shortened 16. 11% ± 3.1% （ P 〈 0. 01 ） and 9. 99 % ± 4. 2% （ P 〈 0. 01 ）. And the degree of AERP shortening induced by rapid pacing was greater at basic cycle lengths of 200 ms （BCL200） than that at BCL150. The AERP of amiodarone, losartan group and ami ＋ los group were not shortened during rapid pacing. （2） In the control group, after the termination of rapid pacing, the AERP gradually increased. The AERP at all of the BCLS examined recovered to almost the 95.78% and 96. 76% of baseline values within the first 10 minutes and recovered to almost the 99.07% and 99.39% of baseline values within the first 30 minutes. Conclusions Short-term atrial rapid pacing can induce the atrial electrical remodeling. Amiodarone and losartan can prevent the electrical remodeling.     

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.     

Atrial fibrillation: mechanistic insights from biatrial (and triatrial) mapping

Percutaneous radiofrequency ablation of pulmonary vein potentials has been shown to eliminate atrial fibrillation in a subset of patients characterized by frequent and repetitive paroxysms of atrial fibrillation. However, pulmonary vein disconnection has had only limited success at curing patients with persistent atrial fibrillation. In those patients, left atrial substrate modification and linear ablation strategies have had substantially higher success rates. Furthermore, in other patients, elimination of right atrial triggers (superior vena cava) or modification of right atrial substrate has been required for elimination of atrial fibrillation. Finally, the realization that the coronary sinus is a third atrial chamber that can both initiate and maintain atrial fibrillation has provided new understanding to the pathogenesis of atrial fibrillation. From a clinical perspective, only careful anatomic and mapping strategies specifically aimed at each subset of patients with atrial fibrillation will allow for pattern recognition and establish which mechanisms are responsible for initiation and maintenance of atrial fibrillation. Only the latter will allow for increased long-term success rates of ablation 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.     

Electrophysiologic Characteristics of a Dilated Atrium in Patients with Paroxysmal Atrial Fibrillation and Atrial Flutter

This study investigated the difference of atrial electrophysiologic characteristics between a normal and dilated atrium and compared them among patients with paroxysmal atrial fibrillation and flutter. Twenty-seven patients with paroxysmal atrial fibrillation and 28 patients with paroxysmal atrial flutter were divided into four subgroups, according to the presence of a normal atrium or bilateral atrial enlargement. Thirty patients without atrial arrhythmia (20 patients with normal atrium and 10 patients with bilateral atrial enlargement) were included in control group. The atrial refractoriness in patients with a dilated atrium was longer than those with normal atrial size. In patients with paroxysmal atrial fibrillation and patients of control group, the P-wave duration and interatrial conduction velocity with or without atrial enlargement were similar. However, in patients with paroxysmal atrial flutter, P-A_PCS (86 ± 10 ms vs. 73 ± 9 ms, p < 0.05) and P-A_DCS (109 ± 9 ms vs. 95 ± 9 ms, p < 0.05) in patients with a dilated atrium were longer than in patients with a normal atrium. The patients with paroxysmal atrial fibrillation or atrial flutter all demonstrated longer P-wave duration and interatrial conduction time than control group. Among the groups with a normal atrium or a dilated atrium, atrial refractoriness in patients with paroxysmal atrial flutter was shorter than that in control group. Moreover, in the patients with a normal atrium, the potential minimal wavelength in control group (6.6 ± 1.7) was longer than that of paroxysmal atrial fibrillation (5.3 ± 1.1), or atrial flutter (5.0 ± 1.2). These findings suggest that atrial electrophysiologic characteristics of a dilated atrium were different from those of normal atrium, and these changes were different between paroxysmal atrial fibrillation and flutter. Multiple factors are considered to be related to the genesis of atrial tachyarrhythmias.     

Heterogeneous changes in electrophysiologic properties in the paroxysmal and chronically fibrillating human atrium

INTRODUCTION: The regional changes in atrial electrophysiologic properties related to atrial fibrillation (AF) in patients with paroxysmal AF (PAF) and chronic AF (CAF) remain unclear. The purpose of this study was to investigate the regional changes in atrial electrophysiology in patients with AF. METHODS AND RESULTS: We evaluated the atrial electrophysiology at different sites (high right atrium, low right atrium [LRA], and distal coronary sinus [DCS]) in 11 patients with CAF, 8 patients with PAF, and 10 controls. Patients with CAF had significantly prolonged interatrial conduction and corrected sinus node recovery time, and shortened atrial effective refractory period (ERP) with loss of rate-related adaptation in the DCS, but had paradoxic prolongation of atrial ERP in the LRA, as compared with patients with PAF and the controls. As a result, the spatial distribution of atrial ERP that was observed in the controls and in patients with PAF was reversed in patients with CAF, without an increase in the dispersion of atrial refractoriness. Patients with PAF showed intermediate changes in atrial conduction times and atrial refractoriness as compared with patients with CAF and controls. CONCLUSION: There was a regional heterogeneity on the changes of atrial electrophysiology in different parts of the atrium, and the "normal" spatial distribution of atrial refractoriness was reversed in patients with CAF. The electrophysiologic changes observed in patients with PAF appear to behave as if in transition from the control state to CAF, suggesting progressive changes in atrial electrophysiologic properties.     

Implantable Atrial Defibrillators

Implantable Atrial Defibrillators. Due to the limited efficacy of antiarrhythmic drugs for atrial fibrillation, several nonpharmacologic therapeutic options have evolved. One of these is an implantable atrial defibrillator. Recent studies have shown that internal atrial defibrillation is feasible with relatively low energies. To date, the optimal electrode configuration involves large surface area catheters in the right atrium and coronary sinus. In humans, atrial defibrillation can generally be achieved with < 2 J using this electrode configuration and a biphasic shock waveform. For shocks < 5 J, there is no significant pathological damage to the atria or coronary sinus. Further investigation is needed to guarantee that atrial defibrillation shocks do not provoke ventricular arrhythmias. Preliminary data suggest that atrial defibrillation shocks synchronized to R waves that are not closely coupled are safe. In addition, the shocks are well tolerated if the shock energy is < 1.5 J. With additional studies to confirm the safety of implantable atrial defibrillators, further reduce shock energy, and improve patient tolerance, an implantable atrial defibrillator can become an acceptable therapy for patients with symptomatic, paroxysmal atrial fibrillation.     

Atrial fibrosis and substrate based characterization in atrial fibrillation: Time to move forwards

Atrial fibrillation (AF) is the most commonly encountered cardiac arrhythmia in clinical practice. However, current therapeutic interventions for atrial fibrillation have limited clinical efficacy as a consequence of major knowledge gaps in the mechanisms sustaining atrial fibrillation. From a mechanistic perspective, there is increasing evidence that atrial fibrosis plays a central role in the maintenance and perpetuation of atrial fibrillation. Electrophysiologically, atrial fibrosis results in alterations in conduction velocity, cellular refractoriness, and produces conduction block promoting meandering, unstable wavelets and micro-reentrant circuits. Clinically, atrial fibrosis has also linked to poor clinical outcomes including AF-related thromboembolic complications and arrhythmia recurrences post catheter ablation. In this article, we review the pathophysiology behind the formation of fibrosis as AF progresses, the role of fibrosis in arrhythmogenesis, surrogate markers for detection of fibrosis using cardiac magnetic resonance imaging, echocardiography and electroanatomic mapping, along with their respective limitations. We then proceed to review the current evidence behind therapeutic interventions targeting atrial fibrosis, including drugs and substrate-based catheter ablation therapies followed by the potential future use of electro phenotyping for AF characterization to overcome the limitations of contemporary substrate-based methodologies.     

Reduced Peak Atrial Systolic Mitral Annular Velocity Predicts the Development of Nonvalvular Atrial Fibrillation

We investigated whether the echocardiographic parameters of the left atrium (LA) can predict the development of nonvalvular atrial fibrillation (AF). Among 14,062 patients ( > 20 years old) who underwent an echocardiographic examination were evaluated, 2,606 patients who underwent follow-up ECG with an interval of > 6 months were investigated. Newly developed AF was noted in 42 (1.6%) patients with follow-up duration of 31.8 ± 8.9 months. Cox regression analysis revealed that a higher left atrial volume index (hazard ratio [HR ]= 1.06; 95% confidence interval [CI] 1.03–1.09, P < 0.001), relative wall thickness (RWT) of ≥ 0.407 (HR = 2.74, 95% CI 1.39–5.41, P = 0.004), a reduced peak atrial systolic mitral annular velocity (HR = 0.845, 95% CI 0.72–0.99, P = 0.037), and an advanced age (HR = 1.04, 95% CI 1.01–1.07, P = 0.009) were independently related to the development of nonvalvular AF. Therefore, reduced A ' , which is parameter of LA contractile function, might be an important predictor for the development of nonvalvular AF.     

Left atrial isthmus: anatomic aspects relevant for linear catheter ablation procedures in humans

INTRODUCTION: The success rate of catheter maze ablation procedures for atrial fibrillation depends upon adequate electrical isolation by performing linear ablation lesions. However, recurrence of atrial arrhythmias is not uncommon, particularly in the so-called left atrial isthmus, between the orifice of the left inferior pulmonary vein and the mitral valve annulus. The focus of the present study is the anatomy of this area. METHODS AND RESULTS: Twenty human hearts were studied. The distance between the left inferior pulmonary vein and the mitral valve, the thickness of the left atrial myocardium, and the extent of left atrial myocardium toward the mitral valve were measured. The AV groove contained a fat pad harboring the great cardiac vein. The distance between the vein and the valve varied considerably (range 17-51 mm). The great cardiac vein coursed along the inferior left atrial wall, approximately 1 cm above the level of the mitral valve. Myocardial thickness also varied considerably (distal: range 1.4-7.7 mm, midway: range 1.2-4.4 mm, proximal: range 0-3.2 mm). Left atrial myocardium extended onto the mitral valve in two hearts, and the left atrial myocardium ended above the level of the mitral valve (range 1.8-5.1 mm) in six hearts. An important variable because it raises the question of how much energy should be used--and at which point--to achieve an adequate transmural ablation line. CONCLUSION: The great cardiac vein is not an adequate marker for the level of the mitral valve, left atrial myocardium may continue onto the mitral valve, the distance between the left inferior pulmonary vein and mitral valve varies considerably, and left atrial myocardial thickness is highly variable and not uniform.     

The Impact of the Distance between the Atrial Electrode and the Atrial Wall on Atrial Undersensing in Patients with VDD Pacemakers: Long‐Term Follow‐Up

Aim: Atrial undersensing (AUS) in single‐lead VDD pacemakers may be due to diminished P‐wave amplitude secondary to local inflammation beneath the electrodes closer to atrial wall. The aim of this study was to assess the potential effect of distance between atrial electrode and atrial wall on immediate and long‐term atrial sensing stability in VDD systems. Methods: A total of 275 patients with normal sinus node function who received VDD pacemakers were enrolled into the study and were followed up for a median duration of 33 months. During each control visit, a standard 12‐lead electrocardiogram (ECG) was obtained and standard pacemaker function assessment was performed including testing for pacing threshold and atrioventricular synchrony. The distance between atrial electrode and atrial wall was measured from chest X‐ray. Results: Of the 275 patients, AUS was detected in 59 patients. Univariate predictors of AUS were use of closely spaced bipolar ring atrial electrode (CSBR) (P = 0.01), wider atrial ring‐spacing (P = 0.03), and atrial sensitivity programmed to a higher level (P = 0.001). Use of CSBR (P = 0.04) and atrial sensitivity ≥0.3 mV (P = 0.02) were observed to be the independent predictors for AUS. When the distance between atrial electrode and atrial wall was <7 mm, AUS was less with diagonally arranged bipolar ring electrodes (DABR) than it was with CSBRs (P = 0.02). Conclusions: The distance between atrial electrode and atrial wall does not appear to affect AUS incidence in VDD pacemakers. For VDD electrodes closer to atrial wall, AUS was significantly less likely in DABR‐type electrodes.