High Right Atrium Pacing Research Articles

A work flow to build and validate patient specific left atrium electrophysiology models from catheter measurements.

Biophysical models of the atrium provide a physically constrained framework for describing the current state of an atrium and allow predictions of how that atrium will respond to therapy. We propose a work flow to simulate patient specific electrophysiological heterogeneity from clinical data and validate the resulting biophysical models. In 7 patients, we recorded the atrial anatomy with an electroanatomical mapping system (St Jude Velocity); we then applied an S1-S2 electrical stimulation protocol from the coronary sinus (CS) and the high right atrium (HRA) whilst recording the activation patterns using a PentaRay catheter with 10 bipolar electrodes at 12 ± 2 sites across the atrium. Using only the activation times measured with a PentaRay catheter and caused by a stimulus applied in the CS with a remote catheter we fitted the four parameters for a modified Mitchell-Schaeffer model and the tissue conductivity to the recorded local conduction velocity restitution curve and estimated local effective refractory period. Model parameters were then interpolated across each atrium. The fitted model recapitulated the S1-S2 activation times for CS pacing giving a correlation ranging between 0.81 and 0.98. The model was validated by comparing simulated activations times with the independently recorded HRA pacing S1-S2 activation times, giving a correlation ranging between 0.65 and 0.96. The resulting work flow provides the first validated cohort of models that capture clinically measured patient specific electrophysiological heterogeneity.

The effect of atrial pacing site on electrophysiological properties of the atrioventricular junction and induction of atrioventricular nodal reentry in patients with typical atrioventricular nodal reentrant tachycardia.

Clinical studies in humans have shown the site of atrial stimulation to influence atrioventricular (AV) conduction times and refractory periods, the demonstration of dual AV nodal (AVN) pathways, and induction of AVN reentry. These studies often found conflicting results. Moreover, among enrolled patients a minority of them were found to have AVN reentrant tachycardia (AVNRT). The purpose of this study was to investigate the effect of right and left atrial pacing on the electrophysiological properties of the AV junction in the typical AVNRT population. Ninety-two consecutive patients with typical AVNRT were included. Atrial pacing was performed from the high right atrium (HRA) and the left atrium via the proximal coronary sinus (CS). Stimulation from either the HRA or the CS could result in dual AVN physiology and AVNRT. No site-dependent differences in the ease of induction of dual AVN pathways with variability of initiation from either site were found. However, AVNRT was easier to induce from the HRA. With CS pacing the leftward but not the rightward AVN approaches were the entry point to the AV node because of significantly shorter AH conduction times compared to HRA pacing. Conduction over the leftward AVN extensions could initiate the tachycardia with significantly shorter critical AH interval compared to conduction over the rightward AVN extensions; however, the AH interval during AVNRT and its cycle length were not significantly different. Rightward and leftward AVN extensions are regular features of the AV node. Their different electrophysiological properties lead to variation in the demonstration of discontinuous AVN conduction and AVNRT during right and left atrial pacing. Despite the observation that the left AVN extensions could compose the entry point to the reentrant circuit, there is no evidence that they constitute the critical component of sustained typical AVNRT.

The utility of atrial pacing for identifying the electrical breakthrough sites between the left atrium and pulmonary veins

BackgroundCircumferential pulmonary vein (PV) isolation for atrial fibrillation (AF) is occasionally difficult to achieve because electrical breakthrough sites (EBSs) between the left atrium (LA) and PVs cannot be identified during ablation especially in the carina regions. MethodsThe left PVs (Lt.PVs) of 60 AF patients and the right PVs (Rt.PVs) of 37 patients undergoing PV isolation were studied. When PV isolation was not achieved after the initial circumferential PV isolation, atrial pacing was repeatedly performed from the distal coronary sinus (CSd) and high right atrium (HRA), and the time interval from the stimulus to the earliest PV potential (stimulus-PV interval) was measured using circular mapping catheters at each PV until PV isolation was achieved. When PV isolation was achieved via local Radiofrequency (RF) deliveries, those regions were diagnosed as final EBSs. We classified the final EBSs into six segments for each PV (anterior and posterior PV walls of the roof, carina, and bottom) and investigated the relationship between the final EBSs and stimulus-PV intervals. ResultsFor Lt.PVs, the stimulus-PV intervals during CSd pacing were significantly shorter than during HRA pacing at the Lt.PV anterior carina and bottom (90±28ms vs. 125±26ms, P<0.001 and 84±20ms vs. 148±24ms, P=0.028, respectively), but there was no significant difference in the Lt.PV roof and any posterior segments. For Rt.PVs, the stimulus-PV interval from both pacing sites exhibited no significant difference between either segment. ConclusionsThis pacing method may help to identify whether EBSs are located in the anterior Lt.PVs. Improved recognition of EBSs through pacing from different sites would be helpful for achieving PV isolation.

Effects of acute autonomic modulation on atrial conduction delay and local electrograms duration in paroxysmal atrial fibrillation

Slowed atrial conduction may contribute to reentry circuits and vulnerability for atrial fibrillation (AF). The autonomic nervous system (ANS) has modulating effects on electrophysiological properties. However, complex interactions of the ANS with the arrhythmogenic substrate make it difficult to understand the mechanisms underlying induction and maintenance of AF. Aim To determine the effect of acute ANS modulation in atrial activation times in patients (P) with paroxysmal AF (PAF). Methods and results 16P (9 men; 59 ± 14 years) with PAF, who underwent electrophysiological study before AF ablation, and 15P (7 men; 58 ± 11 years) with atrioventricular nodal reentry tachycardia, without documentation or induction of AF (control group). Each group included 7P with arterial hypertension but without underlying structural heart disease. The study was performed while off drugs. Multipolar catheters were placed at the high right atrium (HRA), right atrial appendage (RAA), coronary sinus (CS) and His bundle area (His). At baseline and with HRA pacing (600 ms, shortest propagated S2) we measured: i) intra-atrial conduction time (IACT, between RAA and atrial deflection in the distal His), ii) inter-atrial conduction time (interACT, between RAA and distal CS), iii) left atrial activation time (LAAT, between atrial deflection in the distal His and distal CS), iv) bipolar electrogram duration at four atrial sites (RAA, His, proximal and distal CS). In the PAF group, measurements were also determined during handgrip and carotid sinus massage (CSM), and after pharmacological blockade of the ANS (ANSB). AF was induced by HRA programmed stimulation in 56% (self-limited — 6; sustained — 3), 68.8% (self-limited — 6; sustained — 5), and 50% (self-limited — 5; sustained — 3) of the P, in basal, during ANS maneuvers, and after ANSB, respectively ( p = NS). IACT, interACT and LAAT significantly lengthened during HRA pacing in both groups (600 ms, S2). P with PAF have longer IACT ( p < 0.05), a higher increase in both IACT, interACT ( p < 0.01) and electrograms duration ( p < 0.05) with S2, and more fragmented activity, compared with the control group. Atrial conduction times and electrograms duration were not significantly changed during ANS stimulation. Nevertheless, ANS maneuvers increased heterogeneity of the local electrograms duration. Also, P with sustained AF showed longer interACT and LAAT during CSM. Conclusion Atrial conduction times, electrograms duration and fractionated activity are increased in PAF, suggesting a role for conduction delays in the arrhythmogenic substrate. Acute vagal stimulation is associated with prolonged interACT and LAAT in P with inducible sustained AF and ANS modulation may influence the heterogeneity of atrial electrograms duration.

Alternate Site Atrial Pacing in the Young: Conventional Echocardiography and Tissue Doppler Analysis of the Effects on Atrial Function and Ventricular Filling

Although the right atrial appendage (RAA) is typically used for atrial pacing lead implant, recent studies have shown benefits of alternate site atrial pacing (ASAP) in the elderly. However, comparable studies in the young are lacking. To investigate effects of ASAP on cardiac function and atrioventricular mechanical interactions in the young, 26 subjects (ages 10 to 23 years) with normal cardiac anatomy, function, and atrioventricular node conduction underwent echocardiography during electrophysiology studies while in sinus rhythm (NSR), and with temporary pacing from high right atrium (HRA), RAA, mid septal right atrium approximating Bachmann's bundle (BB), and left atrium (LA) via the distal coronary sinus (CS). After a paced steady state of 10 minutes, left atrial total and systolic ejection fractions, color-guided mitral inflow, and annular tissue Doppler indices were obtained. Left ventricular ejection fraction and myocardial performance indexes (MPI) were calculated. The total and systolic LA ejection fractions were higher during the NSR compared to all ASAP. Mitral inflow velocities changed significantly with ASAP. The passive/active ventricular filling ratio (E/A) deteriorated from NSR to HRA to BB to CS. There were significant changes in late diastolic tissue Doppler velocities during ASAP compared to NSR. The MPI during ASAP differed from those during the NSR. HRA and Bachmann bundle pacing provided better MPIs than RAA or CS pacing. The location of atrial pacing leads has an acute impact on cardiac function and atrioventricular mechanical interaction. Pacing close to sinus node location may be beneficial in the young.

Effects of verapamil on superior vena cava electrical remodeling induced by short-term pacing from right atrium and superior vena cava in human

Background Although the superior vena cava (SVC) may be involved in the triggering or maintenance of atrial fibrillation (AF), the electrophysiological properties of SVC in human are ill-defined. Methods The baseline effective refractory periods (ERPs) of high right atrium (HRA), SVC and the conduction time (CT) between HRA and SVC were measured at pacing cycle lengths (PCL) of 600 and 400 ms respectively in 20 patients (12 females, age 46 ± 13 years) with paroxysmal supraventricular tachycardia. Immediately after acute electrical remodeling (ER) induced by constant HRA or SVC pacing at PCL of 400 ms for 5 min, ERPs of HRA, SVC and the CT between HRA and SVC were determined. After verapamil was administered, the same protocols for determining ERPs of HRA, SVC and the CT between HRA and SVC were repeated. Results The baseline ERP of SVC was significantly longer than that of HRA. The CT from SVC to HRA was significantly longer than that from HRA to SVC. After acute ER, both the ERPs of HRA and SVC were significantly shortened. However, no significant changes of the CT between HRA and SVC could be demonstrated. After verapamil infusion, significant shortening of the ERP of HRA and SVC still occurred following acute ER and the ERP of SVC was still longer than that of HRA. Conclusions In human, ER can occur both in HRA and SVC after a short and moderately rapid heart rate pacing either from HRA or SVC. Verapamil cannot prevent such ER from occurring.

Two LBBB‐Like Tachycardias with Identical QRS Morphology: What Is the Mechanism?

Case Presentation A 17-year-old boy was referred for an electrophysiological (EP) study because of recurrent palpitations due to a left bundle branch block (LBBB) shaped wide QRS tachycardia. The baseline ECG showed a normal QRS complex during sinus rhythm, but intermittently broad QRS complexes were noted on telemetric monitoring before the study. Three diagnostic quadripolar catheters (Biosense Webster, USA) were introduced and placed in the high right atrium (HRA), His bundle region (His), and right ventricular apex (RVa), respectively. A decapolar catheter (St. Jude Medical, USA) was inserted into the coronary sinus (CS). Two kinds of tachycardia with identical LBBB-shaped QRS morphology (width 120 ms) but different cycle lengths were easily induced by programmed atrial stimulation. Tachycardia 1 (Fig. 1, left panel), having a heart rate of 150 beats per minute (bpm), was similar to the clinical tachycardia and, according to the patient, duplicated his symptom. Tachycardia 2 (Fig. 1, right panel) was even faster, with a heart rate of 190 bpm. Both tachycardias showed a superior frontal plane axis (−60 ◦ ). No definite P waves could be identified. Overdrive HRA pacing during tachycardia 1 led to a shift to the faster tachycardia 2 (Fig. 2) and vice versa. What was the mechanism of these two tachycardias? The EP Study and Differential Diagnosis Although a negative concordant pattern was present in the precordial leads, the initiation of the tachycardia by atrial pacing, the width, and configuration of the QRS complex in lead V1, V2, and the clearly 1:1 V/A relationship made a ventricular origin unlikely. Both tachycardias in this case showed same QRS morphology and same concentric VA ac

Correlation of Electrotonic Monophasic Action Potential Shortening with Short‐Term Memory in Human Atrium

To determine the presence of memory in human atria, we recorded monophasic action potential (MAP) at the high right atrium (HRA) in 21 patients. After reaching a steady state at 600 ms, HRA pacing was switched to the coronary sinus (CS) pacing to alter the activation sequence. After 20 minutes of CS pacing, pacing was continued at HRA to record the memory effect of CS pacing. Atrial memory was defined as the change in HRA MAP duration (MAPd) after 20 minutes of altered activation sequence. Baseline MAPd was 229 +/- 31 ms, which was shortened to 226 +/- 24 ms immediately after CS pacing. After 20 minutes of CS pacing, HRA MAPd during HRA pacing was 220 +/- 28 ms, which was significantly shorter than the baseline MAPd (P = 0.003). The degree of atrial memory was associated with the degree of initial electrotonic MAPd changes caused by the altered activation sequence. These results suggest that memory phenomenon exists in human atria, and it can be expressed as a change in MAPd.

763 Is age correlated with dynamic atrial decremental conduction properties?

Atrial fibrillation (AF) has been associated with premature beats and decreased atrial conduction velocities. On the other hand, prevalence of AF is increased in the elderly. The aim is to evaluate and analyze the relation between age, atrial size and a new index of dynamic interatrial conduction time (iaCT) in a homogeneous population of patients (pts) with structurally normal heart without AF.45 patients (pts) without structural heart disease aged 53 +/- 20 years referred for electrophysiologic study were analyzed. To examine the atrial electrophysiologic characteristics we studied interatrial conduction time (iaCT), double potentials and fragmented atrial activity during premature stimulation of high right atrium; prior to investigation, all antiarrhythmic drugs were withdrawn for an appropriate period of time. The following parameters were assessed: baseline iaCT (iaCTb) between high right atrium (HRA) and distal coronary sinus (CS), iaCT during HRA pacing S1S1 600ms (iaCTS1), maximum prolongation of iaCT during S2 and S3 delivery (iaCTS2, iaCTS3). We calculated a derived parameter: maximum prolongation iaCT/decremental index (DI)= iaCT S3-ia CTS1/iaCTS1%. The following echocardiograhic parameters were assessed: left atrial dimensions and surface (LAs), right atrial dimension and surface (RAs), total atrial surface (TAs=LAs+RAs) and left atrial volume (LAv) calculated using ellipse formula.iaCT ranged from 42 to 87ms; DI ranged from 16 to 52%. Simple regression analysis demonstrated a statistically significant linear correlation between the age of pts and HRA DI (r = 0.76, r2 = 0.55, p <0.0001). A trend toward a significant correlation was found between TAs and DI (r=0.64, r2=0.41, p<0.0001) LAv and DI (r=0.59, r2=0.35, p<0.0001). No significant correlation was found in this group between age and iaCT. Atrial double potentials and fragmentated electrograms were recorded using HRA stimulation in CS leads in 7 pts (15%) all aged >35 years. Pts were divided into two groups: 17 pts with normal electrophysiologic findings and 28 pts with junctional reentrant tachycardia. There were no significant differences between subgroups concerning the main studied parameters.This study shows a direct better correlation for age than atrial size in the relation with the dynamic behaviour interatrial conduction, suggesting that higher incidence in AF in the elderly might be also a consequence of the higher incidence of atrial conduction disturbances.

Mechanism of Atrial Fibrillation:

Atrial fibrillation (AF) has been associated with premature beats and decreased atrial conduction velocity. This study examined a new index of dynamic inter-atrial conduction time (iaCT) in patients with paroxysmal AF (PAF). We compared 42 consecutive patients with paroxysmal AF (mean age = 52 +/- 16 years) without structural heart disease with 39 age-matched patients (mean age = 49 +/- 15 years) who underwent ablation of junctional tachycardias. Prior to investigation, all antiarrhythmic drugs were discontinued for an appropriate period of time. The following measurements were made: baseline iaCT (iaCTb) between high right atrium (HRA) and distal coronary sinus, iaCT during HRA pacing S1S1 600 ms (iaCTS1), maximum prolongation of iaCT during S2 and S3 delivery (iaCTS2, iaCTS3). We then derived the decremental index (DI), the maximum percent prolongation of iaCT = iaCT S3-iaCTS1/iaCTS1%. In patients with PAF, iaCTb was 81.3 +/- 24 ms versus 59.5 +/- 14 ms in controls (P = 0.0001). Atrial fibrillation was reproducibly and easily induced with a prominent increase in iaCT in 11 patients with AF. In this subgroup DI was 92 +/- 17%, compared to 45 +/- 21% in the other patients with AF (P = 0.0001) and 21 +/- 15% in the control group (P = 0.0001). Spontaneous isolated or repetitive ectopic activity was observed in 11 patients with AF (26%), and decremental atrial conduction was observed in 76% of patients with AF. This study supports the role of dynamic inter-atrial conduction disturbances in patients with lone PAF. The DI may be a new index of vulnerability to paroxysmal AF.

Human study of biatrial electrical coupling: determinants of endocardial septal activation and conduction over interatrial connections.

The relative contribution of the atrial septum and interatrial connections to biatrial activation is a fundamental concept of human cardiac electrophysiology that has yet to be fully characterized. The purpose of the present study was to determine how both atria are coupled electrically. Twenty patients (16 men; mean age 54+/-11years) with a history of symptomatic atrial fibrillation (AF) underwent simultaneous biatrial noncontact mapping before catheter ablation of AF. The multiple electrode array catheters were positioned, respectively, in the left atrium (LA; transseptally) and the right atrium (RA). In all but 2 patients, isopotential maps revealed that endocardial septal activations of the RA and LA were separate, independent, and asynchronous of each other. Interatrial conduction was related to the site of initial atrial depolarization, revealing conduction over Bachmann's bundle in all patients during sinus rhythm, high RA pacing, and pacing from the LA appendage. Pacing from the coronary sinus was associated with conduction over the interatrial connection at the level of the coronary sinus in all patients, and conduction over Bachmann's bundle also occurred in 5 (26%) of 19 patients. Interatrial conduction over the fossa ovalis occurred in only 2 (2%) of the 116 segments analyzed. Electrical coupling of the RA and LA in humans is predominantly provided by muscular connections at the level of Bachmann's bundle and the coronary sinus. The true septum (the fossa ovalis and its limbus) of the RA and LA is asynchronous and discordant, usually without contralateral conduction during sinus rhythm or atrial pacing.

Global P wave duration on the 65-lead ECG: single-site and dual-site pacing in the structurally normal human atrium.

Pacing is believed to prevent atrial fibrillation by reducing atrial activation time. Exact correlation between P wave duration (PWD) on surface ECG and endocardial atrial activation time is still unexplored. In 15 patients without structural heart disease (9 women, age 45 +/- 14 years), single site [high right atrium (HRA), coronary sinus ostium (CSos), distal CS (CSd), high RA septum (Bachmann's bundle, BB)] and dual-site pacing (various combinations) was performed after ablation of supraventricular tachycardia. A 65-lead surface ECG was recorded simultaneously. Endocardial atrial activation time was measured off-line (stimulus - last bipolar recording), and the respective PWD was assessed using the root mean square and 65-channel summary plots. PWD during pacing from BB was significantly shorter (96 +/- 12 msec) than during HRA (121 +/- 15 msec), CSos (108 +/- 9 msec), and CSd pacing (126 +/- 14 msec; P < 0,01, respectively). PWD during dual-site pacing (HRA+BB, 91 +/- 14 msec; HRA+CSos, 96 +/- 7 msec; HRA+CSd, 90 +/- 7 msec; BB+CSd, 96 +/- 12 msec) was not significantly shorter than during pacing from BB. Correlation between endocardial atrial activation time and PWD was 0.83. PWD during single-site and dual-site atrial pacing represents endocardial atrial activation time and can be measured precisely using the 65-lead surface ECG. The fact that high septal pacing results in the shortest PWD may have implications for preventive pacing in patients with atrial fibrillation.

The electromechanical effects of pacing at different sites within the right atrium.

To compare high right atrium (HRA) with right atrial appendage (RAA) pacing with respect to atrial electromechanical function. Eleven patients undergoing elective electrophysiological studies were studied in order directly to compare atrial conduction acutely associated with HRA and RAA pacing. Twenty-five patients with chronically implanted, active fixation leads in the HRA were compared with an age and sex matched group of 25 patients with chronically implanted, passive fixation leads in the RAA. For both studies recordings were taken in sinus rhythm then repeated when paced. Measured time intervals were intra- and interatrial activation times. P wave duration and time to onset of atrial systolic blood flow. Right atrial pacing, when compared with sinus rhythm, significantly prolongs the interatrial activation time, the P wave duration and the time to onset of right and left atrial blood flow irrespective of site paced. Comparing the RAA group with the HRA group, there were no statistical differences for any of the measured parameters. High right atrial free wall or the right atrial appendage pacing, when compared with sinus rhythm, is significantly detrimental to atrial electromechanical function. There is, however, no demonstrable difference between the two sites.

Atrial electrophysiological properties evaluated by right and left atrial pacing in patients with or without atrial fibrillation.

Coronary sinus (CS) pacing has been shown to prevent induction of atrial fibrillation (AF) by suppression of the propensity of atrial premature beats at high right atrium (HRA) to induce local conduction delay at the posterior triangle of Koch. However, other mechanisms of CS pacing in preventing induction of AF have not been explored. This study investigated whether a differential conduction delay exists between the HRA and distal CS pacing in patients with paroxysmal AF but not in patients without AF. Nine patients with atrioventricular reentrant tachycardia utilizing a left accessory pathway undergoing catheter ablation were included in this study. Group 1 consisted of 5 patients with clinically documented paroxysmal AF and group 2 4 patients without a history of AF. The effective refractory periods (ERPs) of HRA, distal CS, and four different left atrial sites were determined. The interatrial conduction time and conduction delay between the HRA and distal CS during HRA or distal CS pacing were measured. The interatrial conduction delay (ICD) from the HRA to the distal CS during HRA pacing was significantly longer than that from the distal CS to the HRA during distal CS pacing in patients of group 1. However, the ICD from the HRA to the distal CS during HRA pacing was not significantly longer than that from the distal CS to the HRA during distal CS pacing in group 2 patients. A differential conduction delay between the HRA and the distal CS pacing is present in this specific population of patients with paroxysmal AF but not in patients without AF. The shorter conduction delay during DCS pacing may contribute to the prevention of induction of AF.

Monophasic action potentials of the right atrium in patients with paroxysmal atrial fibrillation.

To investigate the mechanism of atrial fibrillation (AF), monophasic action potentials (MAPs) from the atrial myocardium were studied in 7 patients with paroxysmal AF (PAF) and in 7 control individuals. The MAPs were recorded using a contact catheter during sinus rhythm and continuous pacing at the high right atrium (HRA) with pacing cycle lengths of 600, 500 and 400 ms. MAPs were obtained from 6 sites in each participant. The MAPD90 was measured from onset to 90% of MAP repolarization. Average, maximal and minimal MAPD90 (avMAPD90, maxMAPD90 and minMAPD90) were obtained from all participants. The dispersion of MAPD90 (dispMAPD90) was defined as the difference between maxMAPD90 and minMAPD90. The width of each atrial potential (WAP) and the wavelength index (WLI=MAPD90/WAP) were determined. Average, maximal and minimal WLI (avWLI, maxWLI and minWLI) were obtained from all participants. The avMAPD90 and maxMAPD90 did not significantly differ between the 2 groups. The minMAPD90 in the PAF group was significantly smaller than that in the control group at HRA pacing with cycle lengths of 500 and 400 ms (210+/-18ms vs 245+/-14 ms, p<0.05; 207+/-23 ms vs 238+/-20 ms, p<0.05; respectively). The dispMAPD90 was significantly longer in the PAF group than in the control group during sinus and HRA pacing. The WAP value did not differ between the 2 groups. The minWLI in the PAF group was significantly smaller than that in the control group at HRA pacing with cycle lengths of 500 and 400 ms (3.3+/-0.5 vs 3.8+/-0.3, p<0.05; 3.2+/-0.4 vs 3.7+/-0.3, p<0.02). A shortened and widened dispersion of atrial refractoriness may play an important role in the genesis of AF. Furthermore, smaller wavelengths may form in the atrium of patients with PAF.

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 inducibility 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.

Effects of Different Atrial Pacing Modes on Atrial Electrophysiology

Multiple-site atrial pacing has been shown to prevent recurrence of atrial fibrillation. However, information about the mechanisms of different atrial pacing modes in prevention of atrial fibrillation was not clear. Forty-two patients without structural heart disease were classified into group 1 and group 2 according to absence or presence of clinical atrial fibrillation, respectively. Atrial conduction time and electrogram width of the right posterior interatrial septum (RPS) were measured during drive-train stimulation (S1) and early extrastimulation (S2). The locations of S1 were the high right atrium (HRA), distal coronary sinus (DCS), or both sites simultaneously. Effective refractory periods (ERPs) of the HRA and DCS were also determined during S1 stimulation at each site and during biatrial pacing. The ERPs were not different between single-site atrial pacing and biatrial pacing. In contrast, early S2 stimulation at the HRA caused greater atrial conduction delay and greater increment of electrogram width of the RPS in patients with a history of atrial fibrillation. Biatrial pacing significantly reduced the conduction delay and electrogram width of the RPS caused by HRA extrastimulation. In addition, in 17 group 2 patients, atrial fibrillation was induced by an early HRA S2 coupled to HRA pacing. However, with the same coupling interval of S2 at HRA, only 6 of them had the arrhythmia induced during biatrial pacing. Furthermore, conduction delay and increase of electrogram width caused by early S2 at the HRA were reduced by biatrial pacing only in patients whose arrhythmia induction was successfully prevented by biatrial pacing. Biatrial pacing reduced both the atrial conduction delay and increase of electrogram width at the RPS caused by early S2 at HRA, and these effects could prevent induction of atrial fibrillation.