Atrial Septal Pacing: A Method for Pacing Both Atria Simuhaneously

By pacing both atria simultaneously, one could reliably predict and optimize left-sided AV timing without concern for IACT. With synchronous depolarization of the atria, reentrant arrhythmias might be suppressed. We studied four male patients (73 ± 3 years) with paroxysmal atrial fibrillation and symptomatic bradyarrhythmias using TEE and fluoroscopy as guides; a standard active fixation screw-in lead (Medtronic model #4058) was attached to the interatrial septum and a standard tined lead was placed in the ventricle. The generators were Medtronic model 7960. The baseline ECG was compared to the paced ECG and the conduction time were measured to the high right atrium, distal coronary sinus and atrial septum in normal sinus rhytbm, atrial septal pacing, and AAT pacing. On the surface ECG, no acceleration or delay in A V conduction was noted during AAI pacing from the interatrial septum as compared with normal sinus rhythm. The mean interatrial conduction time for all 4 patients was 106 ± 2 ms; the interatrial conduction time measured during AAT pacing utilizing the atrial septal pacing lead was 97 ± 4 ms (P = NS). During atrial septal pacing, the mean conduction time to the high right atrium was 53 ± 2 ms. The mean conduction time to the lateral left atrium during atrial septal pacing, was likewise 53 ± 2 ms. We conclude that it is possible to pace both atria simultaneously from a single site using a standard active fixation lead guided by TEE and fluoroscopy. Such a pacing system allows accurate timing of the left-sided AV delay.     

The Importance of the Left Atrioventricular Interval during Atrioventricular Sequential Pacing

During atrioventricular (AV) sequential pacing from the right heart, the interval between the left atrium and ventricle may vary from the programmed AV interval depending on the position of the atrial and ventricular electrodes and interatrial and interventricular conduction. The aim of this study was to determine the hemodynamic effects of altering the left AV interval while keeping the programmed AV interval constant. Four male and 17 female patients, aged 49 ± 15 years were studied. The left AV interval was measured by a catheter in the coronary sinus. Stroke volume and mitral flow were measured by simultaneous echo Doppler during AV sequential pacing from the right atrial appendage and right ventricular apex at programmed AV intervals of 100. 60, and 6 ms. The atrial catheter was then positioned on the atrial septum and the measurements repeated. With the atrial catheter in the right atrial appendage, interatrial activation time (118 ± 20 ms) was similar to interventricular activation time (125 ± 21 ms) and the left AV interval was almost identical to the programmed right AV interval. There was a significant correlation between interatrial and interventricular activation times (r = 0.8; P < 0.001). Positioning the atrial electrode on the septum decreased interatrial activation time by 39 ± 12 ms and increased the left AV interval by a similar amount. At a programmed AV interval of 60 ms, the left AV interval increased from 67 ± 15 ms to 105 ± 17 ms after the atrial catheter was repositioned from the appendage to the septum (P < 0.001). Compared to pacing from the right atrial appendage, atrial septal pacing increased mitral A wave velocity integral (2.8 ± 1.4 vs 4.4 ±1.7 cm at a programmed AV interval of 60 ms, P < 0.01), decreased E wave velocity integral (8.1 ± 2.2 vs 6.1 ± 2.4 cm, P < 0.001) but did not alter stroke volume (44.8 ± 10.6 vs 44.9 ± 10.1 mL). In contrast, a 40 ms decrease in the programmed right AV interval from 100 to 60 ms decreased stroke volume from 48.0 ± 10.0 to 44.9 ± 10.2 mL (P < 0.001). There was a strong relationship between interatrial and interventricular conduction so that patients with prolonged interatrial conduction still had equivalent left and right AV intervals during atrioventricular sequential pacing from the right atrial appendage and right ventricular apex. Positioning the atrial electrode on the septum decreases interatrial activation time and increases the left AV interval by about 40 ms but has minimal hemodynamic effect in patients without heart failure.     

Failure of coronary sinus pacing in reducing local atrial conduction delay in patients with atrial fibrillation after successful internal cardioversion

Recent studies suggested that distal coronary sinus (CS) pacing may prevent atrial fibrillation (AF) by reducing site dependent intraatrial conduction delay. The aim of this study was to investigate the effect of high right atrial (HRA) and distal CS pacing on local conduction delay in patients with AF. The study population consisted of 10 patients with persistent AF after transvenous atrial defibrillation and 10 control subjects. The local conduction delays along the anterolateral right atrium (RA), in the CS, and at the right atrial septum (RAS), and the incidence of AF in response to an atrial extrastimulus during HRA and distal CS pacing at a drive cycle length of 400, 500, and 600 ms were evaluated. In patients with AF, distal CS and HRA pacing are associated with more prominent and similar extent of conduction delay within the atria, without any significant difference in the dispersion of conduction delay and susceptibility to AF induction (70% vs 60%, P = 0.9). In normal controls, distal CS pacing reduces the conduction delay at the RAS and CS ostium and decreases the dispersion of conduction delay and the propensity for AF induction (0% vs 50%, P = 0.03) compared to HRA pacing. The pacing drive cycle length has no significant effect on conduction delay in patients with AF and normal controls (P > 0.05). Compared to normal controls, patients with AF have significantly longer conduction delay at the RAS and along the anterolateral RA during HRA and distal CS pacing. The result of this study demonstrates that the effect of HRA and distal CS pacing on the local atrial conduction delay in patients with and without AF differ significantly. These patients with AF may have more diffuse atrial anisotropy causing the changes in conduction, and pacing from distal CS in these patients dose not reduce the propensity for AF.     

The effect of the atrial pacing site on the total atrial activation time

The effect of dual site pacing for prevention of atrial fibrillation may be due to synchronization of right and left atrial activation. Little is known, however, about the effect of pacing from single right atrial sites on differences in interatrial conduction. Twenty-eight patients without structural heart disease were studied following radiofrequency catheter ablation of supraventricular arrhythmias. Pacing was performed using standard multipolar catheters from the presumed insertion site of Bachmann's bundle, the coronary sinus ostium, the high lateral right atrium, and the right atrial appendage (n = 8 patients). Bipolar recording was performed from the distal coronary sinus, the high and low lateral right atrium, and the posterolateral left atrium (n = 13 patients). The longest conduction time from each pacing to each recording site was considered the total atrial activation time for the respective pacing site. During high right atrial pacing, the total atrial activation time was determined by the conduction to the distal coronary sinus (118 +/- 18 ms), during coronary sinus ostium pacing by the conduction to the high right atrium (94 +/- 18 ms), and during Bachmann's bundle pacing by the conduction to the distal coronary sinus (74 +/- 18 ms). The total atrial activation time was significantly shorter during pacing from Bachmann's bundle, as compared to pacing from other right atrial sites. Thus, in normal atria, pacing from the insertion of Bachmann's bundle causes a shorter total atrial activation time and less interatrial conduction delay, as compared to pacing from other right atrial sites. These findings may have implications for alternative pacing sites for prevention of atrial fibrillation.     

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.     

Interatrial Conduction During Cardiac Pacing

DDD pacemakers sense and pace right-sided cardiac chambers. The relationship of atrial to ventricular systole on the left side of the heart is of importance for systemic hemodynamics. Effective atrioventricular synchrony is partially determined by interatrial conduction time (IACT). At the time of DDD pacemaker implantation, interatrial conduction was measured using an intraesophageal pill electrode in 25 patients who were on no cardiac medications. Mean interatrial conduction time for all patients prolonged from 95 ± 18 ms during sinus rhythm to 122 ± 30 ms during right atrial pacing (p < 0.001). In 16 patients with P wave duration < 110 ms interatrial conduction prolonged from 85 ± 10 ms during sinus rhythm to 111 ± 9 ms during right atrial pacing (p < 0.01) compared to 114 ± 20 ms prolonging to 111 ± 19 ms (p < 0.01] in 9 patients with P wave duration > 110 ms. In each patient, while atrioventricular conduction prolonged with incremental right atrial pacing, interatrial conduction times did not vary. Interatrial conduction prolongs from baseline during atrial pacing and remains constant at all paced rates from 60–160 heats per minute. In addition to longer interatrial conduction times during sinus rhythm, patients with electrocardiographic P wave prolongation have longer interatrial conduction times during right atrial pacing than do normals (p < 0.0001). Based on interatrial conduction times alone, the AV interval during DDD cardiac pacing should be approximately 25 ms longer during AV pacing as compared to atrial tracking.     

Left Origin of the Atrial Esophageai Signal as Recorded in the Pacing Site

Clear atrial depolarizations from inside the esophagus have always been recorded in electrocardiology, but their precise origin is still under discussion. Though atriol signals are recorded along most of the esophagus, pacing of the atria is possible only in a short tract, probably where the esophagus is in contact with the posterior left atrium wall. In order to ascertain which portion of atria gives rise to the esophageai atrial signal recorded in the atrial pacing segment, we examined 37 patients with normal P waves on the standard ECG by inserting esophageai and endocavitary catheters. The interval between the earliest start of the P wave and the bipolar atrial deflection, was measured both through the esophagus (PA-Eso) and the Hisian region (PA-His) (the latest depolarization of interatrial septum). The former was longer than the latter (P < 0.001) in 36 of 37 patients, showing that the esophagus recorded atrial signal, at the site of effective pacing, originates outside the interatrial septum. As the atrial depolarization recorded through the esophagus is significantly delayed compared with the Hisian region recording, a pure left origin of the esophageai signal can be hypothesized. This is supported by the well-known delayed depolarization, during sinus rhythm, of the left atrium posterior wall compared with the right atrium and interatrial septum. Measuring the interval between the standard ECC P wave and atrial depolarization recorded through esophagus in the site of effective pacing, provides a reliable noninvasive estimate of interatrial time conduction.     

Impact of transisthmus linear ablation of typical atrial flutter on coronary sinus activation time

Complete or incomplete bidirectional isthmus conduction block after linear ablation of atrial flutter is difficult to interpret without detailed multiple electrodes mapping along the tricuspid annulus and the low right atrial isthmus area. The influence of isthmus block on the intraatrial septal and coronary sinus activation has not been assessed by endocardial mapping. This study was designed to analyze the intraartial and interatrial activation times in a retrospective fashion to investigate (1) whether isthmus conduction block can change the coronary sinus activation sequence during low lateral right atrial pacing, and (2) the correlation between change of coronary sinus activation time and isthmus conduction block. Sixty-five consecutive patients (mean age, 57 +/- 18 years) with clinically documented typical atrial flutter were studied. A 20-pole "Halo" catheter was placed around the tricuspid annulus including the entire low right atrial isthmus to verify complete bidirectional isthmus block. Activation time from ostium to distal coronary sinus (OCS-->DCS), and interatrial septum and isthmus activation times during right atrial pacing were analyzed and compared before and after incomplete or complete isthmus block. Complete bidirectional isthmus block was achieved in 50 (77%) patients. During low lateral right atrial pacing, linear ablation at low right atrial isthmus results in a significant delay of activation in all coronary sinus recording sites with greater extent at the ostium area without influence on interatrial septum activation in complete and incomplete isthmus conduction block. The difference of the OCS-->DCS interval before and after ablation, delta (OCS-->DCS), was well correlated with results of isthmus conduction block and significantly longer in patients with complete than those with incomplete isthmus block (34 +/- 11 vs 11 +/- 8 ms, P < 0.001), thereby allowing a value of 20 ms as a discriminative parameter to differentiate incomplete (< 20 ms) from complete (> or = 20 ms) isthmus counterclockwise conduction block with a sensitivity of 96% and a specificity of 88%. In conclusion, creation of a line of block at the inferior vena cava-tricuspid annulus isthmus could change coronary sinus activation sequence during low lateral right atrial pacing in sinus rhythm. The change of coronary sinus activation time after linear ablation, delta (OCS-->DCS), was well correlated with isthmus conduction block by using a value > or = 20 ms to discern complete counterclockwise isthmus block.     

Interatrial conduction correlates with optimal atrioventricular timing in cardiac resynchronization therapy devices

Background: Echocardiographic optimization of the atrioventricular delay (AV) may result in improvement in cardiac resynchronization therapy (CRT) outcome. Optimal AV has been shown to correlate with interatrial conduction time (IACT) during right atrial pacing. This study aimed to prospectively validate the correlation at different paced heart rates and examine it during sinus rhythm (Sinus). Methods: An electrophysiology catheter was placed in the coronary sinus (CS) during CRT implant (n = 33). IACT was measured during Sinus and atrial pacing at 5 beats per minute (bpm) and 20 bpm above the sinus rate as the interval from atrial sensing or pacing to the beginning of the left atrial activation in the CS electrogram. P‐wave duration (PWd) was measured from 12‐lead surface electrocardiogram, and the interval from the right atrial to intrinsic right ventricular activation (RA‐RV) was measured from device electrograms. Within 3 weeks after the implant patients underwent echocardiographic optimization of the sensed and paced AVs by the mitral inflow method. Results: Optimal sensed and paced AVs were 129 ± 19 ms and 175 ± 24 ms, respectively, and correlated with IACT during Sinus (R = 0.76, P < 0.0001) and atrial pacing (R = 0.75, P < 0.0001), respectively. They also moderately correlated with PWd (R = 0.60, P = 0.0003 during Sinus and R = 0.66, P < 0.0001 during atrial pacing) and RA‐RV interval (R = 0.47, P = 0.009 during Sinus and R = 0.66, P < 0.0001 during atrial pacing). The electrical intervals were prolonged by the increased atrial pacing rate. Conclusion: IACT is a critical determinant of the optimal AV for CRT programming. Heart rate‐dependent AV shortening may not be appropriate for CRT patients during atrial pacing. (PACE 2011; 34:443–449)     

Alternate site atrial pacing in the young: conventional echocardiography and tissue Doppler analysis of the effects on atrial function and ventricular filling

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.     

Placement of a Pacing Lead at the Inferior Portion of the Interatrial Septum Without Special Tools

Introduction: Previous studies have suggested that, among septal sites, the inferior portion of the interatrial septum (IAS) is the most likely to prevent atrial fibrillation, though inserting an active fixation lead at this site can be tedious and time consuming. We describe a relatively straightforward technique to insert a lead at this site without special tools .
Method: We studied 117 consecutive patients (mean age = 76 ± 8 years, 69% men) with ACC/AHA class I and II pacing indications and histories of paroxysmal or permanent atrial fibrillation, undergoing implantation of a dual chamber pacing system. A technique using the "preshaped" stylet and fluoroscopic guidance is described.
Results: The insertion was successful in 111 patients (95%). Acute dislodgement occurred in six patients (5%). The intrinsic P-wave duration was 117 ± 22 ms, and the paced P-wave duration was 90 ± 20 ms (23% shortening, P < 0.001). The mean time required to insert the atrial lead was 12 ± 8 minutes. No complications occurred.
Conclusions: Insertion of an active fixation lead at the inferior portion of the interatrial septum was safe and highly successful in the majority of patients with this technique.     

Atrial Electromechanical Sequence and Contraction Synchrony during Single- and Multisite Atrial Pacing in Patients with Brady-Tachycardia Syndrome

Objectives: Investigation of which atrial pacing modality provides atrial synchrony and the most physiological atrial contraction pattern in patients with brady-tachycardia syndrome.
Methods: Fifteen healthy subjects and 57 patients with sinus node dysfunction, atrial fibrillation recurrences, and prolonged P-wave on the electrocardiogram treated with multisite atrial (MSA) pacing were studied. One atrial lead was implanted in the coronary sinus (CS) ostium area, the other at the right atrial appendage (RAA): RAA+CS group (28 patients), or Bachmann's bundle (BB) region: BB+CS group (29). Sinus rhythm (SR) and CS, RAA, BB, RAA+CS, and BB+CS pacing modalities were evaluated. Electromechanical delay (EMD) in atrial walls was assessed by tissue Doppler echocardiography. Interatrial (ΔinterA), intra-right (ΔRA), and intra-left (ΔLA) atrial dyssynchrony were calculated.
Results: During SR, in the study group versus controls, important ΔinterA: 55 ± 23 versus 22 ± 11 ms (P < 0.01) and ΔLA: 47 ± 21 versus 21 ± 6 ms (P < 0.001) were present. Single-site BB and both MSA pacing modes restored ΔinterA and ΔLA (ΔinterA: 24 ± 16, 20 ± 13 and 14 ± 9 ms, ΔLA: 28 ± 18, 28 ± 13 and 20 ± 10 ms during BB, RAA+CS and BB+CS pacing, respectively). CS pacing prolonged lateral RA EMD, while RAA pacing LA walls EMD, which resulted in ΔinterA persistence. CS pacing induced ΔRA (50 ± 23 vs 16 ± 8 ms, P < 0.0001 vs controls). Atrial contraction sequence during BB pacing resembled that observed in controls.
Conclusions: (1) Single-site BB and both MSA pacing modes restored atrial synchrony. (2) Single-site RAA and CS ostium pacing retained interatrial dyssynchrony; moreover, CS pacing created RA dyssynchrony. (3) Single-site BB pacing provided physiological atrial contraction sequence.     

Nonuniformity of AH Intervals During Stimulation at Different Left Atrial Sites

Studies in humans have found left atrial stimulation via the coronary sinus (CS) to elicit significantly shorter atrium-His (AH) intervals as compared to right atrial stimulation, but whether pacing at dijferent left atrial sites (anterior vs posterior left atrium, i.e., far distal vs proximal CSJ affects the AH interval has not been studied. Hence, in 22 patients, we compared the effects of stimulation from various atriai sites, including anterior high right atrium (HRA), distal CS, mid-CS, and proximal CS, on; stimulus-atrium (SA), AH, and stimuIus-His intervals on the His bundle electrogram. Paced cycle length differed for each patient (range 900–350 msec, mean 532 ± 140 msec), but conduction intervals from different atrial sites were compared using identical cycle length in each patient. The mean SA intervals were 34 ± 10 msec, 57 ± 10 msec, 44 ± 11 msec, and 32 ± 8 msec with stimulation, respectively, from HRA, distal CS, mid-CS. and proximal CS (each significantly different except for HRA vs proximal CSJ. The mean AH intervals were 123 ± 23 msec, 104 ± 28 msec, 95 ± 15 msec, and 90 ± 18 msec with stimulation, respectively, from HRA, distal CS, mid-CS, and proximal CS (each significantly different except for mid-CS vs proximal CSJ. In 13 patients, the discrepancy in AH intervals during distal versus proximal CS stimulation was > 15 msec; in 9 patients this difference was only < 10 msec, considered within the range of measurement error. Thus, in a significant portion of patients, discrepant AH intervals were demonstrated during stimulation from the distal versus proximal CS. These previously undescribed observations suggest that electrophysiological studies on atrioventricular nodal conduction that involve left atrial stimulation must take into account actual location of the stimulation site (anterior or posterior) in order to properly interpret the findings.     

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)     

Atrioventricular Interval Optimization in the Right Atrial Appendage and Interatrial Septum Pacing: A Comparison Between Echo and Peak Endocardial Acceleration Measurements

PADELETTI, et al. : Atrioventricular Interval Optimization in the Right Atrial Appendage and Interatrial Septum Pacing: A Comparison Between ECHC and Peak Endocardial Acceleration. Interatrial septum pacing (IASP) reduces interatrial conduction time and consequently may interfere with atrioventricular delay (AVD) optimization. We studied 14 patients with an implanted BEST Living system device able to measure peak endocardial acceleration (PEA) signal. The aims of our study were to compare the (1) optimal AVD (OAVD) in right atrial appendage pacing (RAAP) and IASP, and (2) OAVD derived by the PEA signal versus OAVD derived by Echo/Doppler evaluation of the left ventricular filling time (LVFT) and cardiac output (CO). Measurements were performed in DDD VDD modes Eight patients (group A) had RAAP and six patients (group B) had IASP. In group A, OAVD measured by LVFT, CO, and PEA was 185 ± 23 ms , 177 ± 19 ms , and 192 ± 23 ms in DDD and 147 ± 19 ms , 135 ± 27 ms , and 146 ± 20 ms in VDD, respectively. OAVD measured by LVFT, CO, and PEA was significantly longer in DDD mode than in VDD (P < 0.01, P < 0.01, P < 0.001 ). In group B, OAVD measured by LVFT, CO, and PEA was 116 ± 19 ms , 113 ± 10 ms , and 130 ± 30ms in DDD and 106 ± 16 ms , 96 ± 15 ms , and 108 ± 26 ms in VDD, respectively. No statistical differences were observed between DDD and VDD. Significant correlations between OAVDs PEA derived and OAVDs LVFT and CO derived were observed (r = 0.71, r = 0.69, respectively ). When new techniques of atrial stimulation, as IASP, are used an OAVD shorter and similar in VDD and DDD has to be considered. The BEST Living system could provide a valid method to ensure, in every moment, the exact required OAVD to maximize atrial contribution to CO.     

Electrophysiological properties of the left atrium evaluated by coronary sinus pacing in patients with atrial fibrillation

Repetitive atrial firing (RAF), marked fragmentation of atrial activity (FAA), and interatrial conduction delay (CD) have been shown to be electrophysiological features of the atrium in patients with atrial fibrillation (AF). Moreover, it has been observed that atrial extrastimuli are more likely to induce AF when delivered from the right atrial appendage (RAA) than from the distal coronary sinus (CSd). We examined the electrophysiological properties of the atrial muscle by CS and RAA stimulation in patients with paroxysmal AF. Patients were divided into two groups: group I, consisting of 18 patients with clinical paroxysmal AF; and group II, consisting of 22 patients with various cardiac arrhythmias in which the substrate does not exist in the atrium. In group I, the following values of electrophysiological parameters of the atrium indicated that AF was more likely to be induced during RAA pacing than CSd pacing: atrial effective refractory period (RAA vs CSd: 201 +/- 28 ms vs 240 +/- 35 ms, P < 0.001), RAF zone (16 +/- 25 ms vs 0 +/- 0 ms, P < 0.03), FAA zone (38 +/- 37 ms vs 5 +/- 19 ms, P < 0.01), maximum interatrial conduction time (144 +/- 19 ms vs 93 +/- 19 ms, P < 0.0001) and CD zone (53 +/- 21 ms vs 9 +/- 18 ms, P < 0.0001). The values of the electrophysiological parameters of the atrium evaluated by CSd pacing in group I patients were not significantly different from those in group II patients. In conclusion, when coronary sinus stimulation is performed, electrophysiological properties of the atrium in patients with AF show a significant decrease in atrial vulnerability compared to stimulation from RAA and also show similar values to those in patients without AF. It might be suggested that the left posterior or posterolateral atrium is electrophysiologically stable even in patients with paroxysmal AF.     

Acute Effects of Different Atrial Pacing Sites in Patients with Atrial Fibrillation: Comparison of Single Site and Biatrial Pacing

It has been reported that a trial single site or biatrial pacing can suppress the occurrence of AF. However, its mechanism remains unclear. The study population included 32 patients with AF (n = 20: AF group), or without paroxysmal AF (n = 12: control group). The mechanism and efficacy of atrial pacing were investigated by electrophysiological studies to determine which was more effective for suppressing AF induction; single site pacing of the right atrial appendage (RAA) or distal coronary sinus (CS-d), or biatrial (simultaneous BAA and CS-d) pacing. In the AF group, AF inducibility was significantly higher with BAA extrastimulus during RAA (12/20; P < 0.0001) or biatrial paced drive (7/20; P < 0.01) than during CS-d paced drive (0/20). In the control group, AF was not induced at any site paced. In the AF group, the conduction delay and other parameters of atrial vulnerability significantly improved during CS-d paced drive. The atrial recovery time (ART) at RAA and CS-d was measured during each basic pacing mode. ART was defined as the sum of the activation time and refractory period, and the difference between ARTs at RAA and CS-d was calculated as the ART difference (ARTD). The ARTD was significantly longer during BAA pacing in the AF group than in control group (155.0 +/- 32.8 vs 128.8 +/- 32.9 ms, P < 0.05). In the AFgroup, ARTDs during biatrial (52.0 +/- 24.2 ms) and CS-d pacing (51.7 +/- 26.0 ms) were significantly shorter than ARTD during RAA pacing. The CS-d paced drive was more effective for suppressing AF induction than biatrial or RAA paced drive by alleviating conduction delay. CS-d and biatrial pacing significantly reduced ARTD compared with RAA pacing.     

Atrial Septal Pacing:

Atrial pacing may prevent the onset of atrial fibrillation (AF) because of: (1) prevention of the relative bradycardia that triggers paroxysmal AF; (2) prevention of the bradycardia induced dispersion of refractoriness; (3)suppression or reduction of premature atrial contractions that initiate reentry and predispose to AF; (4) preservation of AV synchrony, which might prevent switch induced changes in atrial repolarization predisposing to AF. Atrial pacing locations that decrease atrial activation and dispersion of refractoriness may be preferable in patients with a history of AF. Two different interatrial septum sites have been proposed: the Bachmann's bundle and the coronary sinus ostium. The results of two prospective randomized studies indicate that septal pacing, when compared to the traditional right atrial appendage pacing, significantly reduces : (1) paroxysmal AF recurrences and burden; and (2) progression to chronic AF. (PACE 2004; 27[Pt. II]:850–854)     

DDD pacing and interatrial conduction block: importance of optimal AV interval setting

The case of a 83-year-old patient undergoing DDD pacemaker implantation for sick sinus syndrome with postimplant detection of advanced interatrial conduction block is described. At nominal AV interval programming values (175 ms), absence of P wave following an atrial spike was observed, and the presence of an interatrial conduction disturbance was demonstrated by a Doppler transmitral flow pattern analysis and transesophageal ECG recording. AV interval lengthening up to 300 ms resulted in proper timing of atrial and ventricular contractions. Awaiting for conclusive data about biatrial pacing, interatrial conduction blocks can be managed in some cases by proper programming of conventional DDD systems.     

QRS Duration Widening: Reduced Synchronization of Endocardial Activation or Transseptal Conduction Time?

Antegrade activation of the His-Purkinje system (HPS) results in synchronized activation of the right ventricular (RV) and left ventricular (LV) endocardia forming normal, narrow QRS duration (QRSD). An alteration in septal activation and transseptal conduction time have been reported to be the causes for QRSD widening seen with bundle branch block. However, reduced synchronization of activation ofRVand LV endocardia as another potential mechanism for QRSD widening has not been systematically studied. Fifteen consecutive patients underwent radiofrequency ablation (RFA) for treatment of supraventricular tachycardia. After RFA, mean QRSD in normal sinus rhythm was 86 ± 8 ms with mean HV interval of 40 ± 5 ms. Right atrial (RA), coronary sinus (CS), simultaneous (S) RA-CS, RVapex (RVA), LV apex (LVA), and SRVA-LVA pacing were performed. Mean QRSD with RA, CS, SRA-CS pacing was similar to normal sinus rhythm (87 ± 7, 87 ± 8 and 88 ± 8 ms respectively). Mean QRSD was significantly longer with SRVA-LVA and either RVA or LVA pacing alone compared to normal sinus rhythm (106 t 8, 146 ± 12 and 157 ± 13 ms, respectively). However, QRSD was significantly shorter with SRVA-LVA pacing compared to either RVA or LVA pacing alone (P < 0.0001). We conclude that shorter QRSD with SRVA-LVA pacing compared to either RVA or LVA pacing alone is due to elimination of transseptal conduction delay; longer QRSD with SRVA-LVA pacing compared to sinus or atrial paced rhythm is due to reduced synchronization of endocardial activation secondary to ectopic entry of impulses into the HPS network and inability to take advantage of the branching structure of the HPS. Therefore, in addition to transseptal conduction delay, reduced synchronization of endocardial activation is another potential mechanism for QRSD widening.