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.     

Atrial Septal Pacing to Synchronize Atrial Depolarization in Patients with Delayed Interatrial Conduction

The current method of pacing the right atrium from the appendage or free wall is often the source of delayed intraatrial conduction and discoordinate left and right atrial mechanical function. Simultaneous activation of both atria with pacing techniques involving multisite and multilead systems is associated with suppression of supraventricular tachyarrhythmias and improved hemodynamics. In the present study we tested the hypothesis that pacing from a single site of the atrial septum can synchronize atrial depolarization. Five males and two females (mean age 58 ± 6 years) with drug refractory paroxysmal atrial fibrillation (AF) were studied who were candidates for AV junctional ablation. All patients had broad P waves (118 ± 10 ms) on the surface ECG. Multipolar catheters were inserted and the electrograms from the high right atrium (HRA) and proximal, middle, and distal coronary sinus (CS) were recorded. The atrial septum was paced from multiple sites. The site of atrial septum where the timing between HRA and distal CS (d-CS) was ≤ 10 ms was considered the most suitable for simultaneous atrial activation. An active fixation atrial lead was positioned at this site and a standard lead was placed in the ventricle. The interatrial conduction time during sinus rhythm and AAT pacing and the conduction time from the pacing site to the HRA and d-CS during septal pacing were measured. Atrial septal pacing was successful in all patients at sites superior to the CS os near the fossa ovalis. During septal pacing the P waves were inverted in the inferior leads with shortened duration from 118 ± 10 ms to 93 ± 7 ms (P < 0.001), and the conduction time from the pacing site to the HRA and d-CS was 54.3 ± 6.8 ms and 52.8 ± 2.5 ms, respectively. The interatrial conduction time during AAT pacing was shortened in comparison to sinus rhythm (115 ± 18.9 ms vs 97.8 ± 10.3 ms, P < 0.05). In conclusion, simultaneous activation of both atria in patients with prolonged interatrial conduction time can be accomplished by pacing a single site in the atrial septum using a standard active fixation lead placed under electrophysiological study guidance. Such a pacing system allows proper left AV timing and may prove efficacious in preventing various supraventricular tachyarrhythmias.     

AV conduction with atrial rate adaptive pacing in the bradycardia tachycardia syndrome

AV conduction with atrial rate adaptive pacing (AAIR) during exercise was investigated in 43 patients (28 men, 15 female, mean age 68 +/- 7 years) who were paced and medicated with antiarrhythmic drugs for the bradycardia tachycardia syndrome (BTS). Patients were included if they had no second- or third-degree AV block, no complete bundle branch or bifascicular block, and a PQ interval < or = 240 ms during sinus rhythm at rest. The interval between the atrial spike and the following Q wave (SQ) was measured in the supine position at rest (R) with maximum AAI pacing rate (Fmax) achieved below the Wenckebach point (SQ-R-Fmax). Bicycle ergometry was performed using the Chronotropic Assessment Exercise Protocol, and AAI pacing rate was increased stepwise by programming load-adapted increments. Seven patients showed intrinsic rhythm during exercise. In those 36 patients who were atrially paced throughout ergometry (E), SQ was measured with 70 beats/min on the lowest CAEP stage (SQ-E-70) and with Fmax at maximum work load (SQ-E-Fmax). During exercise, no second-degree AV block was observed, but 28 of 36 patients (78%) showed a nonphysiological increase of the SQ interval, and the average SQ-E-Fmax was significantly longer than SQ-E-70 (250 +/- 31 versus 228 +/- 32 ms, P < 0.01). There was only a weak correlation between SQ-R-Fmax and SQ-E-Fmax (r = 0.35824, P < 0.05). When Fmax obtained during exercise was kept during recovery, 14 patients (39%) developed a second-degree AV block between 15 and 240 seconds after ergometry, 8 patients within 90 seconds. Patients who had exhibited a P on T wave in the ECG with Fmax at the end of exercise (11 of 36 patients) were reevaluated by Doppler echocardiography. Using the same exercise protocol and identical, load-adapted rate increments, only 3 of 11 patients showed premature mitral valve closure. It is concluded that patients paced and medicated for BTS are prone to a nonphysiological prolongation of AV conduction with AAIR pacing during and after exercise. As this risk can hardly be predicted by rapid atrial pacing at rest, the pacing system should be dual chamber in this subset of patients. This especially applies to the patients in whom mechanical AV timing is affected by the conduction delay.     

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.     

Impact of the ECG for detection of intraatrial conduction block after atrial flutter ablation

Induction of complete bidirectional conduction block via the posterior isthmus of the right atrium is introduced as a standard endpoint for catheter ablation of atrial flutter. The present study sought to investigate the impact of changes in P wave duration and morphology detected by the surface ECG during coronary sinus and posterolateral right atrial stimulation as a marker for conduction block. Morphology and duration changes of the paced P wave before and after radiofrequency catheter (RFC) ablation were estimated in 22 patients referred for ablation of atrial flutter. We looked for a morphology change of the terminal portion in the 12-lead ECG and an increment of P wave duration. In 16 of 22 patients in whom atrial flutter ablation resulted in a complete bidirectional block, the conduction block was unidirectional in 4 patients and conduction times remained unchanged in 2 patients. After induction of complete bidirectional block a change of the terminal portion of the P wave towards a more positive morphology in one or more inferior leads was detected in 14 (88%) of 16 patients during coronary sinus stimulation and in 15 (94%) of 16 patients during posterolateral right atrial stimulation. These changes were predominantly observed in the inferior leads. Positive morphology changes of the terminal P wave portion in the inferior leads indicating conduction block with a sensitivity of 86% and a specificity of 100% were observed. An increment of 10 ms or more in P wave duration indicates conduction block with a specificity of 100% and a sensitivity of 67%. There was a significantly larger increment of P wave duration during coronary sinus (CS) stimulation compared to posterolateral right atrial stimulation (38 +/- 21 vs 16 +/- 21 ms). The analysis of P wave duration and morphology in the inferior leads of the surface ECG is a reliable tool to assess the intraatrial conduction after atrial flutter ablation. Different conduction during coronary sinus and posterolateral right atrial pacing may cause a different P wave duration after ablation.     

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)     

Characteristic P wave morphology in patients undergoing the atrial compartment operation for chronic atrial fibrillation with mitral valve disease

The P wave in the surface ECG represents atrial electrical activation and may be altered in certain pathological conditions. Atrial compartment operation has been used to convert chronic AF to sinus rhythm. However, this procedure may result in changes of impulse conduction in various atrial compartments and alters the P wave morphology. This study sought to elucidate the P wave changes after the atrial compartment operation for AF. Fifteen patients undergoing the atrial compartment operation for chronic AF were studied. In the operation, the atrium was divided into three compartments, namely the left atrium, the atrial septum including sinus and AV nodes, and the right atrial compartment. The anatomic connection between adjacent compartments were preserved at the posterior lower margin of incisions. The surface lead P waves were correlated with intracardiac recording and stimulation in various atrial compartments. Fifteen age- and sex-matched control patients without structural heart diseases were compared. The results showed that patients undergoing the atrial compartment operation had a prolonged P wave duration (190 +/- 27 v s95 +/- 14 ms, P < 0.001), a prolonged PR interval (207 +/- 23 vs 155 +/- 20 ms, P < 0.001), and a shortened PR segment (17 +/- 19 vs 60 +/- 17 ms, P < 0.001). The increase in P wave duration was primarily due to a conduction delay from the sinus node to the other atrial compartments as the conduction time from the high right atrium to the right atrial appendage was 132 +/- 57 ms(vs 21 +/- 6 ms for control,P < 0.001), and the conduction time from the high right atrium to the distal coronary sinus was 140 +/- 55 ms(vs 70 +/- 15 ms, P < 0.001). However, the conduction from the high right atrium to the low septal right atrium, which were located in the same compartment, was not impaired. Also, the conduction in the AV node and His-Purkinje system were not impaired. The mean axis of P waves varied greatly, but was not statistically different from that of the control group (60 +/- 48 degrees vs 52 +/- 18 degrees,P > 0.05). Although the patients undergoing atrial compartment operation had a larger left atrial size, their P wave amplitude was smaller (1.0 +/- 0.3 vs 1.3 +/- 0.3 mm, P < 0.01), and an increased negative terminal force in V1 was not seen (0.02 +/- 0.02 vs 0.02 +/- 0.01 mm/s, P > 0.05). Alteration in P wave morphology was seen in 14 patients. All the P waves showed a biphasic configuration with an initial positive and a terminal slurred negative deflection in leads II, III, and aVF. The terminal components represented the activation of right atrial appendage in 5 patients, the left atrium in 1, and the combined activation of right atrial appendage and the left atrium in 8 patients. The P wave morphology suggested that activation of both the right atrial appendage and the left atrial compartments proceeded in a caudocranial direction as a result of the atrial incisions. In conclusion, atrial compartment operation altered the conduction time and direction in the atria and resulted in characteristic P wave changes.     

Atrial pacing lead location alters the effects of atrioventricular delay on atrial and ventricular hemodynamics

The combined role of atrial pacing lead location and AV timing on cardiovascular performance has not been defined. This study tested the hypothesis that atrial pacing lead location can change the dependence of LA and LV hemodynamics on AV timing in vivo. Dogs anesthetized with isoflurane (n = 8) were instrumented for measurement of hemodynamics including LA pressure, LA volume, and pulmonary venous bloodflow. Data were recorded during normal sinus rhythm, and atrial overdrive pacing from the right atrial appendage (RAA), proximal coronary sinus (CS), and LA lateral wall (LAW). The AV node was then ablated and measurements repeated during synchronous ventricular pacing and during dual chamber pacing from each atrial lead location at various AV delays (20, 60, 120, 180, 240, and 350 ms). Hemodynamics during intrinsic sinus rhythm and overdrive atrial pacing from different sites were similar. In contrast, ventricular or dual chamber pacing caused significant (P < 0.05) changes in cardiac output with different AV timing during RAA (3.5 +/- 0.2 vs 2.9 +/- 0.2 L/min at 120 and 350 ms, respectively) and LAW pacing but not CS pacing. A significant interaction between atrial lead location and AV delay was observed for changes in stroke volume, pulmonary venous blood transport, LA volume, and LV preload. The results indicate that the atrial contribution to cardiac output depends on AV timing and atrial lead location in isoflurane-anesthetized dogs with AV nodal conduction block.     

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.     

Conduction properties of the crista terminalis in patients with atrial flutter due to amiodarone therapy for atrial fibrillation

Some patients with atrial fibrillation (AF) treated by antiarrhythmic drugs (AAD) can develop typical atrial flutter, but the mechanism is not clear. This study included 21 patients with AF. Group I (n = 7) had typical atrial flutter due to amiodarone therapy. Group II (n = 7) did not develop atrial flutter after amiodarone treatment. Group III (n = 7) did not receive AAD treatment. A 7 Fr, 20-pole electrode catheter was placed along the CT identified by fluoroscopy and intracardiac echocardiography. After restoration of the sinus rhythm, decremental pacing near the CT was performed until 2 to 1 atrial capture. Complete transverse conduction block was defined as the appearance of double potentials with opposite activation sequence along the CT. Focal transverse conduction delay was defined as the appearance of double potentials at > or = 2 recording sites. Focal transverse conduction delay was observed during pacing at the cycle length of 693 +/- 110 ms in group I, 360 +/- 97 ms in group II and 343 +/- 109 ms in group III (P = 0.001). Complete transverse conduction block was observed during pacing at the cycle length of 391 +/- 118 ms in group I and 231 +/- 23 ms in group II (P = 0.001), but not in group III. In conclusion, focal transverse conduction delay in the CT was common in patients with AF. A predisposition to the line of the conduction block in the CT might contribute to the conversion of AF to typical atrial flutter due to amiodarone therapy.     

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.     

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.     

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.     

Septal His-Purkinje Ventricular Pacing in Canines: A New Endocardial Electrode Approach

Ventricular activation sequences and cardiac performance are influenced by pacing sites. Stimulation of or close to the specialized a trioventricular (AV) conduction system optimizes paced ventricular function compared to alternative epi- or endocardial muscle conduction sites. This study reports a new endocardial electrode implant approach to approximate septal His-Purkinje ventricular pacing. Five 6-month-old beagles were used, A custom, platinum-iridium, exposed helical screw electrode (Medtronic, Inc.), 4.5-mm long, with a 17.8-mm² surface area, was designed with a polyurethane covered 4 filar MP35N nickle conductor lead. An 8 French sheath (USCI, Inc.) was modified as introducer to permit simultaneous implant intracardiac pressure and electrogram recordings. Following a thoracotomy, the introducer was inserted through the right atrial appendage and advanced to record optimal His-bundle electrogram while maintaining atrial pressure along the septal tricuspid valve annulus. After electrode implant, ECG demonstrated narrow paced QRS morphology. Mean implant values showed sensed R wave 6,3 mV, slew rate 0.65 V/sec, pacing impedance 319 ohms, and threshold 0.9 V/3.3 mA at 0.5-msec output. Necropsy showed implant above the tricuspid annulus with electrode extension into and contained within the proximal ventricular septum. This study demonstrates that an endocardial septal approach to His-Purkinje ventricular pacing to optimize paced ventricular function is feasible with a new electrode design and precise septal implant technique. Alternative introducer designs may permit tranvenous application of this approach.     

Atrial threshold variability: implications for automatic atrial stimulation algorithms

BACKGROUND: Automatic management of atrial stimulation by verification of atrial threshold (ACM) has recently been made feasible. We investigated circadian atrial threshold variability over the long term and the predictors of successful automatic atrial threshold measurement, in order to provide practical clues for programming ACM features, in such a way as to achieve daily threshold verification and > 99% effective atrial stimulation. METHODS: Six daily attempts to measure atrial threshold were programmed in patients receiving an EnPulse pacemaker (Medtronic Inc., Minneapolis, MN, USA). Atrioventricular (AV) conduction was maximized by programming Search AV+ (SAV+) to a resting Paced AV delay = 400 ms in the first month, and 600 ms thereafter. RESULTS: Seventy-six patients had a median follow-up of 12 months. Median ACM success was 77%. Concordance between automatically and manually measured thresholds was observed during the entire follow-up (Rho = 0.82, P < 0.001). Daily variability in atrial threshold was < 0.5 V in > 94% of measurements in the first trimester after implantation, and < 0.5 V in > 99% of measurements thereafter, as well as any time after pacemaker replacement. Atrial threshold was measured on 86% of days: the predictors of ACM failure were AV block (AVB), high%Atrial pacing, and atrial fibrillation. Programming SAV+ to achieve 600 ms resting Paced AV decreased%Vpacing in patients with normal AV conduction and first-degree AVB, improving the ability to detect atrial threshold. CONCLUSIONS: The reliability of ACM is high over a long follow-up. On the basis of atrial threshold variability, a practical approach to ACM programming should be two daily atrial threshold measurements in patients with normal AV conduction and%Ap < or = 40%, or with normal sinus activity and AVB, whereas 3-4 measurements should be recommended in patients with first-degree AVB and%Ap > 40% or with recurrent atrial fibrillation and AVB. The lowest adapted stimulation output should achieve at least threshold +1 V in the first trimester after implantation, then threshold +0.5 V thereafter, in order to achieve > 99.5% effective atrial stimulation.     

P wave separation after atrial compartment operation for atrial fibrillation

Surgically induced abnormalities in atrial conduction could result in unusual P wave changes. A 31-year-old woman underwent concomitant mitral valve surgery and atrial compartment operation for mitral stenosis and atrial fibrillation (AF). After operation, the AF was successfully converted to sinus rhythm, whereas an unusual electrocardiogram (ECG) with a discrete negative deflection before the T wave in V1 was noted. Electrophysiological study showed a marked conduction delay from the high right atrium (HRA) to the right atrial appendage (RAA) compartment, which resulted in a separation of P waves. The P wave preceding the QRS complex represented the activation of sinus node and the left atrial compartments, and the P at the vicinity of T wave represented the activation of RAA compartment. The conduction from HRA to RAA was worsened on HRA pacing at a faster rate, and improved after isoproterenol infusion. This report demonstrated that conduction across a surgically created isthmus in the atrium could be severely impaired and result in unusual P wave separation.     

Verapamil suppresses the inhomogeneity of electrical remodeling in a canine long-term rapid atrial stimulation model

Verapamil is known to suppress shortening of the atrial effective refractory period (AERP) during relatively short-term atrial pacing, although the effect of a long-term stimulation model is unclear. The effect of verapamil on electrical remodeling was evaluated in a canine rapid atrial stimulation model. The right atrial appendage (RAA) was continuously paced (400 beats/min) for 2 weeks. Four pairs of electrodes were sutured at four atrial sites; the RAA, right atrium close to the inferior vena cava, Bachmann's bundle, and LA. AERP, AERP dispersion (AERPd), conduction time, and inducibility of AF were evaluated during the pacing phase and the recovery phase. The same protocol was performed under the administration of verapamil. In five control dogs, the AERP shortening was inhomogeneous and the shortening of the AERP was most prominent in the LA. AERPd increased during the rapid pacing phase by 5 +/- 2 ms, but recovered quickly in the recovery phase. The max AERPd was 46 +/- 4 ms in the control group and was larger than that in the verapamil group (31 +/- 3 ms, P = 0.001). At the LA site, the shortening of the AERP was decreased by verapamil administration (-19 +/- 3 vs -5 +/- 2 ms, P = 0.04). However, the AF inducibility was not significantly different between the two groups. The effect of verapamil on electrical remodeling was inhomogeneous, depending on the anatomic portion. As a result, AERPd widening during the rapid pacing phase was suppressed by verapamil, while the AF inducibility was unchanged.     

Atrial Pacing Lead Location Alters the Hemodynamic Effects of Atrial-Ventricular Delay in Dogs with Pacing Induced Cardiomyopathy

HETTRICK, D.A., et al .: Atrial Pacing Lead Location Alters the Hemodynamic Effects of Atrial Ventricular Delay in Dogs with Pacing Induced Cardiomyopathy. The role of atrial lead location in cardiovascular function in the presence of impaired ventricular dysfunction is unknown. We tested the hypothesis that left atrial (LA) and left ventricular (LV) hemodynamics are affected by alterations in AV delay and are influenced by atrial pacing site in dogs with dilated cardiomyopathy. Dogs   (n = 7)   were chronically paced at 220 beats/min for 3 weeks to produce cardiomyopathy and then instrumented for measurement of LA, LV end diastolic pressure (LVEDP) and mean arterial pressure (MAP), LA volume, LV short-axis diameter, and aortic and pulmonary venous blood flow. Hemodynamics were measured after instrumentation and during atrial overdrive pacing from the right atrial appendage (RAA), coronary sinus ostium (CSO) and lower LA lateral wall (LAW). The AV node was then ablated, and hemodynamics were compared during dual chamber AV pacing (right ventricular apex) from each atrial lead location at several AV delays between 20 and 350 ms. Atrial overdrive pacing from different sites did not alter hemodynamics. Cardiac output (CO), stroke volume, LVEDP, MAP and +dLVP/dt demonstrated significant (P < 0.05) variation with AV delay during dual chamber pacing. CO was higher during LAW pacing than RAA and CSO pacing (   2.3 ± 0.4   vs   2.1 ± 0.3   vs   2.0 ± 0.3 l/min   , respectively) at an AV delay of 120 ms. Also, MAP was higher in the LAW than RAA and CSO (   65 ± 9   vs   59 ± 9   vs   54 ± 11 mmHg   , respectively) at an AV delay of 350 ms. Atrial lead location affects indices of LV performance independent of AV delay during dual chamber pacing in dogs with cardiomyopathy. (PACE 2003; 26[Pt. I]:853–861)     

Sinus and paced P wave duration and dispersion as predictors of atrial fibrillation after pacemaker implantation in patients with isolated sick sinus syndrome

The aim of this study was to prospectively evaluate the sinus and the paced P wave duration and dispersion as predictors of AF after pacemaker implantation in patients with isolated sick sinus syndrome (SSS). The study included 109 (69 women, mean age 72 +/- 11 years) patients with SSS, 59 with bradycardia-tachycardia syndrome (BTS). A 12-lead ECG was recorded before pacemaker implantation and during high right atrial and septal right atrial pacing at 70 and 100 beats/min. The ECGs were scanned into a computer and analyzed on screen. The patients were treated with AAIR (n = 52) or DDDR pacing. The P wave duration was measured in each lead and mean P wave duration and P wave dispersion were calculated for each ECG. AF during follow-up was defined as: AF in an ECG at or between follow-up visits; an atrial high rate episode with a rate of > or =220 beats/min for > or =5 minutes, atrial sensing with a rate of > or =170 beats/min in > or =5% of total counted beats, mode-switching in >/=5% of total time recorded, or a mode switching episode of > or =5 minutes recorded by the pacemaker telemetry. The ECG parameters were correlated to AF during follow-up. Mean follow-up was 1.5 +/- 0.9 years. None of the ECG parameters differed between patients with AF and patients without AF during follow-up, nor was there any difference between groups after correction for BTS and age. BTS was the strongest predictor of AF during follow-up (P < 0.001). P wave duration and dispersion measured before and during pacemaker implantation were not predictive of AF after pacemaker implantation in patients with isolated SSS.     

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.