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.     

Adverse Pacemaker Hemodynamics Evaluated by Pulmonary Venous Flow Monitoring

The pacemaker syndrome refers to symptoms and signs in the pacemaker patient caused by an inadequate timing of atrial and ventricular contractions. The lack of normal atrioventricular synchrony may result in a decreased cardiac output and venous cannon A waves. The objective of this study was to define the left atrial and pulmonary venous flow response to ventricular pacing in a group of 14 unselected consecutive patients with total heart block and sinus rhythm. Pulmonary venous flow was assessed by transesophageal pulsed Doppier echocardiography in the VVI and ODD pacing modes. An inappropriate atrial timing caused a marked augmentation of the normally small pulmonary venous z wave in all patients ("negative atrial kick" peak z wave in DDD pacing 14.5 ± 4.6 cm/s, VVI pacing 51.8 ± 15.0 cm/s). Restoration of AV synchrony (DDD pacing, AV interval 100 ms) abolished these "cannon z waves" in all patients, and a normal pattern of pulmonary venous flow was achieved. Abnormal pulmonary venous flow characteristics were observed in 2 of 14 patients during DDD pacing with short AV intervals (100 ms). The Doppier pattern was similar to the findings seen in VVI pacing. Assessment of pulmonary venous flow by transesophageal pulsed Doppier echocardiography may provide a simple, sensitive, and relatively noninvasive technique to evaluate patients with suspected pacing induced adverse hemodynamics.     

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)     

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.     

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 in Patients Undergoing AV Stimulation: Effects of Increasing Right Atrial Stimulation Rate

To evaluate the frequency of spontaneous or rate dependent interatrial blocks, the interatrial conduction time (IACT) was studied on 100 consecutive patients (mean age 78.3 ±7.8 years) during a transvenous dual chamber pacemaker implant. The spontaneous interatrial conduction time (SIACT) was measured from the intrinsic deflection (ID) of the unipolar right atrial signal to the ID of the left atrial signal recorded in a bipoiar way by an esophageal lead. The paced interatrial conduction time (PIACT) was measured from the stimulus artifact to the left atrial ID, when the atrium was paced at a slightly higher rate than the spontaneous rate and during incremental atrial pacing. From these measurements, the maximum increase ofPIACT (MIPIACT) was deduced. In this elderly population, the PIACT was similar (117 ± 26.9 msec) to the data in the literature. However, there were large interindividual variations that were also found in SIACT. We found a close correlation between SIACT and PIACT (P < 0.0001). PIACT was on average 50 msec longer than SIACT. SIACT increased with age (P < 0.03). The MIPIACT was 15.3 ± 15.2 msec. In the majority of patients, the MIPIACT was > 10 msec, and even reached 90 msec in one patient. MIPIACT was longer in patients with a PIACT exceeding 110 msec (P < 0.004). Based on IACT alone, the AV interval must be lengthened on average by 50 msec when changing from atrial tracking-ventricular pacing to atrial pacing-ventricular pacing, but large individual differences must be kept in mind. Elderly people should probably have a longer AV delay.     

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.     

Predictive Value of the P Wave at Implantation for Atrial Fibrillation After VVI Pacemaker Implantation

This study assesses the value of P wave measurements on the surface EGG at implantation, in the prediction of atrial fibrillation in VVI paced patients. From a consecutive series of 320 pacemaker implantations 172 WI paced patients for symptomatic atrioventricular block (AVB) (n = 126; mean age 69 ± 14) or sick sinus syndrome (SSS) (n = 56; mean age 68,6 ± 12] and in sinus rhythm at implantation were used in this study. P wave duration in VI is correlated with the incidence of atrial fibrillation during 5 years of follow-up. VI at implantation was significantly longer (114.6 ± 2.7 msec) in the patients who developed atrial fibrillation than in those who did not (91.9 ± 2.7 msec) (P < 0.001). Although positive predictive accuracy increases progressively for higher VI values for AVB and SSS, the negative predictive and diagnostic accuracy of V1 criteria were Jess in SSS. Application of the Bayes' theorem showed that in SSS the probability to develop atrial fibrillation is 33% for V1 < 110 msec and is for V1 < 90 msec still higher than that reported in DDD paced patients. In the AVB group the probability to develop atrial fibrillation is 8% for V1 < 110 msec and 6% for V1 < 100 msec. It seems, therefore, that atrial stimulation (AAI or DDD) is always indicated in SSS. In AVB with V1 < 100 msec, DDD pacing, if not needed for other indications, apparently does not offer much benefit in the prophylaxis of atrial fibrillation.     

Proposal of a Method for Automatic Optimization of Left Heart Atrioventricular Interval Applicable to DDD Pacemakers

Electrical pacing of the right heart is known to cause delays in the depolarization of left heart chambers, leading to abnormal left heart AV sequence. Interatrial conduction time, defined as the time from the right atrial pacing pulse or intrinsic P to the onset of left atrial P wave, and P wave sensing delay cause a shorter left heart AV interval during atrial pacing-ventricular sensing and atrial sense-ventricular pace. Interventricular conduction time (the time from the right ventricular pacing pulse to the onset of left ventricular depolarization), lengthens left heart AV interval during atrial sensing-ventricular pacing. These delays may add up or partly cancel out, depending on pacing mode. Thus, an algorithm for DDD pacemakers to optimize left heart AV interval by compensating for the above delays is proposed. This algorithm takes into account pacing and sensing delays to deliver a certain AV sequence to the right heart, aimed at producing a physiological left heart AV interval. The optimization of left heart AV interval is achieved by automatically changing right heart AV interval and pacing mode in accordance with known interatrial and interventricular conduction delays, and P wave sense offset.     

Acute Hemodynamic Improvement by Pacing in Patients with Severe Congestive Heart Failure

Since the first report on dual chamber pacing for congestive heart failure (CHF) in 1991, a number of investigators have explored the topic with conflicting results. These conflicts may arise from an incomplete understanding of the mechanisms by which pacing improves cardiac function. Potential mechanisms include: (1) increase in filling time: (2) decrease in mitral regurgitation: (3) optimization of left heart mechanical atrioventricular delay (left heart MAVD); and (4) normalization of ventricular activation. One or more of these mechanisms may be operative in an individual patient, implying that patients may require individuol optimization. Acute pacing studies were conducted on nine CHF patients, NYHA Class II-III to Class IV. Measurements of conduction times in sinus rhythm revealed: (1) normal interatrial conduction times (59 ± 5 ms) in all patients, with wide variations in interventricular conduction times (range, ?15–105 ms); and (2) a wide range of left heart MAVD (range, 97–388 ms). While pacing the right, left, or both ventricles, measurement of high fidelity aortic pressure and mitral and aortic velocities revealed the following: (1) 6 of 9 patients increased mean pulse pressure over sinus value during RV orLV pacing at an optimal A V delay: (2) the maximum aortic pulse pressure was achieved when the atrium was not paced: an 8% increase over sinus pulse pressure with paced RV versus a 5% decrease for paced atrium and RV at optimum AV delay (paired Student's t-test, P = 0.01), and a 0% increase over sinus with paced LV versus 7% decrease for paced atrium and LV at optimum AV delay, P < 0.05: (3) significant dependence on pacing site was noted, with 4 patients doing best with RV pacing. 3 patients achieving a maximum with LV pacing, and 2 patients showing no preference; and (4) 2 of 4 patients with restrictive filling patterns were converted to nonrestrictive patterns with optimum pacing. Patient hemodynamics appear to benefit acutely from individually optimized pacing. Increases in filling time, optimization of left heart MAVD, and normalization of intraventricular activation are the most significant mechanisms. Atrial pacing is inferior to atrial sensed modes if the patient has a functional sinus node.     

Effects of Septal Pacing on P Wave Characteristics: The Value of Three-Dimensional Echocardiography

SZILI-TOROK, T., et al .: Effects of Septal Pacing on P Wave Characteristics: The Value of Three-Dimensional Echocardiography. Interatrial septum (IAS) pacing has been proposed for the prevention of paroxysmal atrial fibrillation. IAS pacing is usually guided by fluoroscopy and P wave analysis. The authors have developed a new approach for IAS pacing using intracardiac echocardiography (ICE), and examined its effects on P wave characteristics. Cross-sectional images are acquired during pullback of the ICE transducer from the superior vena cava into the inferior vena cava by an electrocardiogram- and respiration-gated technique. The right atrium and IAS are then three-dimensionally reconstructed, and the desired pacing site is selected. After lead placement and electrical testing, another three-dimensional reconstruction is performed to verify the final lead position. The study included 14 patients. IAS pacing was achieved at seven suprafossal (SF) and seven infrafossal (IF) lead locations, all confirmed by three-dimensional imaging. IAS pacing resulted in a significant reduction of P wave duration as compared to sinus rhythm (   99.7 ± 18.7   vs   140.4 ± 8.8  ms; P < 0.01   ). SF pacing was associated with a greater reduction of P wave duration than IF pacing (   56.1 ± 9.9   vs   30.2 ± 13.6  ms; P < 0.01   ). P wave dispersion remained unchanged during septal pacing as compared to sinus rhythm (   21.4 ± 16.1   vs   13.5 ± 13.9  ms; NS   ). Three-dimensional intracardiac echocardiography can be used to guide IAS pacing. SF pacing was associated with a greater decrease in P wave duration, suggesting that it is a preferable location to decrease interatrial conduction delay. (PACE 2003; 26[Pt. II]:253–256)     

Relationship Between Atrial Conduction Defects and Fractionated Atrial Endocardial Electrograms in Patients with Sick Sinus Syndrome

The relationship between abnormal atrial electrograms (AAE) recorded during sinus rhythm by endocardial calheter mapping of the right atrium and the afrial conduction defects of sinus impulses or single atrial extrastimuli was investigated in 44 patients with sick sinus syndrome. The patients were divided into two groups on the basis of the presence (n = 29) or absence (n = 15) of AAE recorded during sinus rhythm. The P wave duration in the AAE (+) Group patients was 137 ± 14 msec, and 125 ± 15 msec in (he AAE (−) Group; P < 0.02. The intraatrial conduction time of sinus impulses in the AAE (+) Group was 54 ± 12 msec, and 39 ± 9 msec in the AAE (−) Group; P < 0.001. The interatrial conduction time in the AAE (+) Group was 101 + 14 msec, and 78 ± 16 msec in the AAE (−) Group; P < 0.001. In the AAE (+) Group, H (38%) patients ha d a sinus node recovery time > 4 seconds, whereas in the AAE (−) Group there was only one (6%) patient; P < 0.03. AAE showed a specificity of 93% and a positive predictive accuracy of 91% in predicting inducibility of atrial fibrillation. The sensitivity was 35% and the negative predictive accuracy was 42%. Sustained atrial fibrillation was induced in ten (35%) patients of the AAE (+) Group, and in one (7%) patient of the AAE (−) Group; P < 0.05. These data suggest that in patients with sick sinus syndrome who possess abnormal endocardial eJectrograms in sinus rhythm within the right atrium have: (1) a significantly longer P wave duration: (2) a significantly longer intraatrial and interafrial conduction time of sinus impulses; and (3) a significantly greater sinus node dysfunction and higher incidence of induction of sustained atriai fibrillation. It is concluded that there are significantly greater atrial conduction defects in patients with sick sinus syndrome who possess AAE within the right atrium during sinus rhythm.     

Hemodynamic Findings During Sinus Rhythm, Atrial and AV Sequential Pacing Compared to Ventricular Pacing In a Dog Model

The hemodynamic responses of atrial lAF], atrioventricu-lar sequential (AVP) and ventricuJar pacing (VP) were compared to sinus rhythm (SfiJ in seventeen anesthetized dogs with intact AV conduction. The atrium and/or ventricle were paced at fixed rates above the control sinus rate. An AV interval shorter than normal conduction was selected to capture the ventricle. The changes of pulmonary capillary wedge pressure (PCWP, mmHg). mean aortic pressure (MAP, mmHg), cardiac output (CO, L/min), systemic vascular resistance (SVR, dynes/s/cm⁻⁵), left ventricular stroke work index (SWI) and mean systolic ejection rate (MSER, ml/s) during sinus rhythm, atrial pacing and atrio-ventricular sequential pacing (expressed in percentages of the individual values during ventricular pacing) were:
The importance of atrial systole for cardiac performance was clearly demonstrated in dogs with normally compliant hearts. In both atrial and atrioventricular sequential pacing compared to ventricular pacing there was a reduction of pulmonary capillary wedge pressure (PCWP) (p < 0.01) and systemic vascular resistance (SVR) (p < 0.01) despite an increase in cardiac output (CO). The lesser mean systolic ejection rate (MSER) found during atrioventricular sequential pacing compared to sinus rhythm and atrial pacing may be explained by the abnormal ventricular depolarization in this pacing mode; nevertheless, the mean systolic ejection rate was still greater than that found during ventricular pacing (p < 0.05).     

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.     

Evaluation of atrial conduction time at various sites of right atrial pacing and influence on atrioventricular delay optimization by surface electrocardiography

Cardiac function and electrical stability may be improved by programming of optimal AV delay in DDD pacing. This study tested the hypothesis if the global atrial conduction time at various pacing sites can be derived from the surface ECG to achieve an optimal electromechanical timing of the left heart. Data were obtained from 60 patients following dual chamber pacemaker implantation. Right atrial septal pacing was associated with significantly shorter atrial conduction time (P < 0.0005) and P wave duration (P < 0.005), compared to standard right atrial pacing sites at the right atrial appendage or at the right free wall. The last two pacing sites showed no significant difference. In a group of 31 patients with AV block, optimal AV delay was achieved by programming a delay of 100 ms from the end of the paced P wave to peak/nadir of the paced ventricular complex. Optimization of AV delay resulted in a relative increase of echocardiographic stroke volume (SV) (10.9 +/- 13.7%; 95% CI: 5.9-15.9%) when compared to nominal AV delay (170 ms). Optimized AV delay was highly variable (range 130-250 ms; mean 180 +/- 35 ms). The hemodynamic response was characterized by a weak significant relationship between SV increase and optimized AV delay (R2 = 0.196, R = 0.443, P = 0.047). The study validated that septal pacing is advantageous for atrial synchronization compared to conventional right atrial pacing. Tailoring the AV delay with respect to the surface ECG improved systolic function significantly and was superior to nominal AV delay settings in the majority of patients.     

AV junctional ablation allowing more effective delivery of cardiac resynchronization therapy in patients with intra- and interatrial conduction delay

We report two patients with cardiac resynchronization therapy (CRT) devices and evidence of refractory heart failure in whom impaired intraatrial conduction in one patient, and interatrial conduction in the other, prohibited optimization of the atrioventricular (AV) timing sequence. The patient with intraatrial conduction delay exhibited late right atrial sensing and latency during right atrial pacing that required programming of a short-sensed AV delay and long-paced AV delay (wide differential AV delay). In both patients AV junctional ablation and echocardiography-guided device optimization significantly improved heart failure.     

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.     

Nonphysiological Left Heart AV Intervals as a Result of DDD and AAI "Physiological" Pacing

DDD and AAI pacemakers are considered physiological, since they preserve atrioventricular (AV) synchrony. Artificial pacing, however, is performed largely from right heart chambers, causing aberrant depolarization pathways. Pacing at the right atrial appendage (RAP) is known to delay left atrial contraction due to interatrial conduction time (IACT), and right ventricular (RV) apical pacing (RVP) delays left ventricular (LV) contraction due to interventricular conduction time (TVCT). These delays may render the left heart AV intervals (LAV) either too short or too Jong, thus affecting LV systolic function. The purpose of this study was to evaluate the actual LAV intervals during conventional, right heart AAI and DDD pacing. Resulting LAV intervals were compared to programmed AV values during all DDD pacing modalities. Ten patients with DDD and six patients with AAI pacemakers were studied. IACT was measured from the atrial spike to the onset of left P wave, as recorded by an esophageal lead. Systolic time intervals were measured using either a carotid pulse tracing or a densitogram (photoplethysmography). LV function was appraised by measuring rate-corrected LV ejection time (LVETc). IVCT was measured indirectly as the lengthening of LV preelection period (PEPJ caused by RV pacing, as compared to normal depolarization pathway. Intrinsic‘ACT and IVCT were considered zero. Right heart AV intervals (RAV) were measured from surface ECG and LAVs were calculated according to the following equations: Sinus Rhythm: LAV = RAV; Atrial Pace 4- Ventricular Sense: LAV= RAV ? IACT; Atrial Sense + Ventricular Pace: LAV = RAV + IVCT; Sequential AV Pace: LAV = RAV ? IACT + IVCT, Results: 1. IACT: mean = 73 msec, range: 35–130; IVCT: mean = 50 msec, range: 44–100. 2. Compared to RAVs, LAVs were either too short or too long (?130 to + 300 msec: P < 0.001 J in RAP 4- RVS and RAS + RVP. Conclusions: 1. LAV differed significantly from RAV during AP + VS and AS + VP. 2. “Physiological” RAV intervals in DDD and AAI may cause nonphysiological LAV, possibly affecting LV function. 3. IACT and IVCT should be accounted for when programming DDD PM to provide physiological LAV.     

Comparison of two strategies to reduce ventricular pacing in pacemaker patients

Background: Managed Ventricular Pacing (MVP) and Search AV+ (SAV+) are two pacing algorithms designed to reduce ventricular pacing. MVP promotes conduction by operating in AAI/R mode with backup ventricular pacing during atrioventricular block (AVB). SAV+ operates in DDD/R mode with a nominal AV extension of 290 ms during atrial sensing and 320 ms during atrial pacing. The reduction in ventricular pacing was compared with these two algorithms in pacemaker patients.
Methods: The EnRhythm and EnPulse clinical studies assessed the percentage of ventricular pacing (%VP) after 1 month. Each patient's AVB status was assigned using the following hierarchical categories: persistent third-degree AVB (p3AVB), episodic third-degree AVB (e3AVB), second-degree AVB (2AVB), first-degree AVB (1AVB), and no AVB (nAVB). The%VP was tabulated for each AVB status category.
Results: Data were available from 322 patients of whom 129 received DDD(R) pacing with the MVP algorithm activated and 193 patients with DDD(R) pacing and the SAV+ function activated, each for a month period. MVP resulted in a significantly lower median%VP than SAV+ in all AVB categories except for p3AVB: nAVB (0.3 vs 2.9, P < 0.0001), 1AVB (0.9% vs 80.6%, P < 0.0001), 2AVB (37.6 vs 99.3, P< 0.002), e3AVB (1.2 vs 42.2, P = 0.02), p3AVB (98.9 vs 100, P = 1.00).
Conclusion: MVP resulted in a greater reduction in%VP than SAV+ across all patient groups except persistent third-degree AV block. The greatest reduction in%VP was observed in patients with mildly impaired AV conduction.