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.     

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.     

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.     

Comparison of Intrinsic Versus Paced Ventricular Function

There is increasing evidence supporting the benefits of providing optimum AV delay in cardiac pacing, though controversy exists regarding its value and the benefits of intrinsic versus paced ventricular activation. This study compared various AV delays at rest in patients whose native AV delays were 200 msec. Only patients with DDD pacemakers who had intact AV conduction and normal ventricular activation were included in the study. Nine patients were studied. Methods: Ten studies were performed. Evaluation was done in AAI and DDD modes at paced heart rates of 60/min or as close as possible to the intrinsic heart rate if this was > 60/min. Stroke volume (SV) and cardiac output (COJ were measured. Results: When AV sequential pacing in the DDD mode with an optimum AV delay was compared to AAI pacing with a prolonged AV interval, the average optimum AV delay in the DDD mode was 157 msec and ranged from 125 to 175 msec. The average AV interval in the AAI mode was 245 msec and ranged from 212 to 300 msec. In the DDD mode, there was an overall significant improvement in CO of 11% and SV of 9%. Patients with intrinsic AV conduction times of > 220 msec showed an overall significant improvement in CO of 13% and SV of 11%. In patients with intrinsic AV conduction times of < 220 msec, an improvement in CO of 6% and SV of 4% was seen. Conclusions: (1) An optimum AV delay is an important component of hemodynamic performance; and (2) AV sequential pacing at rest with an optimum AV delay may provide better hemodynamic performance than atrial pacing with intrinsic ventricular conduction when native AV conduction is prolonged > 220 msec.     

Apparent Extension of the Atrioventricular Interval Due to Sensor-Based Algorithm Against Supraventricuiar Tachyarrhythmias

Rapid ventricular tracking response to supraventricular tachyarrhythmia is one major limitation to DDD pacing. In a DDDR pacemaker, sensor-based algorithms have been used to control these arrhythmias. These include the use of an interim rate limit (conditional ventricular tracking limit) or a separate maximum tracking and sensor rate limits (discrepant upper rate). These algorithms limit inappropriate ventricular pacing rate during tracking of pathological supraventricuiar tachyarrhythmia and atrial flutter by Wenckebach-like prolongation of the AV interval. We observed that this may cause an unexpected extension of the AV interval in patients with high atrial rate and intact AV nodal conduction. This was due to P wave rate above the conditional ventricular tracking limit or maximum tracking limit, but AV paced interval prolongation was avoided by the occurrence of intrinsic conduction, albeit at an AV interval longer than the programmed AV interval. This might appear as failure of ventricular pacing on the ECG. This phenomenon is a modified form of "upper rate" behavior occurring in the AV interval, and should be recognized as a normal behavior rather than pacemaker malfunction.     

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.     

Automatic Beat‐to‐Beat Left Heart AV Normalization:

Programming the right heart AV interval to a normal value may cause a nonphysiological left heart AV due to interatrial and interventricular conduction delays, thus affecting cardiac performance. Since AV normalization at rest and exercise may be invalidated by pacing or sensing (mode) changes, the aim of this study was to (1) study the feasibility of a mode independent pacemaker (PM) algorithm for automatic beat-to-beat left AV normalization, (2) establish normal values for the time between mitral flow A wave (Af) and ventricular activation (Va), the AfVa interval, the mechanical surrogate of left AV, and (C) determine the range of values of the interatrial electromechanical delays (IAEMDs) and the effect of RA pacing. To pace with the proper right AV, the previously reported RV-paced interventricular electromechanical delay and the interatrial electromechanical delay, either P-sensed (IAEMDs) or atrial-paced (IAEMDp) are required inputs. Data were collected during diagnostic echo Doppler studies in 84 subjects divided in three groups: (1) control with narrow QRS and no structural heart disease (n = 33, age 50 +/- 21 years, 42% men); (2) patients in sinus rhythm with diverse cardiac pathologies except LBBB (n = 39, age 69 +/- 14 years, 56% men), and (3) DDD-paced patients (n = 12, mean age 71 +/- 6 years). Normal values of AfVa were established from the control group, while IAEMDs and IAEMDp and active atrial flow time (A-peak), in all subjects. The algorithm was tested by computer simulation under all possible modes with the following calculation: RAV = N + IAEMD - IVD, where RAV is the right AV, N is the desired normal AfVa value, IAEMD is either P-sensed or A-paced, and IVD is close to zero for intrinsic narrow QRS and biventricular pacing, or 79 ms for RV pacing. The results demonstrated (1) Normal (controls) AfVa: 85 +/- 15 ms (range 52-110 ms); (2) IAEMDs (All): 84 +/- 16 ms; (3) atrial pacing prolonged IAEMDs by 57 +/- 18 ms (from 93 +/- 15 to 150 +/- 25 ms, P < 0.0001); and (4) Computer simulation of rate and mode changes validated the normalization algorithm. An automatic, beat-to-beat left AV normalization algorithm to preserve a normal AfVa without a hemodynamic sensor is feasible. The normal value of AfVa is 85 +/- 15 ms.     

Differentiation of Sinus Tachycardia From Ventricular Tachycardia with 1:1 Ventriculoatrial Conduction in Dual Chamher Implantable Cardioverter Defibrillators: Feasibility of a Criterion Based on the Atrioventricular Interval

Tachycardia discrimination in future implantable cardioverter defibrillators (ICDs) is likely to be enhanced by the addition of an atrial sensing/pacing lead. However, differentiation of sinus tachycardia (ST) from ventricular tachycardia (VT) with 1:1 VA conduction will remain problematic. We assessed the use of the AV interval as a potential criterion for correctly differentiating ST from VT. Incremental V pacing at the right ventricular (HV) apex served as a “VT” model in each of 41 patients with 1:1 VA conduction to pacing cycle lengths ≤ 450 msec. High right atrial and RV apical electrograms during normal sinus rhythm (NSR) and during incremental V pacing were digitized (simulating ICD sensing). From these signals, AV interval versus pacing cycle length plots were computer generated to identify crossover cycle lengths, each defined as the cycle length at which the AV interval during V pacing equals the AV interval during NSR. At cycle lengths longer than the crossover value, the AV interval during “VT” exceeds the AV interval during NSR. In contrast, the AV interval during ST is physiologically shorter than the AV interval during NSR. Thus, ST can be readily differentiated from “VT” over a range of cycle lengths greater than the crossover value. The overall mean calculated crossover cycle length was 371 ± 52 msec. In 11 patients paced multiple times, each crossover cycle length was reproducible (mean coefficient of variation was 1.2%± 0.9% per patient). AV intervals measured at the RV apex were also analyzed with incremental V pacing during catecholamine stimulation (isoproterenol, n = 5) and during alternate site “VT” (RV outflow tract [n = 8] and left ventricle [n = 2]). In all these cases, the new “VT” plots of AV interval versus pacing cycle length coincided with or fell to the left of those obtained during control RV apical pacing and recording (i.e., these AV interval values crossed the NSR baseline at cycle lengths ≤ the crossover cycle length). Thus, the cycle length range for recognizable differentiation of ST from “VT” remained valid. The data suggest that the described AV interval criterion relying on the crossover cycle length: (1) is a promising approach to improve differentiation of ST from relatively slow VTs with 1:1 VA conduction, and (2) can readily be automated in future dual chamber ICDs, given its computational simplicity.     

Septal Short Atrioventricular Delay Pacing: Additional Hemodynamic Improvements in Heart Failure

Controversy exists as to whether short AV delay pacing is beneficial in left ventricular dysfunction with the studies performed coming to disparate conclusions. The right ventricular apical pacing previously studied results in asynchronous contraction and relaxation sequences and may limit the potential benefits of short AV delay pacing. In this study the hemodynamic effects of septal (resulting in a more physiological activation sequence) and apical right ventricular activation were compared in 15 patients with heart failure. VDD pacing with AV delays of 50,100, and 150 msec was evaluated. Apical VDD pacing did not increase the cardiac output significantly, 4.1 ± 0.75 to 4.45 ± 0.74 L/min, whereas septal VDD pacing increased the cardiac output to 4.86 ± 0.79 L/min (P = 0.037). Apical pacing increased the cardiac output in 10 patients and septal pacing in 11 patients. We conclude that selected patients with ventricular dysfunction benefit from short AV delay pacing. Septal ventricular activation confers significant hemodynamic improvements over apical activation.     

Determination of the optimal atrioventricular interval in sick sinus syndrome during DDD pacing

BACKGROUND: Although the AAI pacing mode has been shown to be electromechanically superior to the DDD pacing mode in sick sinus syndrome (SSS), there is evidence suggesting that during AAI pacing the presence of natural ventricular activation pattern is not enough for hemodynamic benefit to occur. Myocardial performance index (MPI) is a simply measurable Doppler-derived index of combined systolic and diastolic myocardial performance. The aim of this study was to investigate whether AAI pacing mode is electromechanically superior to the DDD mode in patients with SSS by using Doppler-derived MPI. METHODS: Thirty-nine SSS patients with dual-chamber pacing devices were evaluated by using Doppler echocardiography in AAI mode and DDD mode. The optimal atrioventricular (AV) interval in DDD mode was determined and atrial stimulus-R interval was measured in AAI mode. The ratio of the atrial stimulus-R interval to the optimal AV interval was defined as relative AV interval (rAVI) and the ratio of MPI in AAI mode to that in DDD mode was defined as relative MPI (rMPI). RESULTS: The rMPI was significantly correlated with atrial stimulus-R interval and rAVI (r = 0.57, P = 0.0002, and r = 0.67, P < 0.0001, respectively). A cutoff point of 1.73 for rAVI provided optimum sensitivity and specificity for rMPI >1 based on the receiver operator curves. CONCLUSIONS: Even though the intrinsic AV conduction is moderately prolonged, some SSS patients with dual-chamber pacing devices benefit from the ventricular pacing with optimal AV interval. MPI is useful to determine the optimal pacing mode in acute experiment.     

VDD Pacing at Short Atrioventricular Intervals Does Not Improve Cardiac Output in Patients with Dilated Heart Failure

Atrial synchronous pacing with short, nonphysiologicai atrioventricular (AV) intervals has been reported to increase cardiac output in selected patients with severe dilated heart failure. The aim of this study was to determine the acute effect of atrial synchronous pacing with short AV intervals in a consecutive series of patients with dilated heart failure. Twelve patients with a mean ejection fraction of 21 %± standard error 2.5% were studied. Pacing catheters were placed in the high right atrium and right ventricular apex and a balloon flotation catheter in the pulmonary artery for measurement of cardiac output. Simultaneous transthoracic echocardiography was performed for measurement of left ventricular filling time and mitral regurgitation. In a randomized crossover design, measurements were made during VDD pacing at programmed AV intervals of 100 and 60 msec and during a control period in sinus rhythm. Left ventricular filling time increased at AV intervals of 100 and 60 msec (mean difference 37 ± 9 and 34 ± 11 msec, respectively, both P < 0.01 compared to control). Despite increases in ventricular filling time, stroke, and cardiac index declined with short atrioventricular intervals (at an AV interval of 60 msec, stroke index fell by 2.1 ± 0.5 mL/m², P < 0.05 and cardiac index by 125 ± 45 mL/m²; P = NS). Heart rate was unchanged at both AV intervals (78 ± 4.9 at control, 78 ± 5.2 at 100 msec and 79 ± 4.9 beats/min at 60 msec; P = NS). The decrease in stroke index at an AV Interval of 60 msec was inversely related to control left ventricular filling time (r = 0.74; P = 0.01) and ejection fraction (r = 0.69; P = 0.02) and directly related to heart rate (r = 0.77; P < 0.01). The change in stroke index at an AV delay of 60 msec was also inversely related to the change in mitral regurgitation induced by pacing (r = 0.84; P = 0.01). Thus, in a group of patients with stable dilated heart failure, atrial synchronous pacing with short AV intervals did not improve cardiac output. The change in cardiac output with pacing was inversely related to baseline left ventricular function and to the change in mitral regurgitation induced by pacing.     

The Effect of Ventricular Activation Sequence on Cardiac Performance During Pacing

The aim of this study was to evaluate the importance of a normal ventricular activation pattern for cardiac performance. In nine mongrel clogs, atrial pacing was compared to AV synchronous pacing at three different A V delays (150, 100, and 60 nis). In six dogs, proximal septal AV synchronous pacing was compared to apical A V synchronous pacing at three different A V delays. AV synchronous pacing was performed after RF induced complete heart block. Hemodynarnics were evaluated by assessment of positive and negative dP/dt, cardiac output, and left ventricular and pulmonary pressures. Atrial pacing was superior to AV synchronous pacing with respect to positive and negative dP/dt and cardiac output. This difference was present at all AV delays. Proximal septal pacing was associated with a higher positive and negative dP/dl compared to apical pacing at all AV delays. Left ventricular activation time was significantly shorter during proximal septal pacing than during apical pacing (88 ± 4 vs 115 ± 4 ms, P < 0.001). We conclude that atrial and proximal septal pacing improves cardiac function and shortens the ventricular activation time compared to apical AV synchronous pacing independent of the AV interval.     

Experience and Implantation Techniques with a New Single-Pass Lead VDD Pacing System

Thirty-six patients were implanted with a single-lead atrial-synchronous ventricular pacing (VDD) system at our center in the first and second phases of a clinical trial between October 1987 and December 1989. The clinical system comprised a pulse generator in conjunction with a pacing lead incorporating two diagonal atrial bipolar (DAB) electrodes designed to lie in the mid-to upper-right atrium and a distal tip electrode for ventricular pacing and sensing. Twenty five of the patients had complete heart block, ten had second-degree block, and one had AV nodal block. A modified Bruce protocol limiting treadmill speed to 1.7 miles per hour was used to establish sinus node competency as evidenced by sustained sinus rate increase in a more-or-less linear fashion. The mean acute P wave amplitude measured at implant was 1.66 mV +/- 1.04 SD; the mean P wave amplitude (minimum and maximum, both sitting and supine) for all patients at all follow-up (N = 420) was 1.54 mV +/- 0.9 SD. The follow-up interval for all patients ranged from a minimum of 13 days and a maximum of 762 days, with a mean of 261 +/- 206 days as of December 1, 1989. Four dislodgments of the ventricular electrode occurred with the more pliable of two passive fixation mechanisms used on the lead; atrial sensing remained intact at all times with both fixation systems. Changes in atrial sensing threshold were quite frequent during the early follow-up visits due to electrode movement in the right atrium; however, adequate ventricular tracking of the atrial rate was achieved in all cases once the threshold values were established initially, even though several patients required atrial sensing of 0.2 mV at some of the follow-up visits. Two patients presented with pacemaker-mediated tachycardia associated with retrograde conduction, which was resolved with reprogramming; they are presently maintaining atrial synchrony in the VDD mode. Successful single-lead VDD pacing with consistent P wave sensing has been achieved with this atrial rate responsive system.     

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)     

Hemodynamic Consequences of Atrioventricular and Ventriculoatrial Pacing

The effect of atrialventricular versus ventricular pacing and contraction were studied in seven open-chest dogs. Cardiac output, left ventricular, left atrial, right atrial and pulmonary artery pressures were recorded. The right or left ventricular apical areas were consistently superior as ventricular pacing sites.
Appearance of cannon A waves within the pre- or ejection period produced a significant decrease in left ventricular and systemic blood pressure, and cardiac output with a concomitant increase in right atrial, ventricular and pulmonary pressures. Prominent "v" waves were also observed during these periods.
Reducing the basic driving cycle length from 400 to 300 msec caused a marlted deterioration of all hemodynamic parameters with the appearance of mechanical alternans. Random VA conduction or ventricular pacing in the presence of com-plete AV and VA heart block appeared to offer a more favorable hemodynamic result than constant 1:1 VA conduction. It is concluded that maintenance of a physiologic AV interval permitting atrial contraction to appear outside of pre- or ejection period of ventricular systole is an important determinant or ventriculor function during cardiac pacing.     

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).     

Effects of Different Pacing Modes on Left Ventricular Relaxation in Closed-Chest Dogs

Ventricular relaxation is an important determinant of ventricular filling; impaired relaxation may decrease cardiac output and stroke volume. Relaxation hos been shown to occur more quickly following beats with an increased extent of systolic fiber shortening. Since cardiac output and stroke volume are greater during atrioventricular (AV) sequential pacing than during ventricular pacing at identical heart rates, we reasoned that AV sequential pacing would improve relaxation. To assess this hypothesis we studied 11 dogs with chronic (1-3 months) complete heart block (CHB) induced by radiofrequency catheter ablation of the His bundle. Right and left heart pressures, thermodilution cardiac output, und single plane ventriculography were recorded during baseline rhythm (CHB), and VVI, and AV sequential pacing at a heart rate greater than the sinus rate. None had ventriculoatrial conduction. During AV sequential pacing, the AV interval was set at 150 msec. Cardiac output and stroke volume were significantly increased in the AV sequential compared to the VVI pacing mode. Left ventricular pressures, maximal positive and negative dP/dt, and the time constant (T) of isovolumic pressure decay were not different in the two modes. We conclude that despite increased stroke volume in the AV sequential pacing mode, relaxation is unchanged. We believe the lack of change in relaxation is due to nonuniform ventricular activation when depolarization is initiated at the right ventricular apex.     

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.     

A 2:1 AV rhythm: an adverse effect of a long AV delay during DDI pacing and its prevention by the ventricular intrinsic preference algorithm in DDD mode

A 91-year-old woman received a dual-chamber pacemaker for sick sinus syndrome and intermittently abnormal atrioventricular (AV) conduction. The pacemaker was set in DDI mode with a 350-ms AV delay to preserve intrinsic ventricular activity. She complained of palpitation during AV sequential pacing. The electrocardiogram showed a 2:1 AV rhythm from 1:1 ventriculoatrial (VA) conduction during ventricular pacing in DDI mode with a long AV interval. After reprogramming of the pacemaker in DDD mode with a 250-ms AV interval and additional 100-ms prolongation of the AV interval by the ventricular intrinsic preference function, VA conduction disappeared and the patient's symptom were alleviated without increasing unnecessary right ventricular pacing.     

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.