Contribution of Atrioventricular Synchrony to Left Ventricular Systolic Function in a Closed-Chest Canine Model of Complete Heart Block: Implications for Single-Chamber Rate-Variable Cardiac Pacing

This study assessed the impact of atrioventricular (AV) synchrony on characteristics of left ventricular (LV) systolic function during ventricular pacing over a wide heart rate range in a conscious closed-chest canine model of complete AV block. Ten healthy adult dogs underwent thoracotomy during which complete AV block was created by formaldehyde injection, and paired ultrasonic sonomicrometers were positioned on the LV anterior-posterior minor axis. Following recovery from surgery, peak and end-diastolic LV transmural pressure, maximum dP/dt, stroke work, end-diastolic minor axis dimension, and maximum velocity of shortening, were quantitated at heart rates of 80, 100, 120, 140, and 160 beats per minute (bpm) during both ventricular pacing alone and AV sequential pacing with increasing AV intervals (0, 50, 100, 150, 200, 250, and 300 ms). Over the heart rate range tested, parameters of LV systolic function did not differ significantly during ventricular pacing with or without AV synchrony. For example, during ventricular pacing alone maximum LV dP/dt varied from 2110 +/- 70 mmHg/s to 2463 +/- 567 mmHg/s, a range essentially identical to that observed in the presence of AV synchrony. On the other hand, although the impact on LV performance of varying AV interval from 0 to 300 ms was small, differences tended to become more pronounced at higher pacing rates. At 80 bpm, neither stroke work nor maximum LV dP/dt were affected by change in AV interval, while at heart rates greater than or equal to 120 bpm both stroke work and LV dP/dt tended to maximize at AV intervals of 50 and 100 ms and thereafter declined.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

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.     

Full Ventricular Capture Indicated by the QT Interval Function

The atrioventricular (AV) interval is critical in dual chamber (DDD) pacing in patients with hypertrophic obstructive cardiomyopathy (HOCM) to obtain full ventricular capture (FVC) with maximal reduction of the left ventricular (LV) outflow gradient and optimal LV diastolic filling. We studied the relationship of FVC, fusion, spontaneous AV conduction, and the QT interval. Methods: 11 patients with various cardiac diseases and stable AV conduction received a QT sensing Diamond (tm) Vitatron, DDD pacemaker. Software was downloaded into the pacemaker. In the DDD pacing mode, with the QT interval measured from the ventricular pacing stimulus to the end of the T wave, the AV interval was shortened from 400 ms, in 20-ms steps, to 90 ms. At 90 ms the stimulation rate was increased by 30 beats/mm and the AV interval was increased stepwise. FVC and fusion was examined on the surface ECG, Results: At 400 ms interval, spontaneous AV conduction inhibited the pacemaker. Shortening the AV interval resulted in pacing with a short QT interval. Further reduction of the AV interval resulted in a longer QT interval up to a point where the QT interval became stable. This point, the bending point in the plot of measured QT interval versus shortened AV intervals, coincided with the point of FVC. The relation of the QT-AV interval plot and the point of fusion was comparable when lengthening the AV interval at a 30 beats/mm faster stimulation rate. Conclusion: The bending point in the QT interval versus AV interval plots showed a good correlation with the FVC and fusion points observed on ECG. The results suggest that automatic discrimination between fusion and full capture using QT interval measurements may be feasible.     

Early Results of AV Sequential Pacing on Left Ventricular Outflow Obstruction after Senning Procedure

Dual chamber pacing was shown to decrease left ventricular outflow tract (LVOT) obstruction in patients with hypertrophic cardiomyopathy 30 years ago. We report early results of AV sequential pacing from the LV apex in a patient with transposition of the great arteries who is post-Senning procedure. LVOT obstruction resulted from septal deviation and systolic anterior motion of the mitral valve. Pacing was indicated for sinus node dysfunction. AV sequential pacing with a short optimal A V interval of 60 ms demonstrated a 45% reduction in the degree of LVOT obstruction. This article suggests that LVOT obstruction after the Senning procedure can be palliated by asynchronous septal contraction induced by A V sequential pacing, even if the activation is from LV apex, and avoid or postpone surgery in selected situations.     

Morphology of the RV electrogram during LV pacing is related to the hemodynamic effect in cardiac resynchronization therapy

Background: Biventricular (BiV) pacing and left ventricular (LV) pacing both improve LV function in patients with heart failure and LV dyssynchrony. We studied the hemodynamic effect of the atrioventricular (AV) interval and the associated changes in the right ventricular (RV) electrogram (EGM) during LV pacing and compared this with the hemodynamic effect of optimized sequential BiV pacing.
Methods: In 16 patients with New York Heart Association (NYHA) class II to IV, sinus rhythm with normal AV conduction, left bundle branch block (LBBB), QRS > 130 ms, and optimal medical therapy, the changes in RV EGM during LV pacing with varying AV intervals were studied. The hemodynamic effect associated with these changes was evaluated by invasive measurement of LVdP/dt_max and compared with the result of optimized sequential BiV pacing in the same patient.
Results: All patients showed electrocardiographic fusion during LV pacing. The morphology of the RV EGM showed changes in the RV activation that indicated a shift in the extent of fusion from LV pacing. These changes were associated with significant changes in LVdP/dt_max. Baseline LV dP/dt_max was 734 ± 177 mmHg/s, which increased to 927 ± 202 mmHg/s (P<0.0001) with optimized LV pacing and to 920 ± 209 mmHg/s (P<0.0001) with optimized sequential BiV pacing.
Conclusion: The RV EGM is a proper indicator for intrinsic activation over the right bundle during LV pacing and reveals the transition to fusion in the RV EGM that is associated with a decrease in LVdP/dt_max. The hemodynamic effect of optimized LV pacing is equal to optimized sequential BiV pacing.     

Radionuclide Evaluation of Dual Chamber Pacing: Comparison Between Variable AV Intervals and Ventricular Pacing

We prospectively evaluated changes in left ventricular ejection fraction, end diastolic volume, and stroke volume via radionuclide multigated acquisition study, Comparison was made between ventricular pacing and dual chamber pacing with varying AV intervals. The volumes and changes in ejection fraction were determined at rest, at set increased pacing rates, and during physiological stress. AV sequential pacing shows overall improvement in cardiac function in the majority of patients regardless of left ventricular function. The shorter AV interval would be appropriate for the majority of patients who have an atrial tracking mechanism (adequate intrinsic sensed atrial activity followed by ventricular pacing) and who undergo significant physiological stress.     

Invasive optimization of cardiac resynchronization therapy: role of sequential biventricular and left ventricular pacing

BACKGROUND: Aim of this invasive study was to characterize and quantify changes in left ventricular (LV) systolic function due to sequential biventricular pacing (BV) as compared to right atrial triggered simultaneous BV (BV(0)), LV, and right ventricular (RV) pacing in patients with congestive heart failure (CHF). METHODS: In 22 CHF patients, all in sinus rhythm, temporary multisite pacing was performed prior to implantation of a permanent system. LV systolic function was evaluated invasively by the maximum rate of LV pressure increase (dP/dt(max)). Sequential BV pacing was performed with preactivation of either ventricle at 20-80 ms. RESULTS: In comparison to RV pacing, LV and BV(0) pacing increased dP/dt(max) by 33.9 +/- 19.3% and 34.0 +/- 22.6%, respectively (P < 0.001). In 9 patients, optimized sequential BV pacing further improved dP/dt(max) by 8.5 +/- 4.8% compared to BV(0) (range 3.3-17.1, P < 0.05). In 10 patients exhibiting a PR interval < or =200 ms, LV pacing was either superior (n = 6) or equal to BV(0) pacing (n = 4). In these 10 patients, LV pacing yielded a 7.4 +/- 8.0% higher dP/dt(max) than BV(0) pacing (P < 0.05). CONCLUSIONS: Using sequential BV pacing, generally with LV preactivation, moderate improvements in LV systolic function can be achieved in selected patients. Baseline PR interval may aid in the selection of the optimum cardiac resynchronization therapy (CRT) mode, favoring LV pacing in patients with a PR interval < or =200 ms.     

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)     

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.     

What's the Price to be Paid for Rate Response: AV Sequential Versus Ventricular Pacing?

The purpose of this study was to compare the effects of atrioventricular (AV) sequential and ventricular pacing at rest and during exercise on parameters of left ventricular performance. Twenty-five patients were studied by means of first pass radionuclide angiography. Pacing rates increased significantly (P < 0.001) during exercise in both pacing modes, resulting in a significant increase in the cardiac index (P < 0.001). Pulmonary transit times decreased significantly (P < 0.001) during exercise in both pacing modes with a significantly shorter pulmonary transit time for AV sequential pacing at rest (P < 0.01) and during exercise (P < 0.05), indicating impaired left ventricular function in ventricular pacing. Regional left ventricular wall movement deteriorated significantly during exercise in both pacing modes (P < 0.02), with a significantly worse performance during ventricular pacing at rest (P < 0.05) and during exercise (P < 0.05). Therefore, the price to be paid for rate response is a deterioration of regional wall movement. An additional loss of AV synchrony worsens the situation. It is concluded that rate modulated pacing requires preservation of AV coordination to optimize left ventricular performance.     

Effects of AV Sequential Versus Asynchronous AV Pacing on Pulmonary Hemodynamics

We studied the effects of various pacing modes on cardiac hemodynamics and pulmonary gas alterations in chronic heart blocked dogs. Changing the pacing mode from an atrioventricular interval of 100 ms (AV100) to a ventriculo-atrial interval of 100 ms (VA100) caused a significant fall in left ventricular pressure (117.64 +/- 11.91 to 95.60 +/- 16.58 mmHg) and cardiac output from 2.18 +/- 0.24 to 1.46 +/- 0.20 L/min. Following the change in pacing mode from AV100 to VA100, there was an increase in the alveolar-arterial O2 gradient from 23.28 +/- 6.97 to 28.74 +/- 8.43 mmHg and a decrease in the arterial CO2 tension from 32.42 +/- 3.22 to 29.42 +/- 3.22 mmHg. There was also a decrease in arterial CO2 tension when the AV100 pacing mode was compared to asynchronous ventricular pacing (32.42 +/- 3.22 versus 30.56 +/- 2.82 mmHg). The minute volume of O2 also decreased when the pacing mode was changed from AV100 to asynchronous ventricular pacing (0.134 +/- 0.01 versus 0.126 +/- 0.01 L/min) and decreased further at VA100 to 0.114 +/- 0.01 L/min. Other significant changes were also observed: the percent of expired CO2 decreased when the pacing mode was changed from AV100 to VA100 (3.68 +/- 0.13 versus 3.37 +/- 0.26%) or to asynchronous ventricular pacing (3.40 +/- 0.31%). The end-expiratory O2 increased and CO2 decreased when the pacing mode was changed from AV100 to VA100. The breath-by-breath correlation of end-expiratory O2 and CO2 with left ventricular systolic pressure showed an almost immediate increase in O2 and reduction in CO2 concentration associated with decreasing systolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Optimal sensed atrio-ventricular interval determined by paced QRS morphology

BACKGROUND: In cardiac resynchronization therapy (CRT), the atrio-ventricular (AV) and interventricular (VV) intervals have to be optimized. For maximal optimization, the paced and sensed AV intervals have to be determined. We hypothesized that the morphology of the paced QRS complex at the optimal paced AV interval (PAV) can be used to determine the optimal sensed AV (SAV) interval in patients with normal AV conduction. PATIENTS AND METHODS: In 16 patients with implanted CRT devices, the optimal PAV and V-V interval were determined by invasive measurement of left ventricle (LV) dP/dt(max). A 12-lead electrocardiogram (ECG) was recorded at the optimum setting. Subsequently, during atrial sensing ventricular pacing, the SAV interval was changed until the QRS morphology was identical to the morphology at the optimal PAV interval. The optimal SAV interval was verified by repeated measurement of LV dP/dt(max). RESULTS: By optimization of the PAV and VV interval, the LV dP/dt(max) increased from 639 +/- 204 to 789 +/- 223 mmHg/s (+23%; P = 0.0000002). The optimized PAV was 149 +/- 19 ms; the optimized SAV was 100 +/- 20 ms and the corresponding LV dP/dt(max) at this interval was 774 +/- 204 ms (+21%; P = 0.000004). LV dP/dt(max) at optimized SAV - 20 ms and optimized SAV + 20 ms was 747 +/- 213 mmHg/s (P = 0.00004) and 751 +/- 203 mmHg/s (P = 0.0000003), respectively. The mean difference in optimized PAV and optimized SAV was 49 +/- 17 ms, ranging from 20 to 80 ms. CONCLUSIONS: The QRS morphology at optimized PAV can be used as a template to determine the optimal SAV, provided that the patient has normal AV conduction.     

Stimulation rate and the optimal interventricular interval during cardiac resynchronization therapy in patients with chronic atrial fibrillation

Background: Optimization of cardiac resynchronization therapy (CRT) with respect to the interventricular (V‐V) interval is mainly limited to pacing at a resting heart rate. We studied the effect of higher stimulation rates with univentricular and biventricular (BiV) pacing modes including the effect of the V‐V interval optimization. Methods: In 36 patients with heart failure and chronic atrial fibrillation (AF), the effects of right ventricular (RV), left ventricular (LV), simultaneous BiV, and optimized sequential BiV (BiVopt) pacing were measured. The effect of the pacing mode and the optimal V‐V interval was determined at stimulation rates of 70, 90, and 110 ppm using invasive measurement of the maximum rate of left ventricular pressure rise (LV dP/dt_max). Results: The average LV dP/dt _max for all pacing modalities at stimulation rates of 70, 90, and 110 ppm was 781 ± 176, 833 ± 197, and 884 ± 223 mmHg/s for RV pacing; 893 ± 178, 942 ± 186, and 981 ± 194 mmHg/s for LV pacing; 904 ± 179, 973 ± 187, and 1052 ± 206 mmHg/s for simultaneous BiV pacing; and 941 ± 186, 1010 ± 198, and 1081 ± 206 mmHg/s for BiVopt pacing, respectively. In BiVopt pacing, the corresponding optimal V‐V interval decreased from 34 ± 29, 28 ± 28, and 21 ± 27 ms at stimulation rates of 70, 90, and 110 ppm, respectively . In two individuals, LV dP/dt_max decreased when the pacing rate was increased from 90 to 110 ppm. Conclusion: In patients with AF and heart failure, LV dP/dt_max increases for all pacing modalities at increasing stimulation rates in most, but not all, patients. The rise in LV dP/dt_max with increasing stimulation rates is higher in biventricular (BiV and BiVopt) than in univentricular (LV and RV) pacing. The optimal V‐V interval at sequential biventricular pacing decreases with increasing stimulation rates.     

Evaluation of atrial thrombus formation and atrial appendage function in patients with pacemaker by transesophageal echocardiography

BACKGROUND: Physiologic pacing is claimed to be superior to ventricular pacing in as much as it entails lower risk of atrial fibrillation, stroke, and atrial remodeling. There are few data on the relation between atrioventricular (AV) synchrony and atrial clot formation. Utilizing transesophageal echocardiography (TEE), this study sought to evaluate the effect of AV synchrony loss on left atrial physiology, atrial stasis, and clot formation. METHODS: We conducted a cross-sectional study on patients with both AV and ventricular pacing with left ventricular ejection fraction (LVEF) >30%. TEE enabled us to explore atrial and pacing leads thrombi and measure left atrial appendage (LAA) flow velocity. RESULTS: A total 72 patients (mean age, 65 +/- 11.7) were enrolled in the study. The pacing mode was VVI in 53% and AV sequential in 47% of patients. LVEF (mean +/- SD; %) was 53.3 +/- 6.2% in ventricular pacing mode and 52.2 +/- 6.6 in physiologic pacing mode. Thrombus formation on pacing lead (<10 mm in 97% of patients) was observed in 32% of all the patients (23% in patients with AV sequential pacing mode and 39% with VVI mode). Left atrial appendage flow velocity (LAA-FV) was significantly higher among the patients with AV sequential pacing mode (49.44 +/- 18 cm/s vs 40.94 +/- 19.4 cm/s, P value = 0.02). LAA-FV >40 cm/s was detected in 60% of the patients, 60% of whom were in physiologic mode. Left atrial size was significantly larger among the patients with VVI pacing mode (42.3 +/- 2.3 mm vs 37.79 +/- 4.5 mm, P = 0.001). Multivariate analysis showed no relation between LAA-FV and age, hypertension, diabetes mellitus, left atrial size, and left ventricular function. Only one patient had right atrial clot. There was no thrombus in the ventricles and atrial appendage. CONCLUSION: Long-term loss of AV synchrony induced by VVI pacing is associated with the impairment of LAA contraction. Thrombus formation in the LAA is not increased by VVI pacing in patients with relatively good left ventricular (LV) function and 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.     

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.     

AAIR Versus DDDR Pacing in Patients with Impaired Sinus Node Chronotropy: An Echocardiographic and Cardiopulmonary Study

The aim of this study was to compare AAIR and DDDR pacing at rest and during exercise. We studied 15 patients (10 men, age 65 ± 6 years) who had been paced for at least 3 months with activity sensor rate modulated dual chamber pacemakers. All had sick sinus syndrome (SSS) with impaired sinus node chronotropy. The patients underwent a resting echocardiographic evaluation of systolic and diastolic LV function at 60 beats/min during AAIR and DDDR pacing with an AV delay, which ensured complete ventricular activation capture. Cardiac output (CO) was also measured during pacing at 100 beats/min in both pacing modes. Subsequently, the oxygen consumption (VO₂at) and VO₂at pulse at the anaerobic threshold were measured during exercise in AAIR mode and in DDDR mode with an AV delay of 120 ms. The indices of diastolic function showed no significant differences between the two pacing modes, except for patients with a stimulus-R interval > 220 ms, for whom the time velocity integral of LV filling and LV inflow time were significantly lower under AAI than under DDD pacing. At 60 beats/min, CO was higher under AAI than under DDD mode only when the stimulus-R interval was below 220 ms. For stimulus-R intervals longer than 220 ms, and also during pacing at 100 beats/min, the CO was higher in DDD mode. The stimulus-R interval decreased in all patients during exercise. The time to anaerobic threshold, VO₂at ond VO₂at pulse showed no significant differences between the two pacing modes. Our results indicate that, at rest, although AAIR pacing does not improve diastolic function in patients with SSS, it maintains a higher CO than does DDDR pacing in cases where the stimulus-R interval is not excessively prolonged. On exertion, the two pacing modes appear to be equally effective, at least in cases where the stimulus-R interval decreases in AAIR mode.     

Reduction of right ventricular pacing in patients with sinus node dysfunction using an enhanced search AV algorithm

BACKGROUND: Dual chamber pacing typically results in a high percentage of ventricular pacing. A number of studies have been conducted suggesting detrimental effects of ventricular desynchronization produced by long-term RV pacing. Pacemaker algorithms that extend the AV interval to uncover intrinsic AV conduction have been utilized to reduce ventricular pacing. These algorithms are often limited to AV intervals below 250 ms limiting the ventricular pacing reduction. We hypothesized that by allowing AV intervals to extend beyond 300 ms, a marked reduction in RV pacing can be achieved. METHODS: A total of 30 patients (17 men, mean age 71 +/- 9) with standard Brady indications, and implanted with a Medtronic Kappa 700 pacemaker, were randomized to 2-week treatments with default Search AV (KSAV) parameters or Enhanced Search AV (ESAV) parameters. The Enhanced Search AV algorithm included the capability for continuous adjustment of AV delays and the ability to auto disable in patients with persistent AV block. RESULTS: Among patients with intact AV conduction, percent VP was greater in KSAV versus ESAV (70 +/- 40% vs 19 +/- 28%, P < 0.001). In patients with persistent AV block, the algorithm suspended appropriately and there was no significant change in the percent VP between both arms of the study. In 18/22 patients, percent VP was reduced below 40%. CONCLUSIONS: Substantial reduction in ventricular pacing can be achieved by allowing the AV interval parameters to extend beyond 300 ms using the ESAV algorithm. In patients with AV block, ESAV suspended and patients were paced at their nominal settings.