Impact of Right Ventricular Pacing Sites on Exercise Capacity during Ventricular Rate Regularization in Patients with Permanent Atrial Fibrillation

Background: The deleterious effects of right ventricular apical (RVA) pacing may offset the potential benefit of ventricular rate (VR) regularization and rate adaptation during an exercise in patient's atrial fibrillation (AF). Methods: We studied 30 patients with permanent AF and symptomatic bradycardia who receive pacemaker implantation with RVA (n = 15) or right ventricular septal (RVS, n = 15) pacing. All the patients underwent an acute cardiopulmonary exercise testing using VVI‐mode (VVI‐OFF) and VVI‐mode with VR regularization (VRR) algorithm on (VVI‐ON). Results: There were no significant differences in the baseline characteristics between the two groups, except pacing QRS duration was significantly shorter during RVS pacing than RVA pacing (138.9 ± 5 vs 158.4 ± 6.1 ms, P = 0.035). Overall, VVI‐ON mode increased the peak exercise VR, exercise time, metabolic equivalents (METs), and peak oxygen consumption (VO₂max), and decreased the VR variability compared with VVI‐OFF mode during exercise (P < 0.05), suggesting that VRR pacing improved exercise capacity during exercise. However, further analysis on the impact of VRR pacing with different pacing sites revealed that only patients with RVS pacing but not patients with RVA pacing had significant increased exercise time, METs, and VO₂max during VVI‐ON compared with VVI‐OFF, despite similar changes in peaked exercise VR and VR variability. Conclusion: In patients with permanent AF, VRR pacing at RVS, but not at RVA, improved exercise capacity during exercise.     

Comparison of Resting Hemodynamic Indices and Exercise Performance During Atrial Synchronized and Asynchronous Ventricular Pacing

Resting hemodynamic indices and exercise tolerance were measured during atrial synchronized (VAT) and asynchronous ventricular pacing (VOO) in 35 patients with implanted pacemakers which could be externally programmed to function in either pacing mode. Cardiac output and mean systemic arterial pressure were significantly greater during VAT pacing (VAT: 4.5 ± 1.21 /min, 115 ± 28 mmHg; VOO: 3.7 ± 0.8 1/min 105 ± 25 mmHg respectively), although there was no difference in pulmonary artery end-diastolic pressure. Maximal exercise performance was assessed using the Bruce protocol in both pacing modes. Neither the patient nor the supervising physician was aware of the preselected pacing mode; a second physician monitored the electrocardiogram and blood pressure but influenced the point of exercise termination only if a potentially dangerous arrhythmia or hypotension occured. Blood pressure responses were superior and atrial rates lower during VAT pacing, In all but five patients, exercise tolerance was improved by VAT pacing. This amounted to 33 percent or more in 23/35 patients. This improvement was shown to be maintained in the 20 patients who had repeat exercise tests several weeks later. Ventricular arrhythmias, hypotension, and lightheadedness frequently complicated exercise during asynchronous pacing but occurred rarely with atrial synchronized pacing. Resting hemodynamic indices did not predict the extent of improvement gained by physiological pacing.     

Adequacy of Pacing Rate During Exercise in Rate Responsive Ventricular Pacing

Our objective was to determint; the adequate pacing rate during exercise in ventricular pacing by measuring exercise capacity, cardiac output, and sinus node activity. Eighteen patients with complete AV block and an implanted pacemaker underwent cardiopulmonary exercise tests under three randomized pacing rates: fixed rate pacing (VVJ) at 60 beats/min and ventricular rate-responsive pacing (VVIR) programmed to attain a heart rate of about 110 beats/min ar 130 beats/min (VVIR 110 and VVIR 130, respectively) at the end of exercise. Compared with VVI and VVIR 130, VVIR 110 was associated with an increased peak oxygen uptake(VVIR 110:20.3 ± 4.5 vs VVI: 16.9 ± 3.1; P < 0.01; and VVIR 130: 19.0 ± 4.1 mL/min per kg, respectively; P < 0.05) and a higher oxygen uptake at anaerobic threshold (15.3 ± 2.7, 12.7 ± 1.9; P < 0.01, and 14.6 ± 2.6 mL/min per kg; P < 0.05). The atrial rate during exercise expressed as a percentage of the expected maximal heart rate was lower in VVIR 110 than in VVI or VVIR 130 (VVIR 110: 75.9%± 14.6% vs VVI: 90.6%± 12.8%; P < 0.01; VVIR 110 vs VVIR 130: 89.1%± 23.1%; P < 0.05). There was no significant difference in cardiac output at peak exercise between VVIR 110 and VVIR 130. We conclude that a pacing rate for submaximal exercise of 110 beats/min may be preferable to that of 130 beats/min in respect to exercise capacity and sympathetic nerve activity.     

Efficacy of Ventricular Rate Stabilization by Right Ventricular Pacing During Atrial Fibrillation

To assess the effect of right ventricular pacing on rate regularity during exercise and daily life activities, 16 patients with sinoatrial disease and chronic atrial fibrillation (AF) were studied. Incremental ventricular pacing was commenced at 40 beats/min until > 95% of ventricular pacing were achieved during supine, sitting, and standing. Thirteen patients also underwent randomized paired submaximal exercise tests in either a fixed rate mode (VVI) or a ventricular rate stabilization (VRS) mode in which the pacingrate was set manually at 10 beats/min above the average AF rate duringthe last minute of each exercise stage. The pacing interval for rate regularization was shortest during standing (692 ± 26 ms) compared with either supine or sitting (757 ± 30 and 705 ± 26 ms, respectively, P < 0.05). During exercise, VRS pacing significantly increased the maximum rate (119 ± 5.2 vs 106 ± 4.2 ms, P < 0.05), percent of ventricular pacing (85%± 5% vs 23%± 7%, P < 0.05), rate regularity index (5.8%± 1.6% vs 13.4%± 1.9%, P < 0.05), and maximum level of oxygen consumption (12.4 ± 0.5 vs 11.3 ± 0.5 ml/kg, P < 0.05) compared with VVI pacing. There was no change in oxygen pulse or difference in symptom scores in this acute study between the two pacing modes. It is concluded that right ventricular pacing may significantly improve rate regularity and cardiopulmonary performance in patients with chronic AF. This may be incorporated in a pacing device for rate regularization of AF using an algorithm that is rate adaptive to postural and exercise stresses.     

Atrial and Ventricular Stimulation Threshold Development: A Comparative Study in Patients with a DDD Pacemaker and Two Identical Carbon-Tip Leads

The atrial and ventricular pacing threshold development during the first postoperative year was studied in a group of patients receiving DDD pacemakers. Identical carbon-tip endocardial leads were implanted in atrium and ventricle. Atrial and ventricular voltage stimulation thresholds were measured at implantation, and noninvasively at 1 and 12 months thereafter. The atrial amplifier sensitivity required for adequate P wave sensing during follow-up was also determined. The possible influence of a number of factors upon atrial and ventricular threshold evolution was statistically assessed. The threshold data were complete in 57 patients (mean age +/- SD, 65.2 +/- 12.4 years). Thirteen patients had a diagnosis of sinus node disease, whereas 44 had not. Patient age and diagnosis did not significantly influence atrial or ventricular stimulation threshold development. Atrial sensing thresholds were not related to atrial stimulation thresholds during follow-up. Atrial pacing thresholds were higher than ventricular thresholds at pacemaker implantation (P less than 0.00005), but the postoperative threshold rise and thresholds at 1 and 12 months postoperatively did not differ significantly between the atrium and ventricle. The ratio of chronic to acute stimulation thresholds was higher on the ventricular than on the atrial level (0.001 greater than P greater than 0.0005). The chronic atrial threshold showed a logarithmic relation to the threshold at implantation (P = 0.0006); postoperative threshold rise was not a significant determinant of the chronic atrial threshold (P = NS). On the ventricular level, the reverse was seen: The chronic threshold was related to the postoperative threshold rise (P = 0.0015, logarithmic relation), but not to the implantation threshold (P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)     

A Double-Blind Study of Submaximal Exercise Tolerance and Variation in Paced Rate in Atrial Synchronous Compared to Activity Sensor Modulated Ventricular Pacing

To assess the variation in paced rate during everyday activity and the importance of atrioventricular synchronization (AV synchrony) for submaximal exercise tolerance, atrial synchronous (DDD) and activity rate modulated ventricular (VVI,R) pacing were compared in 17 patients with high degree AV block. The patients were randomly assigned to either mode and evaluated by treadmill exercise to moderate exertion and by 24-hour Holter monitoring after 2 months in the DDD and VVI,R modes, respectively. At the end of the study, the patients were programmed to the pacing mode corresponding to the preferred study period. During the treadmill test, the mean exercise time to submaximal exertion (Borg 5/10), exertion ratings and respiratory rate did not differ between pacing modes despite a significantly lower ventricular rate in the VVI,R mode. The atrial rate during VVI,R pacing was significantly higher than the ventricular rate, but did not differ from the ventricular rate during DDD pacing. There was a diurnal variation in paced rate in both pacing modes. Paced ventricular rate was, however, higher and variation in paced rate greater in DDD compared to VVI,R pacing. Nine patients preferred the DDD mode, three patients preferred the VVI,R mode, while five subjects did not express any preference. The results from this study indicate that the variation in paced rate during activity sensor-driven VVI,R pacing does not match that during DDD pacing neither during everyday activities nor during submaximal treadmill exercise. Nevertheless, no differences in exercise time, Borg ratings, and respiratory rate during submaximal exercise were found. Thus, for most patients with high degree AV block, DDD and VVI,R pacing seem equally satisfactory for submaximal exercise.     

Plasma Levels of Natriuretic Peptides During Ventricular Pacing in Patients with a Dual Chamber Pacemaker

The mechanism(s) responsible for the release of brain natriuretic peptide (BNP), a cardiac hormone of ventricular origin, are still not completely understood. We measured plasma atrial natriuretic peptide (ANP) and BNP in 15 subjects (10 men, mean age 67 ± 3 years) with a dual chamber pacemaker and unimpaired heart function during ventricular pacing, which is known to induce an increase in atrial pressure and plasma ANP concentration. Under ECC monitoring, all subjects received sequential atrioventricular pacing for 30 minutes and ventricular pacing for 30 minutes, at the same rate of 80 beats/min. Arterial pressure and plasma BNP and ANP levels were measured every 10 minutes throughout the study. Ventricular pacing led to atrioventricular dissociation in eight subjects and to retrograde ventriculo-atrial conduction in seven. Arterial pressure remained unchanged in all subjects. In the group with atrioventricular dissociation, plasma ANP increased from 10.14 ± 0.58 to 16.72 ± 0.92 fmol/mL at the 60th minute (P < 0.0001), whereas plasma BNP did not change at all (fiom 1.26 ± 0.07 to 1.16 ± 0.09 fmol/mL). In the group with retrograde conduction, plasma ANP concentration doubled (fiom 10.95 ± 1.66 to 21.40 ± 1.51 fmol/mL, P < 0.0001), BNP increased 1.5-fold (from 1.16 ± 0.06 to 1.64 ± 0.14 fmol/mL, P < 0.001), and the ANP: BNP ratio augmented fiom 10:1 to 13.4:1. These results indicate that the release of ANP and BNP is regulated by different mechanisms, supporting the view that there is a dual natriuretic peptide system, comprising ANP fiom the atria and BNP fiom the ventricles.     

Ventricular Protection Against Atrial Arrhythmias in DDD Pacing Based on a Statistical Approach: Clinical Results

Atrial arrhythmias (AA) are commonly encountered in DDD paced patients. Newer dual chamber pacemakers (PM) possess mode switching functions that convert pacing to an asynchronous mode when AAs are detected. The lack of a reliable mode switch leading to rapid, irregular ventricular responses may result from AA undersensing. To avoid this, the DDDR PM Chorum 7234 Eta Medical AA diagnosis is based on a statistical approach: the PM constantly compares arrhythmic and sinus cycles and, based on "strong" and "weak" criteria, provides for rapid or slower mode switch. The aim of the study was to evaluate the efficiency and reliability of these two criteria. Thirty-one patients with a Chorum 7234 implanted for AV block (11), sinus dysfunction (10), both (5), or hypertrophic obstructive cardiomyopathy (5) were evaluated at 24 hours and 1 month using the internal memory (IM) of the PM, surface 24-hour Holter recordings, and exercise testing. Interrogation of the IM on the first day of study showed that 8 patients had mode switching episodes, based only on the strong criterion confirmed by the surface Holter recording. At I month, the IM revealed mode switching episodes in 12 patients, 6 of whom had used the weak criterion. No inappropriate mode switching episode was recorded during exercise testing at the 1-month follow-up. These results confirm the reliability and efficiency of this algorithm as well as the requirement for a specific algorithm to compensate for transient loss of sensing during AA.     

Microvolt T-Wave Alternans During Atrial and Ventricular Pacing

Introduction: Assessment of microvolt T-wave alternans (MTWA) by the spectral analysis (SA) method requires the heart rate to be stable within a certain range. This can be achieved by ventricular pacing (VP). We compared MTWA during short-term VP versus atrial pacing (AP).
Methods: Patients presenting for evaluation of risk of sudden cardiac death underwent an invasive electrophysiologic study. The concordance of results of MTWA-VP with MTWA-AP was evaluated, as well as the specificity, sensitivity, negative, and positive predictive values of MTWA-VP versus MTWA-AP. The maximum recorded amplitude of MTWA (MValt) in concordant positive results, as well as noise levels in all, were compared in both pacing modes.
Results: We studied 42 consecutive patients, of whom 31 completed both tests (32 by AP, 40 by VP). Compared to AP, VP—MTWA SA had a sensitivity of 93%, specificity of 71%, negative predictive value of 92%, and positive predictive value of 72%. The results were concordant in 25 patients (80%, κ= 0.62, P < 0.001). The noise level was significantly higher during VP than AP (1.4 ± 0.8 vs 1± 0.8, P< 0.01), and there was a trend toward a higher amplitude of TWA by VP (10.7 ± 5.3 vs 7.8 ± 3.9, P = 0.058).
Conclusions: MTWA SA is more likely to be completed during VP than AP. Overall there was concordance between both tests. VP generates higher amplitudes and noise, and a higher percentage of nonnegative results.     

Failure of Plasma Atrial Natriuretic Peptide Levels to Increase During Exercise in Patients with Chronic Atrial Fibrillation

It is generally accepted that plasma atrial natriuretic peptide release occurs secondary to atrial stretch. The influence of coordinated atrial contraction (AC) upon this process is not fully appreciated. The aim of the study was to determine the importance of coordinated AC upon peripheral atrial natriuretic peptide levels (α-hANP) during exercise. Peripheral α-hANP levels were measured at rest and during exercise in 12 patients with complete heart block (CHB) and permanent rate responsive pacemakers. Seven patients had coordinated AC and five had chronic atrial fibrillation (AE). Each patient performed three treadmill exercise tests. Maximal inspired oxygen volume (VO₂ max) was determined during test 1. Tests 2 and 3 were performed to 70% VO₂ max, the pacemaker being programmed to either VVI or VVIR mode. Plasma α-hANP was measured using a two-site immunoradiometric assay. At rest there was a small but significant difference between the two patient groups: AF 60.2 pg/mL versus AC 97.6 pg/mL; P = 0.03. During exercise in the AC patients, there was a significant increase in α-hANP levels, in VVIR mode, to 238.4 pg/mL, and in VVI mode, to 207.9 pg/mL, P = 0.002 and 0.003, respectively. In those patients with chronic AF, there was no significant rise or fall in α-hANP levels in either pacing mode, VVIR 65.2 pg/mL, VVI 46.6 pg/mL. Previous workers have suggested that α-hANP release by nonfunctioning atria is normal. We have shown that the presence of coordinated AC is required for the release of α-hANP during exercise in patients with CHB, and that this appears to be independent of ventricular rate.     

Atrial Synchronized Ventricular Pacing: Contribution of the Chronotropic Response to Improved Exercise Performance

In contrast to asynchronous ventricular pacing (VOO, VVI), alrial synchronized ventricular pacing (VAT, VDD, DDD) maintains the normal sequence of cardiac chamber activation and permits a chronotropic response to exercise. thereby improving exercise performance. To assess the separate contributions of these two factors to improved work capacity. 14 patients with implanted programmable VAT pacemakers were exercised according to the Bruce protocol, in three different pacing modes, selected in a random orderand on a double blind basis: (a) VAT: (b) chest wall stimulation triggered ventricular (V-CWS-T) pacing, during which the pacemaker was programmed to VAT mode but driven externally using chest wall stimulation at rates fractionally above the patients'atrial rate, thereby providing a chronotropic response to exercise without atrioventricular synchronization; and (c) VOO mode at 70 beats per minute. There was a significant improvement in exercise performance in all patients during both VAT and V-CWS-T pacing as compared to VOO mode; the average increase in work capacity being similar: VAT: 44 ± 31, (range, 12 to 140) percent and V-CWS-T; 40 ± 24 (range, 5 to 85) percent. It is concluded that in patients with adaptive pacing systems, the chronotropic response is the major determinant of any improvement in exercise performance.     

DDD Pacing: An Effective Treatment Modality for Recurrent Atrial Arrhythmias

We performed atrial EP studies (atrial substrate evaluation) on 10 patients. These patients had evidence of paroxysmal, sustained, recurrent atrial arrhythmias (7 men and 3 women with a mean age of 64 ± 15 years). All patients combined a brady-tachy syndrome; 7 patients had a sick sinus syndrome (SSS) and 3 patients a typical vagally induced atrial arrhythmia. No anti-arrhythmic drug was allowed in 3 patients with SSS, 1 drug failed in 4 patients and the combination of 2 drugs failed in 3 patients during the first to eighth years prior to pacemaker implantation. Atrial substrate evaluation was feasible in all these patients off anti-arrhythmic therapy and showed important abnormalities of atrial loco-regional conduction parameters and long refractory periods (RP). The remarkable point was, in 7 patients, a paradoxical improvement in intra-atrial conduction delay at rapid pacing rate. The DDD pacing mode was chosen in all patients. No technical problem occurred during implantation. Atrial pacing rate was programmed to be slightly higher than the mean diurnal heart rate calculated on Holter monitoring. After implantation, the mean follow-up period was 18 ± 25 months with an average of one Holter every 4 months during the first 2 years. The 7 patients who improved intra-atrial conduction at rapid pacing rate were controlled without drugs, 2 patients were controlled with 1 drug, and 1 patient with 2 drugs. Atrial pacing in the DDD mode in a selected group of patients prevents paroxysmal and drug-resistant atrial arrhythmias. Atrial substrate evaluation is a sensitive tool for assuring the long-term benefit of atrial pacing. In this subset of patients, maintenance of AV synchrony by DDD pacing is preferable to catheter ablation of the His bundle.     

Comparison of Ventricular Function in Atrial Rate Adaptive Versus Dual Chamber Rate Adaptive Pacing During Exercise

The hemodynamic effects of two different pacing modes—rate adaptive atrial (AAIR) versus dual chamber (DDDR) pacing—were assessed in 12 patients with DDDR pacemakers during upright bicycle exercise first-pass radionuclide angiography using a multiwire gamma camera with tantalum-178 as a tracer. All patients had sinus node disease with intact AV conduction. Patients exercised to the same heart rate in random order in these two different pacing modes, AAIR and DDDR with AV delay (of 100 msec) selected to maintain 100% ventricular capture. Cardiac output in creased significantly above baseline values during exercise in both pacing modes: 154 ± 41% (mean ± SEM, P = 0.002) with AAIR, versus 95 ± 24% (P = 0.004) with DDDR (P = NS between the two modes). The peak filling rate, likewise, increased in both pacing modes (2.3 ± 0.21 end-diastolic volumes/sec to 3.8 ± 0.31 end-diastolic volumes/sec in AAIR [P = 0.0004] and 2.2 ± 0.18 end-diastolic volumes/sec to 3.4 ± 0.27 end-diastolic volumes/sec in DDDR [P = 0.0008]). LV ejection fraction was normal at rest (60 ± 4%, SEM) and did not significantly change with submaximal exercise in either pacing mode (both 56%, P = NS). No significant changes in end-diastolic volume or stroke volume indexes occurred with exercise in either pacing mode. Our study demonstrates that in patients with normal resting LV function, AAIR and DDDR pacing are equally effective in attaining appropriate increases in cardiac output and LV filling during exercise.     

Failure to Sense P Waves During DDD Pacing

ECG tracings of three patients in whom AV universal (DDD) pacemakers were implanted intermittently demonstrated dropped P waves. In one patient, true atrial undersensing was present; in the others, sensing of the atrial electrode was appropriate, but sensing of sinus P waves was intermittently blocked by normal pacemaker operation. In this report we discuss the electrocardiographic diagnosis of atrial undersensing in order to avoid unnecessary reinterventions.     

Atrial Natriuretic Peptide During Different Pacing Modes in a Comparison with Hemodynamic Changes

The study investigates the response of atrial natriuretic peptide (ANP) to different cardiac pacing modes in comparison with hemodynamic changes. Ten patients underwent Swan-Ganz catheterization during pacemaker implant. Atrioventricular and ventricular pacing were performed consecutively at three pacing rate levels (80, 100, and 110 ppm). Blood samples were taken from the pulmonary artery for ANP determination, both basally and at the end of each pacing period. Concomitantly, mean pulmonary capillary wedge pressure (PCWP) and mean pulmonary artery pressure (PAP) were measured. Cardiac output (CO) was determined by thermodilution both basally and during the 110 ppm steps. During atrioventricular pacing, whereas no significant changes were observed for ANP, PCWP and PAP, CO increased significantly (P less than 0.0005). At the beginning of ventricular pacing hemodynamic parameters and ANP levels were comparable with those of baseline conditions. During subsequent ventricular pacing PCWP and ANP increased significantly at the 110 ppm rate step (P less than 0.05). PAP did not change significantly, whereas CO decreased in all cases (P less than 0.01). A positive correlation was observed between ANP and PCWP during ventricular (P less than 0.001), but not atrioventricular pacing. The results, while confirming the hemodynamic advantages of atrioventricular pacing, point to a major stimulation of ANP secretion during ventricular pacing. This fact, together with the observed drop in CO and the correlation between ANP and PCWP, suggest that the increase of ANP in ventricular pacing may be the expression of a compensatory mechanism to the hemodynamic disadvantages of atrioventricular asynchrony.     

Acute and Chronic Changes in Atrial Natriuretic Factor Induced by Ventricular Pacing: A Self Controlled Clinical Trial

A self controlled clinical trial was carried out to study the acute and chronic effects of ventricular pacing (VVI) on the atrial natriuretic factor (ANF). Eleven people were selected from a pool of 20 DDD paced patients. Pacemakers were programmed to the VVI mode for 1 month and their effectiveness tested by ECG at rest and after an effort test. ANF was measured by radioimmunoassay at baseline, after 15 minutes, and again 1 month after programming. The reliability of the radioimmunoassay was confirmed using the coefficients of variation between (12.5%) and within assay (9.7%). Data analysis was done using Wilcoxon's test. Our results showed that the onset of WI pacing led to a sudden sharp rise in ANF in all patients (P < 0.0001). During VVI pacing, three patients were dropped from the study (2 were withdrawn because of symptoms and 1 voluntarily withdrew). After 1 month of WI pacing, a significant increase of ANF above the baseline was observed (P < 0.05). The results showed that ventricular pacing led to an immediate rise in ANF and, that with long-term VVI pacing, there was an increase in ANF levels as well. The role of these findings in the pathophysiology of the pacemaker syndrome calls for further research.     

Importance of Heart Rate Response During Exercise in Patients Using Atrioventricular Synchronous and Ventricular Pacemakers

Atrioventricular synchronous pacing offers advantages over fixed-rate ventricular (VVI) pacing both at rest and during exercise. This study compared the hemodynamic effects at rest and exercise of ventricular pacing at a rate of 70 beats/min, ventricular pacing where the rate was increased during exercise and dual chamber pacing. Ten patients, age 63 +/- 8 years, with multiprogrammable DDD pacemakers were studied using supine bicycle radionuclide ventriculography. Radionuclide data during dual chamber pacing was acquired at rest and during a submaximal workload of 200-400 kpm/min. The pacemakers were then programmed to VVI pacing at a rate of 70 beats/min, and 1 week later, studies were repeated in the VVI mode at rest, during exercise at a rate of 70 beats/min, and during exercise with the VVI pacemaker programmed to a rate adapted to the DDD pacing exercise rate. At rest, the cardiac output was lower in the VVI compared with the AV sequential mode (4.1 +/- 1.1 vs 5.7 +/- 1.1 1/min, P less than 0.01). During exercise, the cardiac output increased from resting values in the DDD and VVI pacing modes, however cardiac output in the rate-adapted VVI mode was higher than in the VVI mode with the rate maintained at 70 beats/min (8.1 +/- 1.5 vs 6.3 +/- 1.1 1/min, P = 0.02). Three patients completed lower workloads with VVI pacing at 70 beats/min compared with AV synchronous pacing. At rest, AV sequential pacing was superior to VVI pacing, suggesting the importance of the atrial contribution to ventricular filling. With VVI pacing during exercise, cardiac output was improved with an increased pacemaker rate, suggesting that the heart rate response during exercise was the major determinant of the higher cardiac output.     

Pacemaker Electrocardiography of Rate Smoothing During DDD Pacing

A rate smoothing option is available in a new bipolar AV universal (DDD) pacemaker. In three patients, two with intact retrograde conduction and one with retrograde block, rate smoothing values of 3% and 6% were programmed. Irregular pacemaker-mediated tachycardia occurred in one patient and AV synchrony was temporarily lost in the other two patients. In this report, we describe the pacemaker electrocardiography of rate smoothing during DDD pacing.     

Left Atrial Size and Wall Motion in Patients with Permanent Ventricular and Atrial Pacing

KUBICA, J., ET AL.: Left Atrial Size and Wall Motion in Patients with Permanent Ventricular and Atrial Pacing. It is well known that during permanent ventricular pacing atrial arrhythmias and embolic complications occur much more frequently in comparison to permanent atrial or sequential pacing. He-modynamic disturbances caused by ventriculoatrial conduction (VAC) are thought to be responsible for those complications. The aim of this study was to compare the left atrial size and its wall motion in three groups of patients with sick sinus syndrome. Group 1: 58 patients with VVI pacing and VAC observed (22 males, 36 females, aged 31–86, mean 62.3). Group 2: 43 patients with primary AAI pacing (13 males, 30 females, aged 27–74, mean 57.8). Group 3: 13 patients with AAI or DDD replacing the primary VVI mode due to pacemaker syndrome and/or heart failure, all with VAC present during VVI pacing (7 males, 6 females, aged 26–80, mean 59.8). Two-dimensional/M-mode echocardiography was performed in all these patients. In group 1 mean diastolic as well as mean systolic atrial diameters were significantly greater (p < 0.005) and wall motion significantly smaller (p < 0.005) in comparison to the other groups. Left atrial wall motion amounted to only 7.4% of the mean diastolic diameter in this group. Mean left atrial diastolic and systolic diameters and wall motion in patients with pacemakers preserving atrioventricular synchrony (group 2 and group 3) were almost identical and wall motion amounted to about 22% of the diastolic diameter in both these groups. We conclude that ventriculoatrial conduction leads to significant enlargement of left atrium and to the atrial wall-motion decrease. This predisposes to arrhythmias and embolic complications. Changes in atrial size and performance seem to be reversible with restoration of the physiological atrioventricular synchrony.     

Stability of the DDD Pacing Mode in Patients 80 Years of Age and Older

We reviewed the records of 119 consecutive patients aged 80 years or older (mean age 84 ± 3.7 years) in whom a dual chamber pacemaker was implanted between 1984 and 1991. Follow-up data was available up to February 1993. Immediate postimplantation complications were rare. Nine patients were lost to follow-up, all within 6 months of implantation. An additional seven patients died within 6 months of implantation. Long-term follow up for at least 6 months from implantation was available for 103 of the 119 patients (87%). Of these 89 (66%) remained in functioning DDD mode for a mean of 22 ± 15 months from implantation. Nine patients were reprogrammed to VVI mode, six due to atrial fibrillation and three due to failure of atrial sensing or pacing. One patient was programmed DVI for failure of atrial sensing; 94 of 112 patients (84%) whose status was definitely known in February 1993 remained in functioning DDD mode until death or last follow-up. Cumulative survival in DDD mode was 78% at 30 months. We conclude that DDD pacing is stable in the great majority of patients in their nineth and tenth decades who present with rhythms amenable to dual chamber pacing and who have no history of sustained atrial fibrillation.