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J Am Coll Cardiol, 2003; 42:614-623, doi:10.1016/S0735-1097(03)00757-5 © 2003 by the American College of Cardiology Foundation |
* Department of Cardiology, Skejby Hospital, Aarhus University Hospital, Aarhus, Denmark
Department of Medicine, Viborg County Hospital, Viborg, Denmark
Manuscript received October 2, 2002; revised manuscript received January 6, 2003, accepted January 30, 2003.
* Reprint requests and correspondence: Dr. Henning R. Andersen, Department of Cardiology, Skejby Hospital, University of Aarhus, Brendstrupgaardsvej, 8200 Aarhus N, Denmark.
henning.rud.andersen{at}dadlnet.dk
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Abstract |
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BACKGROUND: In patients with SSS and normal atrioventricular conduction, it is still not clear whether the optimal pacing mode is AAI or DDD pacing.
METHODS: A total of 177 consecutive patients (mean age 74 ± 9 years, 73 men) were randomized to treatment with one of three rate-adaptive (R) pacemakers: AAIR (n = 54), DDDR with a short atrioventricular delay (n = 60) (DDDR-s), or DDDR with a fixed long atrioventricular delay (n = 63) (DDDR-l). Before pacemaker implantation and at each follow-up, M-mode echocardiography was done to measure LA and LV diameters. Left ventricular fractional shortening (LVFS) was calculated. Analysis was on an intention-to-treat basis.
RESULTS: Mean follow-up was 2.9 ± 1.1 years. In the AAIR group, no significant changes were observed in LA or LV diameters or LVFS from baseline to last follow-up. In both DDDR groups, LA diameter increased significantly (p < 0.05), and in the DDDR-s group, LVFS decreased significantly (p < 0.01). Atrial fibrillation was significantly less common in the AAIR group, 7.4% versus 23.3% in the DDDR-s group versus 17.5% in the DDDR-l group (p = 0.03, log-rank test). Mortality, thromboembolism, and congestive heart failure did not differ between groups.
CONCLUSIONS: During a mean follow-up of 2.9 ± 1.1 years, DDDR pacing causes increased LA diameter, and DDDR pacing with a short atrioventricular delay also causes decreased LVFS. No changes occur in LA or LV diameters or LVFS during AAIR pacing. Atrial fibrillation is significantly less common during AAIR pacing.
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The primary aim of the present randomized study was to compare the echocardiographic changes in LA size and LV size and function during rate-adaptive AAI and DDD pacing in patients with SSS and relatively normal AV conduction.
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Methods |
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220 ms for patients 70 years and PQ interval 260 ms for patients >70 years, as used in a prior study (the AAI vs. VVI trial) (2,5). In a one-year period, patients were furthermore enrolled at the neighboring Viborg County Hospital.
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150 ms) (DDDR-s), and DDDR pacemaker programmed with a fixed long AV delay (300 ms) (DDDR-l). Medical history and physical examination were done before implantation. Echocardiography was done before, and again within 24 h after, pacemaker implantation. Follow-up visits were after three months, 12 months, and then once a year. The follow-up visits included physical examination, electrocardiogram (ECG) recordings, pacemaker check-up, and echocardiography. Physical examination and echocardiography were done unblinded regarding randomization and pacing mode. Echocardiography was done blinded regarding prior echocardiographic examinations.
Echocardiography. A Vingmed CFM 750 echocardiograph (Vingmed, Horten, Norway) with a 3.25 MHz transducer was used for echocardiograms.
M-mode echocardiography was done to measure LA, LV end-systolic (LVES) and end-diastolic (LVED) diameters, and LVFS was calculated by the formula LVFS = (LVED diameter – LVES diameter)/LVED diameter. M-mode echocardiography was done in accordance with the recommendations of the American Society of Echocardiography, using the leading-edge methodology (6).
Two-dimensional echocardiography was used to measure LA, LVED, and LVES volumes, allowing calculation of the LVEF. Echocardiographic images were digitally stored on optic disc and analyzed off-line using Echopac 6.0 (VINGMEDsound, Horten, Norway) software. The biplane disc summation method was used for calculation of ventricular volumes (7,8). Each LV volume was averaged from three beats. If only one of the two apical standard views could be obtained, the single plane disc summation method was used. At follow-up of patients in the DDDR-s group, echocardiographic parameters were initially obtained in that pacing mode the patient presented—typically with ventricular pacing. If ventricular pacing was present at that first echocardiogram, another echocardiogram was done 5 min after programming the pacemaker in AAI mode, same rate (DDDR-s-AAI). Echocardiographic parameters at the end of follow-up were defined as the measurements obtained at the last follow-up of each patient, which could be in the range from three months to five years. All echocardiograms were obtained and analyzed by one of three experienced echocardiographers.
Variability. Thirty consecutive patients underwent independent and separate M-mode echocardiographies by two observers on the same day. Left atrial diameter and LVED and LVES diameters were measured, and LVFS was calculated. The bias (the mean intra-individual difference) was low in all four parameters, whereas the limits of agreement (the mean intra-individual difference ± twice the SD of the differences) were quite wide: –6.6 to 6.4 mm (LA diameter), –9.5 to 8.7 mm (LVES diameter), –9.1 to 8.3 mm (LVED diameter), –0.19 to 0.20 (LVFS) (9). Two-dimensional echocardiography was performed and analyzed by the same examiner in 10 consecutive patients, in whom paired standard apical two- and four-chamber views were available, on two separate days. For these two-dimensional parameters, the bias was acceptable, and the limits of agreement were quite wide: –6.9 to 11.7 ml (LVES volume), –19.5 to 34.3 ml (LVED volume), –0.09 to 0.11 (LVEF).
During follow-up, good quality paired standard apical two- and four-chamber views were available in only 50% to 60% of the patients. At the three-month follow-up, they were available in 53% of the patients. In most of the remaining patients, only one of the two apical views was available and could be used to calculate the LV volumes.
Clinical end points. Atrial fibrillation was diagnosed only by standard 12-lead ECG at planned follow-up visits. Stroke was diagnosed when neurological symptoms of presumably cerebral ischemic origin persisted for more than 24 h or if patients died within 24 h from an acute cerebrovascular event. Peripheral embolus was diagnosed if verified at embolectomy or necropsy. Cause of death was obtained by interviewing the doctors who had care of the patient and by review of hospital and necropsy reports. Cardiovascular death included sudden death, death due to congestive HF, arterial thromboembolism, or a pulmonary embolus. Heart failure was classified according to New York Heart Association (NYHA) criteria and quantitated by the daily dose of diuretics.
Pacemaker telemetry data. Numbers of sensed and paced events were retrieved from the pacemaker event counters at every follow-up, and mean proportions of paced events in the atrium and in the ventricle during the entire follow-up period were calculated for each patient.
Pacemaker implantation. Standard rate-adaptive single-chamber pacemakers and dual-chamber pacemakers (Cardiac Pacemakers Inc. [St. Paul, Minnesota], Pacesetter [St. Paul, Minnesota], Medtronic [Minneapolis, Minnesota]) were used, all fulfilling the study requirements for reporting cumulative numbers of paced and sensed events for a 12-month period.
All atrial leads were implanted in the upper parts of the right atrial wall. Among patients randomized to AAIR pacing, 19 patients had unipolar leads, and 35 patients had bipolar leads. Among patients randomized to DDDR pacing, 37 patients had unipolar leads, and 86 patients had bipolar leads in the right atrium. All patients randomized to DDDR pacing had unipolar leads with passive fixation implanted in the RV apex. Atrial fibrillation at the time of pacemaker implantation was not a reason for implanting another pacemaker rather than according to the randomized mode.
During implantation, an atrial pacing test at 100 beats/min was performed; 1:1 AV conduction was required for an atrial pacemaker to be implanted. If Wenckebach block occurred at a rate of 100 beats/min, the patient received a DDDR pacemaker.
The rate response function was active in all but two patients. Lower and upper rates were programmed individually. Mode-switch function was active in all patients implanted with DDD pacemakers.
In patients randomized to DDDR-l pacing, the AV delay was fixed at 300 ms. In four patients a shorter AV delay had to be programmed to avoid induction of endless loop tachycardia during initial pacemaker testing. In patients randomized to DDDR-s pacing, the AV delay was 150 ms and rate adaptive but even shorter if necessary to obtain ventricular pacing with full capture.
Analysis. Power calculations were based on M-mode echocardiographic data from the AAI versus VVI study (2). With a statistical power of 80% and a 0.05 level of significance, a total of 450 patients were to be included in the study to detect a 10% difference between the AAIR group and the DDDR group in LA diameter. No differences between the DDDR-s and the DDDR-l groups were expected. However, inclusion was stopped after randomization of 177 patients, because at that time a national multi-center trial of AAIR versus DDDR pacing in patients with SSS was initiated and started in Denmark (the Randomized comparison of AAIR and DDDR pacing in 1,900 patients with SSS [DANPACE] trial) (10). Patients included in the present study were not rolled over into the DANPACE study.
The last patient included was to be followed up for at least one year before data were analyzed, which was March 2000. Analysis was on an intention-to-treat basis. Continuous variables were expressed as mean ± SD. Treatment groups were compared by the chi-square test for discrete variables. Paired two-tailed t test was used for within-group comparisons. One-way analysis of variance (ANOVA) was used to compare continuous variables between groups. Correlation analysis between proportion of pacing and changes in echocardiographic parameters was done. Kaplan-Meier survival curves were compared by log-rank test. A Cox regression analysis was done to calculate the relative risk proportion of AF adjusted for brady-tachy syndrome. A p value <0.05 (two-sided) was considered statistically significant. No correction was done for multiple comparisons. SPSS 10.0 was used for statistical analysis. The Institutional Scientific Ethical Committee approved the study.
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Results |
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The 177 consecutive patients were randomized to AAIR (n = 54), DDDR-s (n = 60), or DDDR-l (n = 63) pacing. Mean follow-up was 2.9 ± 1.1 years (range, 6 days to 5.3 years) and similar in the three groups. No patients were lost to follow-up. Baseline characteristics of the three groups were similar (Table 2). The programmed minimum rate was 63 ± 8 (range, 40 to 80) versus 60 ± 4 (range, 50 to 70) versus 61 ± 5 (range, 50 to 70) beats/min, in the AAIR, DDDR-s, and DDDR-l groups, respectively (p = 0.04, ANOVA). The programmed maximum rate was 120 ± 8 (range, 100 to 130) versus 120 ± 5 (range, 100 to 130) versus 108 ± 8 (range, 90 to 120), respectively (p < 0.01, ANOVA).
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Echocardiographic changes.
M-mode
The within-group comparisons of the M-mode parameters obtained before pacemaker implantation and at the end of follow-up are listed in Table 3. The within-group differences (delta values) did not differ between groups for any of the parameters.
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The changes observed in the LA and LV diameters during follow-up were similar after exclusion of the patients who had AF at echocardiography before pacemaker implantation or at one or more of the follow-up visits (Table 3).
Two-dimensional parameters. The within-group comparisons of the two-dimensional echocardiographic parameters obtained before pacemaker implantation and at the end of follow-up are listed in Table 4. The within-group differences did not differ between groups for any of the parameters. Left atrial, LVED, and LVES volumes did not differ between groups at baseline or at last follow-up, nor did LVEF differ between groups at baseline or at last follow-up.
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In the AAIR group and in the DDDR-s group, LVES volume increased, and LVEF decreased significantly during follow-up (Table 4).
Pacemaker telemetry data. Mean proportion of pacing during follow-up was, in the atrium: 69% in the AAIR group, 57% in the DDDR-s group, and 67% in the DDDR-l group (p = 0.08, ANOVA); in the ventricle: 90% in the DDDR-s group and 17% in the DDDR-l group (p < 0.001, ANOVA). Correlation between mean proportion of pacing in the ventricle during follow-up and the relative changes in LA diameter, LVES and LVED diameters, and LVFS from before implantation until end of follow-up was done for the DDDR-s and the DDDR-l groups. Correlation between mean proportion of pacing in the atrium during follow-up and the relative change in LA diameter was done for all three randomization groups. No significant linear correlation was observed.
Clinical end points. During follow-up, AF at one or more ambulatory visits was significantly less common in the AAIR group, 7.4% (n = 4) versus 23.3% (n = 14) in the DDDR-s group versus 17.5% (n = 11) in the DDDR-l group (p = 0.03, log-rank test). Kaplan-Meier plots of the proportions of patients in the three groups without AF during follow-up are shown in Figure 3. Brady-tachy syndrome at pacemaker implantation was strongly associated with AF during follow-up (relative risk 3.3 [95% confidence interval 1.3 to 8.1], p = 0.01). The risk of developing AF in the AAIR group compared with the DDDR-s group was still significantly decreased after adjusting for brady-tachy syndrome (relative risk 0.27 [95% confidence interval 0.09 to 0.83], p = 0.02). Programmed lower rate was not different among patients with and without AF during follow-up (61.3 beats/min vs. 61.7 beats/min, p = 0.74).
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A total of 37 patients died during follow-up, nine patients (16.7%) in the AAIR group, 14 patients (23.3%) in the DDDR-s group, and 14 patients (22.2%) in the DDDR-l group (p = 0.51, log-rank test). Annual rate of mortality was 5.4%, 8.4%, and 8.0%, respectively. Cardiovascular mortality was 7.4% versus 11.7% versus 14.3% (p = 0.43, log-rank test).
Before pacemaker implantation, there were no differences in NYHA functional class or consumption of diuretics between the AAIR, DDDR-s, and DDDR-l groups. During follow-up, 31% versus 30% versus 46% of patients in the three groups increased at least one NYHA class (p = 0.17, chi-square test), and increase in consumption of diuretics was observed in 28% versus 32% versus 21% of patients in the three groups (p = 0.34, chi-square test).
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Discussion |
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In the present trial, DDDR pacing with 90% RV pacing induced changes identical to the changes observed in the VVI group in the AAI versus VVI trial (1,2), with a decrease in LVFS and an increase in LA dilation, and DDDR-l pacing (with a mean 17% of RV pacing) caused only an increase in LA diameter, with no change in LVFS. These findings support that a high proportion of RV pacing causes a decrease in LV function. This is in accordance with recent findings from the randomized MOST (The Mode Selection Trial in Sinus-Node Dysfunction) (11) trial, where increasing proportions of pacing in the RV was associated with increase in the risk of hospitalization for HF (12).
The persistent LA dilation and LVFS decrease in the DDDR-s group after programming to AAI mode (DDDR-s-AAI) indicate that the effects of long-term RV pacing on LV function and LA size also persist after cessation of pacing. The echocardiographic study in AAI mode was, however, done only 5 min after programming to AAI mode, and it is not known whether the LA dilation and LVFS decrease would revert, given a longer period without RV pacing. In dogs, long-term AV synchronous LV pacing has been reported to induce ventricular remodeling with asymmetrical hypertrophy of the LV wall, thinning of the earliest activated free wall, and thickening of the late-activated septum (13,14). The present results do not answer whether a similar remodeling occurs during long-term RV pacing in humans.
In the present study, LA diameter increased significantly in both DDDR groups but not in the AAIR group. The LA dilation is possibly caused by the abnormal activation sequence and mechanical contraction pattern of the ventricles induced by RV pacing (3,4,15,16) associated with a decrease in the LV systolic (3,4) and diastolic function (15) and an increase in the right atrial pressure and the pulmonary capillary wedge pressure (3,17,18). The LA dilation was more marked in the DDDR-s group with 90% RV pacing than in the DDDR-l group with 17% RV pacing, supporting an association between these two parameters. The non-significant increase in LA diameter observed in the AAIR group could represent a feature in the natural evolution of the SSS and/or be related to increasing age (19). In the present study, the ventricular lead was implanted in the RV apex. Using RV septal pacing might have influenced the present results (20,21).
Patients with DDDR pacemakers were programmed with either a short rate-adaptive AV delay or a long fixed AV delay. Optimizing the AV delay individually might have influenced the present results (22). However, the study was designed to evaluate effects of different proportions of ventricular pacing rather than DDDR pacing with an optimized AV delay. Despite programming of a fixed long AV interval, pacing in the RV was reduced to a mean of only 17%. The explanation of this finding probably is RV fusion beats, RV pacing during AF, and RV pacing during different forms of pacemaker tachycardias, as previously documented (22).
When the present study was designed in the early 1990s, two-dimensional echocardiography was expected to yield more precise information of the changes over time in LA and LV dimensions than M-mode echocardiography. The results of our two-dimensional echocardiographic studies do not support the findings done by M-mode echocardiography. The changes observed in left chamber volumes and LVEF during follow-up were all small in size and within the 95% confidence intervals of repeated two-dimensional echocardiographic studies (23,24). Measuring the LA volume by two-dimensional echocardiography has never found any place in clinical or scientific echocardiography. Furthermore, in contrast with LA diameter measured by M-mode echocardiography (25), LA volume has never been found predictive of later cardiovascular events.
The correlations between mean proportion of RV pacing and the changes in LA and LV diameters during follow-up and the correlations between mean proportion of pacing in the atrium and changes in LA diameter were all non-significant, most likely because of the insufficient accuracy of echocardiography (23,26).
In the present trial, AF was significantly more common in the two DDDR groups, indicating that RV pacing may promote AF, most likely because it causes LA dilation. Similar changes in the echocardiographic parameters were observed after excluding patients who had AF at their echocardiographic examinations, indicating that AF was not the cause of the echocardiographic changes observed. We observed no differences in occurrence of thromboembolism, congestive HF, or death between pacing modes during follow-up, indicating that AAIR and DDDR pacing is similar regarding these outcomes. The limited sample size must, however, be kept in mind when interpreting these data. The incidence of high-degree AV block in the AAIR group was comparable to the annual rate of 1.7% observed in a recent retrospective study of 399 consecutive patients treated with AAI(R) pacing in our institution (27).
At present time, AAI(R) pacing mode seems to be the optimal treatment for isolated SSS. In the future, new mode switching abilities between DDD and AAI pacing may enable AAI pacing the majority of the time and, in addition, protect the patients from severe bradycardia due to AV block. The currently ongoing DANPACE trial (10) is expected to answer whether the risks associated with AAI(R) pacing and AV block are less than the risks associated with RV pacing in DDD(R) mode.
Study limitations. In our previous study, the differences between pacing modes increased markedly during long-term follow-up (2,28). In the present study the mean follow-up was just below three years. The present results cannot be extrapolated beyond this period after pacemaker implantation. Our study was initially designed to include 450 patients, but inclusion was stopped prematurely after randomizing 177 patients, reducing the statistical power.
The echocardiographic measurements were done un-blinded with regard to pacing mode and randomization group. Furthermore, at the ambulatory follow-up visits, echocardiography was done in the AAI mode 5 min after echocardiography in the DDD mode when ventricular pacing had been present in that mode. These factors may have introduced an observer bias. However, results from prior echocardiographic studies of any particular patient in the study were not known at the time of later echocardiographic studies or analyses of echocardiographic data in that patient.
For evaluating the proportions of pacing and sensing in the chambers, we had to rely on telemetered data. Far-field over-sensing of R waves in the atrium and of T waves in the ventricle as well as under-sensing of small atrial electrograms during AF may have influenced these data. To reduce these sense problems, bipolar atrial leads were used in the majority of patients. It is unlikely that the reliability of telemetered data should be different between randomization groups.
Conclusions. Our study is the first randomized trial comparing AAIR and DDDR pacing in patients with SSS and normal AV conduction. The study indicates that long-term DDDR pacing induces LA dilation and, in the case of a high proportion of LV pacing, also reduces LV function. Furthermore, AF is significantly less common during AAIR pacing. These findings support AAIR pacing as the preferred pacing mode in this group of patients.
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E. Occhetta, M. Bortnik, A. Magnani, G. Francalacci, C. Piccinino, L. Plebani, and P. Marino Prevention of Ventricular Desynchronization by Permanent Para-Hisian Pacing After Atrioventricular Node Ablation in Chronic Atrial Fibrillation: A Crossover, Blinded, Randomized Study Versus Apical Right Ventricular Pacing J. Am. Coll. Cardiol., May 16, 2006; 47(10): 1938 - 1945. [Abstract] [Full Text] [PDF]
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M. O. Sweeney and A. S. Hellkamp Heart Failure During Cardiac Pacing Circulation, May 2, 2006; 113(17): 2082 - 2088. [Abstract] [Full Text] [PDF]
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L. Padeletti and N. Musilli Pacemaker selection: time for a rethinking of complex pacing systems: reply Eur. Heart J., May 1, 2006; 27(9): 1127 - 1127. [Full Text] [PDF]
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