Europace Advance Access originally published online on February 1, 2007
Europace 2007 9(3):194-199; doi:10.1093/europace/eul186
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CARDIAC PACING
Single-chamber ventricular pacing increases markers of left ventricular dysfunction compared with dual-chamber pacing
1 Divsion of Cardiology, Department of Internal Medicine; 2 Zentrallabor, Stadtspital Triemli, Birmensdorferstrasse 497, CH-8063 Zürich, Switzerland
Manuscript submitted 6 June 2006. Accepted after revision 10 November 2006.
* Corresponding author. Tel: +41 44 466 11 11; fax: +41 44 466 25 99. E-mail address: barbara.naegeli{at}triemli.stzh.ch
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Abstract |
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Aims Large randomized trials comparing DDD with VVI pacing have shown no differences in mortality, but conflicting evidence exists in regard to heart failure endpoints. Here we evaluated the effect of pacing mode on serum levels of brain natriuretic peptide (BNP) and amino-terminal-proBNP (NT-proBNP).
Methods Forty-one patients (age 73 ± 10 years) with dual-chamber pacemakers were included in a prospective, single-blind, randomized crossover study evaluating the impact of DDD(R)/VDD versus VVI(R) mode on objective and functional parameters. Data were collected after a 2-week run-in phase and after 2 weeks each of VVI(R) and DDD(R)/VDD pacing or vice versa.
Results BNP and NT-proBNP levels during DDD(R)/VDD stimulation (151 ± 131 and 547 ± 598 pg/mL) showed no change compared with baseline (154 ± 130 and 565 ± 555 pg/mL), but a significant 2.4-fold increase was observed during VVI(R) mode [360 ± 221 and 1298 ± 1032 pg/mL; P < 0.001 compared with DDD(R)/VDD]. The assessment of functional class, the presence of pacemaker syndrome [49% in VVI(R) mode] and the patients' preferred pacing mode showed significant differences in favour of DDD(R)/VDD pacing.
Conclusion Patients can differentiate between DDD(R)/VDD and VVI(R) pacing, and prefer the former. Compared with DDD(R)/VDD pacing, VVI(R) stimulation induces a two- to three-fold increase in serum BNP and NT-proBNP levels.
Key Words: Pacing, Natriuretic peptides, Pacemaker syndrome, Echocardiography
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Introduction |
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Current guidelines do not advocate the use of dual chamber [DDD(R)/VDD] rather than right ventricular [VVI(R)] pacing to improve survival, to prevent stroke, or even to prevent heart failure in bradycardia patients.1
These recommendations are based on recently published large randomized controlled trials such as the Canadian Trial of Physiologic Pacing, the Mode Selection Trial in Sinus Node Dysfunction, and the United Kingdom Pacing and Cardiovascular Events trial. None of these trials found any difference in mortality when comparing DDD with VVI pacing.2–4 These studies and their conclusions, however, have been criticized for various reasons: (i) It has been argued that superiority of a certain pacing mode might only be demonstrated if patients are pacemaker dependent for longer periods of time. (ii) The follow-up period of about 3 years might be too short for the impact of subtle changes in haemodynamic performance to result in differences in hard endpoints. (iii) When assessing quality of life and symptom relief, it may be inappropriate to compare the pre-implantation period with bradycardia-related symptoms with the post-implantation period, when most of the symptoms are abolished by any type of pacemaker. Therefore, the issue of whether to use DDD or VVI mode is not yet settled.
In this study, we investigated the impact of pacing mode on cardiac function using brain or B-type natriuretic peptides, which are considered to be sensitive markers of heart failure. The biologically active hormone brain natriuretic peptide (BNP) and an inactive amino-terminal fragment (NT-proBNP) are the cleavage products of an intracellular prohormone proBNP. BNP and NT-proBNP are secreted predominantly by cardiomyocytes in response to ventricular volume expansion and pressure overload.5 Although secretion occurs on an equimolar basis, their molar ratio in plasma is not 1:1 because BNP has a shorter plasma half-life than NT-proBNP.6 Plasma levels of BNP and NT-proBNP have been found to be reliable markers of the haemodynamic status. They correlate well with left ventricular size and the degree of both systolic and diastolic dysfunction.7 Natriuretic peptides have been shown to be useful in the emergency room evaluation of acute dyspnoea and may be used successfully to guide treatment of congestive heart failure.8–10 Their prognostic relevance is proven in almost all conditions in which they have been studied, including heart failure, acute coronary syndromes, and even in those who are asymptomatic.11–15 We chose to measure levels of both BNP and NT-proBNP, since their relative sensitivity and specificity is still a matter of debate.
Therefore, the primary endpoint of the present study was to analyse the impact of DDD(R)/VDD pacing versus VVI(R) stimulation on BNP and NT-proBNP levels. Secondary endpoints were echocardiographically determined parameters of systolic and diastolic function as well as the patient-reported endpoints of dyspnoea (functional class), pacemaker syndrome, and patients' preference for a certain stimulation mode.
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Study population
The study population was recruited from patients in our pacemaker clinic with dual-chamber pacemakers. Participating patients were required to >18 years of age, have a chronically implanted DDD(R) or VDD pacemaker, and no recent changes in their cardiovascular medication. Exclusion criteria were symptoms of overt heart failure or documented atrial fibrillation at the time of study entry, and any form of acute coronary syndrome within the past 4 weeks.
Study design
A prospective single-blinded randomized crossover design was used (Figure 1). Randomization was performed by a person unaware of the study protocol in blocks of four using sealed envelopes. At enrolment clinical baseline characteristics were assessed. In each patient, a 12-lead surface ECG was obtained to determine underlying conduction abnormalities and to exclude atrial fibrillation. After a run-in phase of 2 weeks with stable medical treatment, patients were randomized to either atrioventricular pacing or to VVI(R) stimulation for a period of 2 weeks. Thereafter, patients crossed over to the opposite pacing mode for another period of 2 weeks (Figure 1). In DDD and VVI modes the lower rate was programmed to 60 bpm. In patients with sinus node dysfunction or binodal disease, in whom sensor parameters had already been activated, these parameters were left unchanged at study entry. At crossover to VVI mode, rate-response parameters were left in place in these patients. In patients with isolated atrioventricular nodal disease, in whom chronotropic competence is intact by definition, sensor parameters were programmed to nominal settings at crossover to VVI mode. This was done to prevent sudden chronotropic incompetence, which might have biased the patients' choice of desired pacemaker mode. The percentage of ventricular paced beats in each stimulation mode was assessed by pacemaker telemetry at the end of each period. At randomization and at the end of each period, blood samples were taken under standardized conditions for BNP and NT-proBNP measurements. At the end of each period, a transthoracic echocardiography study was performed. Furthermore, all patients completed a questionnaire to assess functional class and personal preference of stimulation mode. Symptoms consistent with the presence of pacemaker syndrome were defined in advance as recurrent lightheadedness, syncope, increasing level of dyspnoea, intolerable pulsations in the neck or abdomen, palpitations, or symptoms accompanying a fall in blood pressure of 
20 mmHg during ventricular pacing compared with normal sinus rhythm or atrioventricular stimulation.16 Written informed consent was requested of all patients. The protocol was approved by the local ethics committee.
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Measurements of BNP and NT-proBNP levels
Peripheral blood samples for BNP and NT-proBNP determination were obtained by direct venipuncture of an antecubital vein after the patient had been in a supine position for at least 15 min. At randomization and at the end of each study period, a venous blood sample was collected in tubes containing potassium EDTA. All samples were centrifuged at 3000 rpm (15ºC for 10 min) and separated plasma was immediately assayed. Plasma natriuretic peptide concentrations were measured with a specific immunoradiometric assay for human BNP and NT-proBNP using commercial kits (Triage, Biosite, San Diego, USA; Elecsys, Roche Diagnostics, Mannheim, Germany).
Echocardiographic studies
Two experienced operators performed all echocardiographic studies using a commercially available system (Vivid 7, GE Medical Systems, Horton, Norway). Patients were examined at rest in the left lateral supine position. All studies were performed at the end of each 2-week period, immediately prior to reprogramming of pacing parameters. Of the systolic parameters, biplane ejection fraction was determined using the Simpson method, and the velocity time integral in the left ventricular outflow tract was obtained from an apical five chamber view by pulsed wave Doppler measurement.17 Diastolic function was assessed with two methods: mitral flow propagation was quantified in the colour M-mode profile of mitral inflow, E to E' ratio was calculated from pulsed wave Doppler measurements of mitral inflow and tissue Doppler imaging of mitral annulus velocity, respectively.18,19
Statistical analysis
Statistical analyses were performed with the SPSS/PC software package (version 11.0, SPSS Inc.,Chicago, IL, USA). Results are presented as means ± SD. A P value <0.05 was considered to indicate statistical significance. Comparisons were made with the use of Student's t test or the 
2 test, as appropriate.
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Patients
The study cohort consisted of 41 consenting patients with a dual-chamber pacemaker, 32 with a DDD(R), and 9 with a VDD pacemaker system. The mean age was 73 ± 10 years (range 49–85 years), 66% were male. The primary implant diagnosis was sick sinus syndrome in 16 patients, high degree AV block in 21 patients, and a combination of these two disorders (binodal disease) in 4 patients (Table 1). At baseline, 28 patients had an unpaced heart rate
60 bpm and were thus termed pacemaker-dependent.20
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Pacing data during the study
All patients completed the study per protocol. The telemetrically assessed percentage of ventricular paced beats was 91 ± 22% in the DDD(R)/VDD mode and 82 ± 28% in the VVI(R) mode (P = 0.009). Predominant right ventricular pacing (
95% paced beats) was present in 35 patients (85%) during DDD(R)/VDD mode and in 27 patients (66%) during VVI(R) mode (P = 0.04). No patient had atrial fibrillation during the study.
BNP and NT-proBNP measurements
Compared with baseline, no increase in BNP (154 ± 130 and 152 ± 131 pg/mL, respectively) or NT-proBNP (565 ± 555 and 548 ± 598 pg/mL, respectively) levels was obtained during DDD(R) or VDD pacing. In contrast, 2 weeks after changing the pacing mode to VVI(R), a highly significant 2.4-fold increase in both BNP [DDD(R)/VDD: 152 ± 131 versus VVI(R): 360 ± 222 pg/mL, P < 0.0001] and NT-proBNP levels [DDD(R)/VDD: 548 ± 598 versus VVI(R): 1298 ± 1033 pg/mL, P < 0.0001] could be observed (Figure 2). This pattern of natriuretic peptide increase during VVI(R) pacing was consistently present throughout all subgroups analysed (Table 2). It was present for different pacing indications, in different underlying heart diseases, in different age groups, in patients with and without left ventricular systolic dysfunction, in patients with New York Heart Association (NYHA) I functional capacity and those with NYHA class >I, and in both pacemaker-dependent and independent patients.
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Echocardiographic parameters
The echocardiographic findings, as secondary endpoints, were quite similar in both stimulation modes. None the less, atrioventricular pacing was associated with a mild but significant increase in left ventricular ejection fraction (50.9 ± 10.0 versus 48.9 ± 10.7%, P = 0.036), and a trend towards increased velocity time integral in the left ventricular outflow tract (36.9 ± 15 versus 35.1 ± 14.2 cm, P = 0.10). There were no significant changes in diastolic function (transmitral flow propagation rate and the E to E' ratio).
Subjective parameters
The assessment of patients' functional class, the presence or absence of pacemaker syndrome, and the patients' preference of a certain pacing mode, all showed significant differences in favour of DDD(R) or VDD pacing (Table 3). New York Heart Association functional class deteriorated during VVI(R) pacing in 21 of the 41 patients, including 8 of 10 patients who were completely without symptoms while on DDD(R) or VDD stimulation. Diuretics had to be added to baseline medications in two patients because of progressive dyspnoea while on VVI(R) mode. Symptoms of pacemaker syndrome were present in almost 50% of patients during VVI(R) stimulation. The preferred pacing mode was DDD(R) or VDD in 29 of the 41 patients (71%), whereas the remaining 12 patients had no preference. No patient preferred the VVI(R) mode. Interestingly, both baseline levels of BNP and NT-proBNP and their magnitude of increase during VVI(R) pacing were comparable between patients with and without a pacing mode preference.
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Discussion |
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It is still a widespread opinion that optimal pacing strategies should include the restoration of atrioventricular synchrony and the provision of rate adaptation whenever possible, thus favouring the use of dual-chamber rather than single-chamber ventricular pacemakers.21
However, recent large prospective randomized trials consistently demonstrated the absence of an overall survival benefit with DDD(R) pacing compared with VVI(R) stimulation.2–4 These findings have questioned the justification for implanting DDD(R) pacing systems.
The purpose of this study was to evaluate if DDD(R)/VDD pacing, compared with VVI(R) pacing, would positively impact cardiac function in a way what would be detectable using the objective, sensitive, and prognostically relevant parameters BNP and NT-proBNP. Our main result shows that patients experience a highly significant, two- to three-fold increase of BNP and NT-proBNP levels during VVI(R) pacing compared with synchronized atrioventricular pacing (Figure 2). This finding was consistently present in all subgroups analysed (Table 2). The reversibility of this finding in our crossover study design suggests that the loss of atrioventricular synchrony while on VVI(R) stimulation is directly responsible for the increased levels of natriuretic peptides, most likely as a result of increased atrial and ventricular wall stretch and pressure.22
Elevated natriuretic peptide levels have been shown to predict adverse long-term cardiovascular outcomes in a wide array of clinical settings.10–15 The observed increase in BNP and NT-proBNP release while on ventricular-based pacing might be interpreted to suggest an unfavourable prognosis in response to atrioventricular dyssynchrony. This assumption, however, is in contradiction to the lack of survival benefit found for atrioventricular sequential pacing in the large randomized controlled trials.2–4 This apparent discrepancy might be related to the large proportion (68%) of pacemaker-dependent patients in our cohort. In an analysis of the CTOPP trial results, it was shown clearly that pacemaker-dependent patients (defined as an unpaced heart rate at first follow-up 60 bpm) randomized to atrioventricular pacing had improved survival.20 In contrast, patients with an unpaced heart rate >60 bpm, who would be paced only infrequently, had no significant changes in outcome with VVI pacing compared with DDD pacing. Unfortunately, a subgroup analysis based on pacemaker dependency has not been presented for either the MOST or UKPACE trial.3,4 With respect to other hard endpoints, some trials have shown a significant reduction in the frequency of atrial fibrillation and hospitalization for heart failure with atrioventricular sequential pacing in specific subgroups such as patients with sinus node disease and patients <75 years of age.2,3,23,24
The subtle improvement in haemodynamic performance detected by natriuretic peptides in DDD(R)/VDD mode was associated with a mild but significant increase in left ventricular ejection fraction (P = 0.036). These mild changes in left ventricular function may not be clinically relevant, but need to be interpreted with regard to the short time periods in our study design. It is conceivable that larger changes may become evident over periods >2 weeks. Moreover, measurements at rest may not be representative for cardiac performance over 24 h in physically active patients.
In the present study, >50% of patients deteriorated in NYHA functional class during VVI(R) pacing (from NYHA class 1.8 ± 0.5 to NYHA class 2.4 ± 0.6), a rate which is consistent with previously published results from studies of a similar design.25,26 Almost 50% of the cohort met the pre-specified criteria for pacemaker syndrome while in VVI(R) mode. Considering the high incidence of symptomatic deterioration during VVI(R) stimulation, it is not surprising that the preferred mode was DDD(R) or VDD in 71%—chosen by the patients while blinded to their pacing mode. The remaining 12 patients had no preference, but no patient preferred the VVI(R) mode. These data are comparable with the study of Heldman et al., in which 83% of patients complained of symptoms consistent with pacemaker syndrome, and to the study of Rediker et al., where 42% of patients reported the occurrence of pacemaker syndrome in VVI mode.25,26 By contrast, in the CTOPP study, in which surgical revision was required to upgrade from VVI(R) pacing to physiological pacing, the incidence of pacemaker syndrome was reported to be 2.7% at 3 years.2 In studies in which all patients received a dual-chamber pacemaker and could have it reprogrammed, the reported incidence of pacemaker syndrome was much higher.27,28 In the PASE trial, the crossover rate from the VVI(R) to the DDD(R) group due to pacemaker syndrome was 26%, and in a recent publication from the MOST cohort 18.3%.27,28 The most likely explanation for the high rate of pacemaker syndrome in the present study is the study design. The trials mentioned above compared the pre-implantation period, in which most of the symptoms were bradycardia-related, with the post-implantation period, when most symptoms are abolished by any type of pacemaker. In contrast, we included patients in a steady state after pacemaker implantation, chronic DDD(R)/VDD pacing. An additional reason for the higher incidence of pacemaker syndrome in our study cohort and the deterioration of functional class while on VVI(R) pacing might be, on the one hand, the selected base rate of 60 bpm in VVI(R) mode, given by the study design, on the other hand, there was the high percentage of ventricular stimulated complexes in our study [91% ventricular paced beats in DDD(R)/VDD mode; 82% ventricular paced beats in VVI(R) mode]. This is reflected in the fairly large proportion of patients with an unpaced heart rate of 60 bpm. In contrast, the percentage of ventricular paced beats was only around 50% in the MOST cohort, and no details are reported on percent paced beats of those patients in the PASE and CTOPP trial who had been programmed to VVI mode.28 Many patients with sick sinus syndrome whose pacemakers are programmed to VVI rarely require pacing. For this reason, the effect of pacing mode would be less impressive than in patients with complete heart block.
Clinical implications
BNP and NT-proBNP measurements can differentiate easily and efficiently between more or less physiological pacing parameters. Therefore, those markers may be a useful instrument to optimize pacemaker parameters in individual patients. Furthermore, if medium-term changes of natriuretic peptides translate to long-term changes in prognosis, as it has been shown in almost all circumstances investigated, then our study results suggest an adverse long-term prognostic effect of VVI(R) pacing.
Limitations
This study was performed using a single-blind design, thus introducing potential for bias in data collection. However, the main endpoints of the study, the plasma levels of BNP and NT-proBNP, are objective measurements not at risk of bias. Similarly, assessment of patient-reported parameters (functional class, pacemaker syndrome, and personal preference) was performed using a questionnaire, which the patients completed at each stage independently of the study physicians. Finally, echocardiographic measures were acquired by physicians unaware of the patients' current pacing assignment. Nonetheless, in some cases VVI pacing might have been identifiable due to transmitral Doppler flow profiles and ECG monitoring.
An additional limitation is the relative short study period. Although a 2-week time frame might appear to be a short period to evaluate medium- to long-term effects of various pacemaker settings, we considered it sufficient, since prior studies have shown that acute haemodynamic changes seen with different pacemaker settings are representative of changes seen with long-term pacing.29,30 Furthermore, other authors have found the same time interval useful to reveal differences resulting from altered pacemaker settings.31,32 Similarly, prognostically relevant changes in natriuretic peptide levels have been found after even shorter time periods when used in other clinical settings.10
Finally, the number of patients with different underlying cardiac diseases was relatively small in this study. Although subgroup analysis showed neither significant differences, nor a trend in favour of one of these subgroups, the data resulting from these analyses should be considered as preliminary observations.
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Conclusions |
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Despite being blinded to their pacing mode, most patients can differentiate between DDD(R)/VDD and VVI(R) pacing, and the vast majority prefer the former. Compared with DDD(R)/VDD pacing, VVI(R) stimulation induces a two- to three-fold increase in the prognostically relevant serum levels of BNP and NT-proBNP. This is accompanied by worsening functional class and a high rate of pacemaker syndrome. These data support the concept that DDD(R) or VDD pacing is superior to VVI(R) stimulation.
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Acknowledgements |
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David J. Kurz receives financial support from the Swiss Heart Foundation.
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