|Year : 2016 | Volume
| Issue : 1 | Page : 52-59
Early effects of right ventricular pacing on the left ventricle in single-chamber and dual-chamber pacemakers
Alaa S Algazzar1, Mohamed A Moharram2, Azza A Katta1, Ghada M Soltan2, Walaa F Abd Elaziz2
1 Cardiology Department, National Heart Institute, Cairo, Egypt
2 Cardiology Department, Faculty of Medicine, Menofia University, Menufia, Egypt
|Date of Submission||04-Jan-2014|
|Date of Acceptance||29-Sep-2014|
|Date of Web Publication||18-Mar-2016|
Alaa S Algazzar
Msc, Zaki Gomaa st, Aldalgamoon, kafr Elzayat, Gharbeia Governorate
Source of Support: None, Conflict of Interest: None
Our study aimed at demonstrating the early impacts of right ventricular apical pacing induced by single-chamber (VVI) and dual-chamber (DDD) pacemakers on left ventricular (LV) functions, and to assess whether brain natriuretic peptide (BNP) after 2 months of implantation is correlated for LV dyssynchrony.
Long-term effects of right ventricular apical pacing have been studied, and not much information is available on the early effects of right ventricular pacing on the LV function and dyssynchrony.
Patients and methods
The study was conducted on 40 patients who came for the implantation of permanent pacemakers. Patients were divided into two groups of 20 patients each: group A included patients who were implanted with VVI pacemakers and group B included patients who were implanted DDD pacemakers. Both groups were examined before implantation and after 2 and 6 months of implantation for BNP and predetermined parameters for LV dyssynchrony and systolic and diastolic functions by echocardiography. After 6 months, patients with DDD pacemakers were crossed over to the VVI mode of pacing by programming for a period of 2 weeks, and then a blood sample was collected for BNP.
The mean BNP level in VVI pacing (group A) was 196.5 123 pg/dl, which was higher than that in DDD pacing (group B 79.35 65.36 pg/dl), after 2 months, with P value equal to 0.001, while a comparison after 6 months showed P value equal to 0.023. There was a statistically significant difference between groups in their myocardial performance index with a P value of 0.03. Results of the aortic pre-ejection delay showed a significant difference with a P value of less than 0.05. BNP was correlated to aortic pre-ejection delay (r = 0.651 and P = 0.001) and the pacing percentage (r = 0.687 and P = 0.00).
Loss of atrioventricular synchrony in the VVI mode leads to a significant difference in LV dyssynchrony between both groups. Myocardial performance index was affected more than the other parameters for systolic and diastolic functions. The BNP level was correlated to LV dyssynchrony and the pacing percentage.
Keywords: Brain natriuretic peptide, dyssynchrony, pacing
|How to cite this article:|
Algazzar AS, Moharram MA, Katta AA, Soltan GM, Abd Elaziz WF. Early effects of right ventricular pacing on the left ventricle in single-chamber and dual-chamber pacemakers. Menoufia Med J 2016;29:52-9
|How to cite this URL:|
Algazzar AS, Moharram MA, Katta AA, Soltan GM, Abd Elaziz WF. Early effects of right ventricular pacing on the left ventricle in single-chamber and dual-chamber pacemakers. Menoufia Med J [serial online] 2016 [cited 2020 Dec 3];29:52-9. Available from: http://www.mmj.eg.net/text.asp?2016/29/1/52/178977
| Introduction|| |
Cardiac pacing at any point of the ventricle alters the natural heart activation and contraction pattern, as the stimulus conduction velocity is slower across the ventricular myocardium when compared with that resulting from the specialized His-Purkinje system ,.
Right ventricular (RV) apical pacing can induce both interventricular dyssynchrony [between the RV and the left ventricle (LV)] and intraventricular dyssynchrony (within the LV) . It has been demonstrated that the presence of ventricular dyssynchrony is associated with an increased risk of cardiac morbidity  and mortality  in heart failure patients. In addition, it has been suggested that the presence of mechanical dyssynchrony after long-term RV apical pacing is associated with reduced LV systolic function and deterioration in the functional capacity .
However, there are only a few studies that have demonstrated a direct relation between pacing-induced ventricular dyssynchrony and clinical heart failure. This suggests that an abnormal activation pattern (left bundle branch block during RV apical pacing) or ventricular dyssynchrony may be directly related to a deterioration of LV function. Therefore, the assessment of ventricular dyssynchrony may provide important information in patients with permanent RV apical pacing ,.
| Patients and methods|| |
The study was carried out during the period between April 2012 and November 2013, and included 40 patients with implantation of single-chamber and dual-chamber permanent pacemakers at the electrophysiology unit of the National Heart Institute. The patients were enrolled into two groups. Group A included 20 patients with implanted single-chamber pacemaker right ventricular pacing (VVI); Group B included 20 patients with implanted dual-chamber pacemaker (DDD).
This study compared the early effects of RV apical pacing on LV functions in VVI and DDD pacemakers using echocardiographically determined parameters of systolic and diastolic functions. Also, we assessed whether brain natriuretic peptide (BNP) after 2 months of implantation is correlated to ventricular dyssynchrony in different cardiac pacing modes.
Adult patients with age less than 75 years with indication for permanent pacing, patients with normal structural hearts and normal LV functions, and patients with a BMI less than 30 kg/m 2 were enrolled in the study after 2 months of implantation if they had more than 60% pacing dependence and if the ventricular lead was in the RV apex.
Patients with a poor echo window and patients with symptoms of overt heart failure, previous cardiac surgery or structural heart diseases (e.g. dilated cardiomyopathy, valvular heart diseases, congenital cardiac anomalies, and prosthetic valves) were excluded from the study. We also excluded patients with documented chronic heart dysrhythmias, patients with previous coronary artery disease detected by evidence of LV regional wall motion abnormalities at the echocardiogram or pathological Q waves in the ECG or any form of acute coronary syndrome within the past 4 weeks, patients with a history of chronic obstructive lung disease, pulmonary hypertension or recent pulmonary embolism, renal impairment, pregnant women, and patients with terminal comorbidities such as end-stage malignancy and end-stage renal or liver diseases.
After obtaining written informed consent, all patients were subjected to the following.
- Full history taking, with a history of medications used and general and cardiac examinations.
- Twelve-lead ECG with measuring the QRS duration. The duration of the QRS complex included the measurement of the time interval between the emission of the pacemaker spike and the end of the QRS complex (ms).
- Chest radiograph to verify the position of the ventricular lead.
- Urea and createnin levels.
- Pacemaker analysis: Pacemaker telemetry was performed under monitoring
- BNP samples were obtained after 2 and 6 months by direct venipuncture of an antecubital vein after the patient had been in a supine position for at least 15 min. A venous blood sample was collected in tubes containing potassium EDTA. All samples were centrifuged at 3000 rpm (15°C for 10 min), and the separated plasma was assayed immediately. Plasma natriuretic peptide concentrations were measured with a specific immunoradiometric assay for human BNP using commercial kits (Human BNP EIA Kit; Ray Bio, Norcross, Georgia, USA). After 6 months, patients in group B were crossed over to the VVI mode of pacing by programming for a period of 2 weeks with a lower rate of 60 beats/min, and then a venous blood sample was collected again for BNP to test the effect of right apical pacing in the VVI mode on the heart. These patients were programmed again to the DDD mode after taking the blood sample.
- Echocardiographic studies were conducted using a commercially available system (Samsung Medison EKO 7, Seoul, Korea) with a 2.5-3.5-MHz transducer. Patients were examined before implantation and again after 2 and 6 months of implantation for the LV dimension, LV systolic and diastolic functions and the myocardial performance index (MPI), and pulsed tissue Doppler imaging was used to obtain septal and lateral velocities for both E and S waves.
Mechanical dyssynchrony was assessed after 2 and 6 months by the following defined conventional parameters.
- Aortic pre-ejection delay (APED) by pulsed wave Doppler is measured between the onset of the QRS complex and the beginning of the aortic flow by pulsed wave Doppler. Intraventricular dyssynchrony is defined by an APED of 140 ms or more ,.
- Interventricular mechanical delay (IVMD) by pulsed wave Doppler: to calculate the IVMD, the time from the onset of the QRS to the onset of pulmonary flow was measured at the parasternal short-axis view, using pulsed wave Doppler, and the difference between it and the APED resulted in the IVMD. Interventricular dyssynchrony is defined by an IVMD of 40 ms ,.
- Septal-posterior wall motion delay (SPWMD) is determined by identifying the time delay from the peak inward septal motion to the peak inward posterior wall. Intraventricular dyssynchrony is defined by an SPWMD of 130 ms ,.
The collected data were tabulated and statistically analyzed using the SPSS version 20.0 for Windows (SPSS Inc., Chicago, Illinois, USA). Comparisons between the groups were performed using the unpaired Student t-test. Comparisons within the group were performed using the paired Student t-test. A probability value of 0.05 was considered to be statistically significant. DDD pacing as compared with VVI pacing was assessed using one-way analysis of variance for repeated measures. Partial correlations were used to measure the linear association between variables while controlling for the effects of one or more additional variables, and multiple linear regression analysis was performed to provide regression analysis, and analysis of variance was used for one dependent variable such as BNP levels and other variables.
| Results|| |
No significant difference was found between both groups regarding baseline characteristics of the study, which are outlined in [Table 1].
In our study, there was no statistically significant difference in the LV ejection fraction (EF), and systolic and diastolic internal dimensions between both groups over time (P > 0.05) as shown in [Table 2]. Also, there was no statistically significant difference for septal and lateral E and S waves by pulsed tissue Doppler in both groups over time (P > 0.05). We found that septal S wave velocity was more affected when compared with the lateral S wave velocity within each group after 6 months, with a P value of 0.005 for group A and a P value of 0.001 for group B as shown in [Table 3].
This study showed that the mean BNP level in VVI pacing (group A) was higher than that in DDD pacing (group B), after 2 months' follow-up: group A showed a mean BNP of 196.5 ± 123 pg/dl compared with 79.35 ± 65.36 pg/dl in group B, with a highly significant difference between both groups (P = 0.001). Comparison of both groups after 6 months showed a mean BNP of 200.85 ± 106.6 pg/dl in group A and a mean of 121.5 ± 105.15 pg/dl in group B, with a statistically significant difference and P value of 0.023. There was a statistically significant difference within repeated measurements of the BNP level in group B after converting pacing from dual chamber (DDD) to single chamber (VVI) for 2 weeks, with mean 172 ± 90 and a P value of 0.001.
|Table 2: Comparison between the studied groups regarding their echocardiographic data|
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|Table 3: Comparison between septal and lateral S waves by tissue Doppler in the studied groups|
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Regarding ventricular dyssynchrony, our results showed no statistically significant difference between both groups at 2 and 6 months in comparison with SPWMD and IVMD in both groups over time (P > 0.05). In contrast, there was statistically significant difference between both groups in the results of APED (P < 0.001 at 2-month interval and 0.026 at 6-month intervals) as shown in [Table 4].
|Table 4: Comparison between the studied groups regarding their brain natriuretic peptide and parameters of dyssynchrony|
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Our results showed a significant correlation between the BNP level and the pacing percentage (r = 0.687 and P = 0.00) as shown in [Figure 1], the APED (r = 0.651 and P = 0.001) as shown in [Figure 2] and the QRS duration (r = 0.42 and P = 0.01) as shown in [Table 5]. On multiple linear regression analysis, the pacing percentage and the APED remained as the only significant and independent predictor of BNP levels, even after adjustment for age and LV EF, with a P value of 0.007 for APED and a P value of 0.0001 for the pacing percentage. Hence, we can infer that the higher the percentage of pacing and the longer the APED, the higher the BNP level.
|Figure 1: A scatter plot graph showing the relationship between brain natriuretic peptide (BNP) and the pacing percentage(r = 0.687, P < 0. 0001).|
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|Figure 2: A scatter plot graph showing the relationship between brain natriuretic peptide (BNP) and the aortic pre-ejection delay (r = 0.651, P < 0. 0001).|
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|Table 5: Partial correlation analysis between the brain natriuretic peptide level and parameters of left ventricular |
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| Discussion|| |
Long-term effects of RV apical pacing have been studied, and not much information is available on the acute and early effects of RV pacing on LV function and LV dyssynchrony . Our study aimed to demonstrate the early negative impact of RV apical pacing induced by single-chamber and dual-chamber pacemakers on LV systolic and diastolic functions in patients with preserved EF.
Effect on left ventricular systolic functions
In our study, there was no statistically significant difference within repeated measurements of the LV EF and systolic and diastolic internal dimensions in both group over time (P > 0.05), and this is due to the short term of follow-up. LV EF is a surrogate parameter that describes myocardial pump function. Even if contractility is reduced, compensatory mechanisms (i.e. ventricular dilatation, geometry changes) can still assure that the stroke volume remains normal at least at rest .
Mohan et al.  in their study found no significant difference in the resting LV EF in the long-term follow-up of AAI-paced and VVI-paced patients of sinus node dysfunction without structural heart disease. Similarly, Anderson et al. , in their study of sick sinus syndrome patients, found no difference in the incidence of clinical congestive heart failure or LV dimensions between AAI and VVI pacing modes on long-term follow-up. In contrast, Pehrsson et al. found an increase in the end-diastolic volume in VVI-paced patients after 3 months . Likewise, Faerestrand et al.  found greater resting LV volumes and lesser EF in patients paced on VVI rather than with the physiological pacing mode. Dwivedi et al.  studied 48 patient with VVI pacing and found that the LV EF decreased progressively from baseline (61.82 ± 10.36%) and was statistically significant at 6 months (52.52 ± 12.11%, P < 0.05). The cardiac dimensions, the LV end-diastolic dimension and the LV end-systolic dimension increased significantly over their corresponding baseline values by 6 months (P < 0.05) . However, the aforementioned study used a higher percentage of pacing (>90%) in all patients, and this may be the cause of early effects on the LV dimension and systolic functions.
The S wave by pulsed-tissue Doppler is another predictor of systolic dysfunction . In our study, there was no statistically significant difference in septal and lateral S waves by pulsed-tissue Doppler in both groups over time (P > 0.05). Our results were the same as Kojuri et al.  in the above-mentioned study. They found no significant difference on comparing EF and S waves by pulsed-tissue Doppler in the DDD, VDD and VVI pacing modes with a P value of 0.45 despite the fact that they had selected patient with more than 90% pacing percentage .
In our study, we found that the septal S wave velocity was more affected when compared with the lateral S wave velocity within each group after 6 months, with a P value of 0.005 for group A and a P value of 0.001 for group B. Ventricular pacing reduces mechanical work in the septum during RV apical pacing by 50% and increases it by 50% in the LV free wall. Under RV apical pacing, the LV septal wall was activated early and forced the LV lateral wall to be pre-stretched at that time. Then, when all regions have been activated, the fiber of the LV lateral wall was longer than the fibers in the septal wall. Therefore, RV apical pacing caused the difference in the local preload between the LV septal and the lateral wall. By virtue of a local 'Frank-Starling' relation, the later activated regions are stronger and shorten more during the ejection phase. Therefore, regional differences in the contraction pattern during ventricular pacing can be regarded as differences in the effective local preload .
The effect on left ventricular diastolic functions
We did not find any statistically significant difference between both groups regarding septal and lateral E′ waves by pulsed-tissue Doppler. This was the same as in previous studies; they also found no significant changes in the diastolic function. Naegeli et al.  conducted a single-blind, randomized crossover study evaluating the impact of the DDD(R) mode as against the VVI(R(mode on objective and functional parameters. They found no significant changes in the transmitral flow propagation rate and the E-E′ ratio . Kojuri et al.  also found no significant changes in E and A′ by pulsed-tissue Doppler between DDD and VVI.
In our study, the mitral deceleration time showed a statistically significant difference between both groups only at 6 months (P = 0.01). Doppler patterns of mitral inflow reflect the pressure gradient between the left atrium and LV, and that transmitral velocities are directly related to the left atrial pressure (preload) and independently and inversely related to ventricular relaxation. Because mitral inflow patterns are highly sensitive to preload and can change drastically as the diastolic dysfunction progresses, the use of mitral valve inflow patterns to assess the diastolic function remains limited. Tissue Doppler assessment of the diastolic function is less load dependent than that provided by standard Doppler techniques. Unlike conventional mitral inflow patterns, E′ is resistant to changes in the filling pressure .
The effect on global left ventrucular systolic and diastolic functions
Our findings showed an increase in the MPI in both groups with a statistically significant difference between both groups at 6 months (P = 0.03). MPI incorporates both systolic and diastolic aspects of the function and has also been shown to correlate well with known invasive indexes of LV systolic and diastolic function . Our data were consistent with previous observations and suggested that LV dyssynchrony was implicated in deteriorating ventricular function in single-chamber pacing [17,22]. This can also be attributed to the shorter LV ejection interval . Choi et al. evaluated 40 patients with sick sinus syndrome before and after (12 months) single-chamber ventricular pacemaker implantation (VVI). MPI significantly increased after 12 months of implantation . Burns et al.  found that RV-paced patients had significantly longer isovolumic contraction times, which is likely a consequence of the slower pressure development during a dyssynchronous LV contraction. Longer isovolumic contraction limits the time available for adequate systolic ejection and diastolic filling. Heart rates were also slightly higher in paced patients, further shortening ejection and filling times. This may be an important mechanism in reducing LV function in RV-paced patients .
The effect on the brain natriuretic peptide level and left ventricular dyssynchrony
This study showed that the mean BNP level in VVI pacing (group A) was higher than in DDD pacing (group B), after 2-month follow-up, with a highly significant difference between both groups (P = 0.001). Comparison of both groups for the BNP level after 6 months showed a statistically significant difference (P = 0.023).
Our results were concordant with previous studies; Nikoo et al.  compared the effects of RV septal with apical pacing on plasma natriuretic peptide levels in VVI and DDD pacemakers and showed that despite the increase in BNP levels in patients with the VVI mode, compared with those with the DDD(R)/VDD mode (P = 0.02), the pacing sites had no effect on BNP levels, irrespective of the pacing mode. They concluded that hemodynamic improvement could be substantially more influenced by the pacing mode than by the pacing site . Kojuri et al.  found that the level of pro-BNP is lower in double-chamber pacing in comparison with single-chamber pacing. Therefore, it seems that dual-chamber pacing causes less LV dysfunction .
In this study, DDD pacemakers were crossed over to the VVI mode of pacing by programming for a period of 2 weeks with a lower rate of 60 beats/min. We found a statistically significant difference within repeated measurements of the BNP level in group B after converting the pacing from DDD to VVI for 2 weeks, with mean 172 ± 90 and a P value of 0.001. The increased BNP level in our crossover design suggests that the loss of atrioventricular synchrony while on VVI 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 .
This cross over was concordant with results from Naegeli et al. , who conducted a single-blind randomized crossover study evaluating the impact of DDD(R)/VDD against VVI(R) mode on objective and functional parameters. They found that patients experience a highly significant (two-three-fold) increase in BNP and NT-pro-BNP levels during VVI(R) pacing compared with synchronized atrioventricular pacing with DDD(R)/VDD pacing (P < 0.001) . Dual-chamber pacing preserves atrial-ventricular synchrony and decreases ventricular end-diastolic pressure and increases the cardiac output [4,22].
Regarding ventricular dyssynchrony, our results showed no statistically significant difference between both groups at 2 and 6 months and for repeated measurement comparisons of SPWD and IVMD in both groups over time (P > 0.05). In contrast, there was a statistically significant difference between both groups in the results of APED (P < 0.05). We believe that the difference was caused by a loss of atrioventricular synchrony and in a larger part by the ventricular pacing percentage.
Sα et al.  observed the prolonging of APED in a small group of patients, who were Chagasic with normal LV EF, throughout an 8-month period. The authors observed that although the APED measurements did not reach the cutoff required for the diagnosis of ventricular dyssynchrony (≥140 ms), this was the only assessed ventricular dyssynchrony measure that showed increases throughout the follow-up .
Our results showed a significant correlation between the BNP level and the pacing percentage, the QRS duration and APED. On multiple linear regression analysis, the pacing percentage and APED remained as the only significant and independent predictors of BNP levels, even after adjustment for age and LVEF, with a P value of 0.007 for APED and a P value of 0.0001 for the pacing percentage. Hence, we can infer that the higher the percentage of pacing and the longer the APED, the higher the BNP level. Results of the DAVID trial revealed that RV-paced patients with LV dysfunction, patients requiring a defibrillator and those who were actively paced in the DDDR-70 mode had a 60% greater risk of hospitalization or death than patients who received minimal back-up pacing in the VVI-40 mode . This can infer the strong relationship between the pacing percentage and the BNP increment.
The correlation between the QRS duration and BNP in our study is explained by a recent study of Chen et al. , who found prolonged paced QRS could be a useful predictor to identify patients who are at risk for heart failure events during RV apical pacing. Abreu CD et al.  demonstrated a significant correlation between the APED and BNP (r = 0.38, P < 0.0001), regardless of the LVEF and the age. The studies MOST , DAVID  and MADIT II , in turn, indicated that ventricular dyssynchrony can create an anatomofunctional substrate capable of impairing heart function in the long term, by observing an increase in the risk of atrial fibrillation, mitral regurgitation and hospital admissions due to heart failure in patients with a high percentage of RV paced beats, particularly in those with ventricular dysfunction before the implant .
The present analysis focuses on the short-term impact of RV apical pacing on LV functions and LV dyssynchrony and does not provide information about the long-term consequences. However, previous studies have demonstrated a close link between ventricular dyssynchrony and the long-term clinical outcome ,,,,. We considered a 6-month follow-up sufficient to detect relevant changes in the natriuretic peptide; however, levels have been found after even shorter time periods when used in other clinical settings ,,. We could not fully achieve the blinding of the echocardiographer because the additional lead was visible in the right atrium and the difference between VVI pacing and the AV synchrony was also apparent. Finally, the number of patients was relatively small in this study, and the data resulting from these analyses should be considered as preliminary observations.
| Conclusion|| |
MPI, which is a combined parameter for systolic and diastolic functions, was affected more than the other parameters. Loss of atrioventricular synchrony in the VVI mode leads to a significant difference in LV dyssynchrony between both groups as observed in the results of APED. Also, we found that the BNP level was correlated to APED and the pacing percentage and can predict LV dyssynchrony in RV-paced patient, which occurs earlier than LV dysfunction.
| Acknowledgements|| |
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]