Objective
The study objective was to compare the left ventricular (LV) dyssynchrony and torsional behavior between right ventricular apical (RVA) and right ventricular septal (RVS) pacing.
Methods
Forty-six patients with symptomatic sick sinus syndrome and preserved LV function were assigned to 2 groups: RVA (n = 23) and RVS (n = 23). Echocardiographic study including two-dimensional speckle tracking imaging was performed in the AAI and DDD modes.
Results
Mean QRS width during DDD mode was significantly longer with RVA pacing than with RVS pacing. Dyssynchrony, torsion, and untwisting rate during DDD mode were significantly worse with RVA than with RVS pacing. In patients with RVA pacing, there was an increase in longitudinal dyssynchrony from AAI to DDD mode that significantly correlated with the deterioration of untwisting rate.
Conclusion
In bradyarrhythmic patients with preserved LV function, RVS pacing resulted in a reduced LV dyssynchrony and better torsional behavior than RVA pacing.
Right ventricular apical (RVA) pacing, the conventional pacing therapy for bradyarrhythmic patients, induces iatrogenic left bundle branch block and left ventricular (LV) dyssynchrony. The Mode Selection Trial demonstrated that chronic RVA pacing increases the risk of atrial fibrillation and congestive heart failure. Therefore, right ventricular septal (RVS) pacing using a standard screw-in lead has been introduced to shorten the wide QRS complex that occurs with RVA pacing.
The recent development of two-dimensional speckle tracking echocardiography (2DSTE) allows the spatial and temporal analysis of myocardial deformation independently of angle correction. Therefore, this method has been used to quantify LV dyssynchrony and torsional behavior. A recent experimental study showed that RVA pacing causes dyssynchrony and exacerbates LV torsional behavior. Accordingly, this study was to test our hypothesis that RVS pacing is a beneficial alternative in terms of less LV dyssynchrony and better torsional behavior compared with RVA pacing in bradyarrhythmic patients with preserved LV function.
Materials and Methods
Study Population
This study included 52 consecutive patients with symptomatic sick sinus syndrome and preserved LV function who were scheduled for permanent pacemaker implantation. Exclusion criteria included patients with chronic atrial fibrillation, significant valvular heart disease, LV ejection fraction less than 60%, and ischemic heart disease confirmed by coronary angiography. We randomly assigned patients into an RVS group or an RVA group. This study was approved by the ethics committee of Ehime University Graduate School of Medicine, and all patients gave informed consent before participation.
Procedure of Pacemaker Implantation
All patients received dual-chamber pacing (DDD) via a transvenous approach. We used a traditional tined-tip pacing to anchor a lead in the right atrial appendage in all patients and in the right ventricular (RV) apex in those patients randomized to the RVA group. In contrast, a screw-in type of ventricular pacing lead was used to anchor a lead in the RV septum in patients randomized to the RVS group. We tried to anchor the ventricular leads at the RV septum using electrocardiographic and fluoroscopic guidance according to the method described by Mond et al.
Echocardiographic Examination
Echocardiographic examination was performed 7 days after pacemaker implantation using a Vivid 7 Dimension ultrasound machine (GE Healthcare, Waukesha, WI) with an M4S probe. Interrogation of the implanted devices before the study showed only atrial pacing (AAI mode) was active. Echocardiographic studies were performed in 2 groups during both AAI and DDD modes. The lower rate limit in AAI mode was programmed to 60 beats/min. When the pacing mode was switched from AAI to DDD mode, the programmed atrioventricular delay was less than the spontaneous atrioventricular delay in the AAI mode to force ventricular pacing. Standard echocardiographic measurements were performed according to the recommendation of the American Society of Echocardiography. In addition, by using color-coded tissue Doppler imaging, the 2 LV dyssynchrony indices, such as basal septal-to-lateral delay from the 4-chamber view (SL delay) and SD in time to peak systolic velocity among 12 LV segments (Ts-SD), were estimated according to previous reports.
Data Analysis from Two-Dimensional Speckle Tracking Imaging
The values of LV strain and rotation derived by 2DSTE were estimated from a high frame rate (65-102 frames per second) gray scale B-mode data with commercially available software (EchoPAC PC BT08: GE Healthcare). We estimated the degree of LV systolic dyssynchrony as the standard deviation of the time from QRS onset to peak systolic longitudinal strain of 18 LV segments (6 basal, 6 mid, and 6 apical segments from apical 4-, 2-, and 3-chamber views) including the apical plane (SDt 18s) in addition to conventional radial dyssynchrony index. LV torsional abnormalities were calculated as described in our recent report. Cases were excluded that had tracking failure in 1 or more myocardial segments judged by the software. All measurements of LV dyssynchrony and rotation were averaged for at least 3 consecutive beats.
Statistical Analysis
Continuous variables were expressed as the mean ± standard deviation. Comparisons of echocardiographic parameters between the AAI and DDD modes in patients receiving RVA or RVS pacing were performed using a paired t test. A 2-way analysis of variance followed by Scheffe’s post hoc test was used to compare the differences in echocardiographic parameters between RVA and RVS pacing in both AAI and DDD modes. Linear regression analysis was performed to evaluate the relationship between the changes of LV dyssynchrony index and that of untwisting rate in both the RVA and RVS groups. The interobserver and intraobserver variabilities were assessed for the SDt 18s and untwisting rate in 10 recordings in 7 randomly selected patients. Interobserver variability was estimated by 2 independent observers who were unaware of the patient data. Intraobserver variability was calculated between the first and second analyses (2-week interval) for a single observer. Values of P less than .05 were considered statistically significant.
Results
This study excluded 6 patients (RVA pacing in 3 patients and RVS pacing in 3 patients) because of the tracking failure in the analysis of 2DSTE. Data for 46 patients (RVA: n = 23, RVS: n = 23) were analyzed.
Table 1 shows that there were no significant differences in age, gender, and atherosclerotic risk factors between the 2 groups. The QRS width in patients receiving RVS pacing during DDD mode was significantly shorter than in patients receiving RVA pacing. Table 2 shows that the SL delay and Ts-SD were significantly greater in patients receiving RVA pacing compared with those receiving RVS pacing in DDD mode. In addition, these values were significantly increased switching from AAI mode to DDD mode in patients receiving RVA pacing but not RVS pacing. The LV radial dyssynchrony index and SDt 18s were also significantly greater in patients receiving RVA pacing compared with those receiving RVS pacing in DDD mode. Furthermore, these values were significantly increased switching from AAI mode to DDD mode in patients receiving RVA but not RVS pacing. The basal LV rotation was significantly lower during DDD mode in comparison with AAI mode in patients receiving RVA pacing (AAI: −9 ± 3 degrees, DDD: −4 ± 2 degrees, P < .01). In addition, the value of apical LV rotation was significantly greater in patients with RVS pacing compared with those receiving RVA pacing during DDD mode (RVA: 7 ± 3 degrees, RVS: 9 ± 4 degrees, P < .05). Consequently, peak torsion in patients receiving RVA pacing during DDD mode was significantly decreased in compared with that during AAI mode but not RVS pacing ( Figure 1 A ). In addition, peak torsion during DDD mode was significantly greater in patients receiving RVS pacing compared with those receiving RVA pacing. The untwisting rate was also significantly decreased during DDD mode compared with AAI mode in patients with RVA pacing ( Figure 1 B) and was significantly decreased in patients receiving RVA pacing compared with those receiving RVS pacing during DDD mode. Figure 2 shows representative cases of 2 groups. LV longitudinal dyssynchrony and untwisting velocity during DDD pacing also deteriorated in a patient with RVA pacing ( Figure 3 A ) compared with RVS pacing ( Figure 3 B). Figure 3 shows the correlation between changes in SDt 18s and that in untwisting rate from AAI to DDD mode in patients with RVA ( Figure 3 A) and RVS ( Figure 3 B) pacing. There was a significant relationship between these parameters in patients with RVA but not RVS pacing.
| Variables | RVA (n = 23) | RVS (n = 23) |
|---|---|---|
| Age (y) | 72.8 ± 7.7 | 73.5 ± 8.1 |
| Male/female (n) | 9/14 | 9/14 |
| Hypertension (%) | 26.1 | 34.8 |
| Diabetes (%) | 21.7 | 26.1 |
| Dyslipidemia (%) | 17.4 | 13.0 |
| Heart rates (beats/min) | ||
| AAI | 66.3 ± 5.2 | 66.3 ± 8.0 |
| DDD | 66.3 ± 4.8 | 66.3 ± 8.0 |
| QRS duration (ms) | ||
| AAI | 92.7 ± 8.8 | 93.1 ± 15.6 |
| DDD | 161.6 ± 15.9 a,b | 141.1 ± 16.8 b |
| LVEF (%) | ||
| AAI | 69.0 ± 4.9 | 69.8 ± 4.1 |
| DDD | 64.5 ± 6.5 | 67.9 ± 5.1 |
| LVEDVI (mL/m 2 ) | ||
| AAI | 39.0 ± 6.8 | 38.1 ± 11.7 |
| DDD | 37.5 ± 8.0 | 36.9 ± 10.2 |
| E/e’ | ||
| AAI | 12.8 ± 4.8 | 13.0 ± 3.5 |
| DDD | 13.4 ± 3.0 | 13.1 ± 2.9 |
| Variables | RVA (n = 23) | RVS (n = 23) |
|---|---|---|
| Septal-to-lateral delay (ms) | ||
| AAI | 32.1 ± 28.3 | 30.4 ± 29.6 |
| DDD | 64.8 ± 42.2 a,c | 32.3 ± 28.6 |
| Ts-SD (ms) | ||
| AAI | 33.8 ± 9.8 | 34.9 ± 13.5 |
| DDD | 54.2 ± 27.8 b,c | 39.2 ± 20.3 |
| Radial dyssynchrony index (ms) | ||
| AAI | 32.4 ± 18.2 | 32.3 ± 15.3 |
| DDD | 84.9 ± 37.0 b,c | 45.3 ± 27.6 |
| SDt 18s (ms) | ||
| AAI | 57.4 ± 15.9 | 55.6 ± 13.9 |
| DDD | 83.1 ± 16.1 a,c | 56.0 ± 11.4 |
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