Background
The purpose of this study was to investigate the acute effect of right ventricular outflow tract (RVOT) pacing and right ventricular apex (RVA) pacing on synchronous ventricular activation and coronary flow dynamics.
Methods
We enrolled 20 consecutive patients who underwent electrophysiologic study. Echocardiographic study including two-dimensional tissue tracking imaging and Doppler guide wire examination was performed during RVOT pacing and RVA pacing.
Results
The improvement of left ventricular radial dyssynchrony (99 ± 12 ms vs. 142 ± 16 ms, P < .001), time-averaged peak velocities of coronary blood flow (54 ± 18 cm/s vs. 47 ± 17 cm/s, P = .007), and coronary microvascular resistance index (2.0 ± 0.8 vs. 2.4 ± 1.1, P = .028) was observed with RVOT pacing compared with RVA pacing.
Conclusion
RVOT pacing might provide favorable effects on the left ventricular function and coronary flow dynamics over RVA pacing.
Right ventricular outflow tract (RVOT) pacing has been reported to deteriorate left ventricular (LV) function less frequently in comparison with right ventricular apical (RVA) pacing. RVOT pacing shortens the wide QRS complex that occurs with RVA pacing and seems to provide a more physiologic ventricular activation. Several clinical studies demonstrated an acute hemodynamic improvement with RVOT pacing. Recent echocardiography investigations showed that RVOT pacing avoids the acute exacerbation in LV dyssynchrony and torsional behavior seen with RVA pacing. However, the effect of LV dyssynchrony induced with right ventricular pacing on coronary blood flow remains unclear.
A Doppler guide wire has been established as a useful modality to evaluate flow dynamics of coronary arteries. With the use of this method, coronary flow velocity and coronary flow reserve could be easily assessed without any flow disturbance in patients with normal coronary arteries. This study compared the acute effect on coronary flow dynamics between RVOT pacing and RVA pacing.
Materials and Methods
Study Population
We studied 20 consecutive patients who underwent electrophysiologic study because of arrhythmia, including 12 with sick sinus syndrome, 3 with complete atrioventricular block, 2 with paroxysmal supraventricular tachycardia, 2 with paroxysmal ventricular tachycardia, and 1 with paroxysmal atrial fibrillation. No patients had persistent atrial fibrillation, left or right bundle blanch block, significant valvular heart disease, congestive heart failure, LV ejection fraction < 50%, or coronary artery stenosis > 25% confirmed by coronary angiography. The institutional review board approved the study, and all patients provided informed consent before participation.
Right Ventricular Pacing
All antiarrhythmic drugs were withheld for periods of at least five times their half lives before the procedure. In addition to standard electrophysiologic catheters deployed in the right atrium and His bundle position, a steerable 6F quadripolar catheter was positioned transvenously via the femoral vein in the RVA and subsequently moved to the RVOT. The ventricular demand pacing was performed with a cardiac stimulator (Cardiac Stimulator SEC-4103; Nihon Kohden Corp, Tokyo, Japan) by use of a 2-ms rectangular impulse at twice the pacing threshold. The pacing rate was set at 100 beats/min.
Echocardiographic Examination
Transthoracic echocardiography was performed in the supine position using a commercially available system (EUB-8500, HITACHI Medical Corporation, Tokyo, Japan) at baseline, RVA pacing, and RVOT pacing. Images were recorded digitally with a 2 to 4-MHz wideband sector transducer and analyzed offline using commercially available software (E-Toolviewer, HITACHI Medical Corporation). Standard echocardiographic measurements were performed according to the recommendation of the American Society of Echocardiography. LV outflow tract velocity-time integral, LV stroke volume, E-wave deceleration time, and grade of mitral regurgitation were measured during right ventricular pacing. Septal-to-posterior wall motion delay was obtained with M-mode from the parasternal long-axis view. By using two-dimensional tissue tracking (2DTT), LV radial dyssynchrony was assessed in the LV short-axis papillary muscle level. A frame rate of 70 to 100 Hz was required for gray-scale imaging. We used 2DTT to track two points on the endocardium and epicardium, and estimated the change of the LV wall thickness [(maximum wall thickness – minimum wall thickness) × 100/minimum wall thickness] by calculating the radial strain between these two points. LV radial dyssynchrony was determined as the time from maximal wall thickening in septum to maximal wall thickening in the lateral wall ( Figure 1 ).
![](https://i0.wp.com/thoracickey.com/wp-content/uploads/2018/06/gr1-426.jpg?w=960)
Coronary Flow Study
Assessment of coronary flow dynamics was performed using a 0.014-inch, 12-MHz Doppler guide wire (FloWire, Volcano Therapeutics, Rancho Cordova, CA). The Doppler guide wire was advanced into the left anterior descending coronary artery through a 6F coronary angiography catheter. During the Doppler study, a 12-lead electrocardiogram (ECG) and coronary artery pressure at the tip of the guiding catheter were monitored continuously. Frequency analysis of the Doppler signal was carried out in real time by fast Fourier transform, using the Doppler velocimeter (FloMap, Volcano Therapeutics). Time-averaged peak velocity (APV) during one cardiac cycle was measured from the phasic coronary flow velocity recordings ( Figure 2 ). The measurements were averaged over five beats. Coronary flow velocity reserve was obtained by the ratio of intravenous adenosine-induced (0.14 mg/kg/min) maximal hyperemia to baseline resting APV. Microvascular resistance index was calculated from the mean coronary pressure at maximal hyperemia divided by the hyperemic APV.
![](https://i0.wp.com/thoracickey.com/wp-content/uploads/2018/06/gr2-311.jpg?w=960)
Statistical Analysis
Statistical analysis was performed with Stat View 5.0J (SAS Institute, Cary, NC). Categoric variables were presented as frequencies. Continuous variables were presented as the mean ± standard deviation and compared using paired t tests. A P value < .05 was considered statistically significant.
Results
Baseline Patient Characteristics
All patients completed the study protocol. Table 1 lists baseline patient characteristics. The mean age of the patients was 54 years. Two thirds of the patients were male; 20% had diabetes mellitus, 20% had hypercholesterolemia, and 25% had hypertension. In the echocardiographic findings at baseline, LV ejection fraction ranged from 54% to 79% and E-wave deceleration time was 187 ± 33 ms.
Age, y | 54 ± 18 |
Male, n (%) | 14 (70) |
Diabetes mellitus, n (%) | 4 (20) |
Hypercholesterolemia, n (%) | 4 (20) |
Hypertension, n (%) | 5 (25) |
Systolic blood pressure, mm Hg | 134 ± 20 |
Heart rate, beats/min | 53 ± 12 |
LVEDV, mL | 99 ± 10 |
LVESV, mL | 38 ± 8 |
LVEF, % | 63 ± 10 |
E wave deceleration time, ms | 187 ± 33 |
IVS thickness, mm | 9.9 ± 1.4 |
PW thickness, mm | 10.2 ± 1.5 |
Mitral regurgitation, grade | 0.9 ± 0.6 |
Right Ventricular Pacing Results
The paced QRS duration was significantly shorter with RVOT pacing compared with RVA pacing (124 ± 15 ms vs. 162 ± 15 ms, P < .001). There was no significant difference in the blood pressure between RVOT and RVA pacing (systole: 120 ± 26 mm Hg vs. 122 ± 24 mm Hg, P = .139; diastole: 81 ± 15 mm Hg vs. 83 ± 15 mm Hg, P = .352).
Echocardiographic Findings
Comparison of echocardiographic findings between RVA pacing and RVOT pacing is shown in Table 2 . LV outflow tract velocity-time integral (18 ± 4 cm vs. 15 ± 4 cm, P < . 001), LV stroke volume (43 ± 7 mL vs. 39 ± 7 mL, P < . 001), and E-wave deceleration time (166 ± 29 ms vs. 144 ± 30 ms, P = .006) were significantly greater with RVOT pacing compared with RVA pacing. The grade of mitral regurgitation was not different between RVOT pacing and RVA pacing. The septal-to-posterior wall motion delay was significantly shorter with RVOT pacing compared with RVA pacing (112 ± 18 ms vs. 135 ± 21 ms, P = .002). LV radial dyssynchrony assessed by 2DTT was also significantly shorter with RVOT pacing compared with RVA pacing (99 ± 12 ms vs. 142 ± 16 ms, P < . 001) ( Figure 3 ).
RVA pacing | RVOT pacing | P value | |
---|---|---|---|
VTI LVOT , cm | 15 ± 4 | 18 ± 4 | <.001 |
LV stroke volume, mL | 39 ± 7 | 43 ± 7 | <.001 |
E-wave deceleration time, ms | 144 ± 30 | 166 ± 29 | .006 |
Mitral regurgitation, grade | 1.1 ± 0.5 | 1.0 ± 0.6 | .163 |
SPWMD, ms | 135 ± 21 | 112 ± 18 | .002 |
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