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 ).

Assessment of LV radial dyssynchrony by 2DTT echocardiography during RVA (A) and RVOT (B) pacing. LV radial dyssynchrony, which was determined as the time from maximal wall thickening in the septum to maximal wall thickening in the lateral wall, was 141 ms with RVA pacing and 98 ms with RVOT pacing. RVA, Right ventricular apex; RVOT, right ventricular outflow tract; LV, left ventricular; ECG, electrocardiogram.

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.

Measurements of coronary flow velocity by using Doppler guide wire during RVA (A) and RVOT (B) pacing. APV with RVA and RVOT pacing was 43 cm/s and 51 cm/s, respectively. Doppler guide wire ( arrow ). RV pacing catheter. RVA, Right ventricular apex; RVOT, right ventricular outflow tract; APV, averaged peak velocity.

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.