Dixit, S., et al., Electrocardiographic patterns of superior right ventricular outflow tract tachycardias: distinguishing septal and free-wall sites of origin. J Cardiovasc Electrophysiol, 2003. 14(1): p. 1-7.
Figure 1. Schematic representation of the right ventricular out?ow tract (RVOT) in which the most superior (sites 1, 2, and 3) septal and free-wall sites
targeted in the study are identi?ed. Left: Location of sites 1 through 3 along the superior septal RVOT as seen in the right anterior oblique ?uoroscopic
projection. Right: RVOT viewed coronally from above the pulmonic valve (PV). Sites 1 (most posterior) through 3 (most anterior) along the septum
and free wall are shown. RV = right ventricle; TV = tricuspid valve.
Figure 2. Twelve-lead ECG pace maps from sites 1, 2, and 3 along the septum and free wall of the right ventricular out?ow tract (RVOT) showing characteristic features. Sites are labeled on the magnetic electroanatomic map in the center of the ?gure and over each pace map. The magnetic electroanatomic map of the RVOT is shown in a coronal projection and was acquired during sinus rhythm. The three-dimensional shape of the RVOT is evident from the magnetic electroanatomic map and the illustration at the bottom of the ?gure. All pace maps show a left bundle branch block morphology and inferior frontal plane axis. Differences in R waves in inferior leads II, III, and aVF between the free-wall and septal pace maps are seen (broader, shorter, and notched for the free-wall sites). The precordial transition pattern for the free-wall sites is late (R to S ratio ≥ 1 by precordial leads V4) compared with the septal locations. Changes in lead I when moving from more anterior and leftward (site 3, negative QRS) to the more posterior and rightward (site 1, positive QRS) are shown. PV = pulmonic valve.
Figure 3. Comparison of QRS amplitude and width in lead II during pace mapping from septal and free-wall sites. Left: Comparison of R wave amplitude in limb lead II between sites 1, 2, and 3 along the septum and free wall. Each line represents R wave amplitude (mV) at the same sites between the septum and the free wall for each patient. Mean R wave amplitudes for the different sites also are shown. At each site, mean R wave amplitude in the septum is signi?cantly greater than that in the free wall. Right: Comparison of R wave duration in limb lead II between sites 1, 2, and 3 along the septum and free wall. Each line represents R wave duration (msec) at the same site in the septum and free wall for each patient. Mean R wave durations for the different sites also are shown. At each site, mean R wave width of the free-wall pace maps is signi?cantly greater than that from the septal pace maps.
Figure 4. Change in QRS amplitude in lead I at sites 1 and 3. Note that for both the septum and free wall, there is a net change from positive forces
in posterior site 1 to negative forces in anterior site 3. This change in QRS amplitude was signi?cant (P ≤ 0.001).
Figure 5. Unique ECG morphologies that help to distinguish site of origin of the clinical arrhythmia in the superior right ventricular out?ow tract.
Left:ECG morphologies of spontaneous arrhythmias from septal sites 1, 2, and 3.
Right: ECG morphologies of spontaneous arrhythmias from free-wall sites 1 and 3.
All of the free-wall sites show notching in the inferior leads and late precordial transition ( ≥ V4). In comparison, all of the septal sites lack both notching of inferior leads and late precordial transition. For both the septal and free-wall locations of the clinical arrhythmias, lead I helps to distinguish anterior and leftward location (site 3, negative polarity) from posterior and rightward location (site 1, positive polarity). Site 2, which lies between sites 1 and 3, manifests multiphasic polarity in lead I (see text for discussion).
Conclusion
In this study, we demonstrated that 12-lead ECG features can be helpful to differentiate sites of origin of pace maps along the septum and free wall in the superior RVOT. Despite an overlap in the measurements, careful comparative ECG analysis for amplitude, width, and notching of the R wave in lead II, coupled with the precordial QRS transition, can reliably distinguish septal site pace maps from their counterpart locations in the free wall. In addition, together with the QRS morphology in lead I, these ECG features were useful in accurately localizing the site of origin of more than 90% of the clinical tachycardias originating from this region in our series. The utility of our proposed ECG criteria is in successfully localizing the likely site of origin of the clinical arrhythmia before ablation so that intracardiac catheter mapping can be targeted at a selected area in the complex three-dimensional anatomy of the RVOT region.
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