Pattern Breaks on the Surface ECG: Can We Anticipate a Long Day Ahead?

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In 1988, Miller et al.1 reported their experience with the correlation between 12‐lead electrocardiograms (ECG) and endocardial sites of ventricular tachycardia (VT) origin in patients with coronary artery disease. In this series of 182 VTs in 108 patients, they noted numerous precordial transition patterns, one of which was a “regression/growth” pattern, with loss of R waves in the mid‐precordial leads and then “regrowth” in the left precordial leads during right bundle branch block morphology VT. Limited additional clinical research has been published on precordial ECG pattern breaks in structural heart disease over the past 29 years. In the idiopathic VT literature, abrupt changes have been described in the LV summit but also on the opposite surface of the heart in the cardiac crux.2 Therefore, it appears that PVCs/VT arising from the basal aspect of the interventricular sulcus are prone to these pattern breaks whether anterior or posterior (Fig. 1).
In the current issue, Hiyashi et al.7 report their retrospective experience with outflow premature ventricular contractions (PVC)/VT demonstrating a pattern break in standard ECG lead V2. Loss of R wave amplitude in V2 relative to V1 and V3 correlated with an origin in close proximity to the left anterior descending artery (LAD) in 12 out of 130 patients in their experience with left bundle branch (LBBB) morphology PVCs. These PVCs demonstrated earliest sites of activation in four related anatomic regions, all with close proximity to the anterior interventricular sulcus: anteroseptal right ventricular outflow tract (RVOT), left coronary cusp (LCC), coronary venous system (anterior interventricular vein), and epicardium. The overall ablation success rate was lower than outflow sites of origin not associated with this ECG pattern (58% vs. 89%, P = 0.0125). Proximity to the left anterior descending (LAD) artery was a major limitation to success in these cases.
The authors, in describing their experience and findings, provide a number of valuable insights:
Idiopathic ventricular arrhythmias originating from the outflow tracts are generally considered “straightforward” from a mapping and ablation standpoint. Ablation success rates overall are high, often reported as greater than 80–90% in retrospective studies. A prospective randomized study by Ling et al.8 showed a 1‐year success rate of 80% in the ablation arm versus 12% in the antiarrhythmic arm. Due to this high reported success rate, these cases are not typically thought to require referral to an experienced VT ablation center. However, the majority of reported studies come from high volume institutions. Therefore, the real world success rate in less experienced centers is likely lower. In addition, a common misconception of idiopathic outflow PVCs/VT is that the origin is almost always from the RVOT. Yet, non‐RVOT origin arrhythmias are common, and due to the complex three‐dimensional anatomy of the outflow tracts and LV summit and the thin walled nature of the outflow tracts, relatively early signals may be seen in the RVOT, even when the actual site of origin is more distant. This fact can lead operators to spend unnecessary time mapping, and even delivering, radiofrequency lesions in the RVOT, which can be risky and result in collateral damage.9
Numerous reports have been published by the current group and others regarding ECG localization of PVCs, which may help avoid the aforementioned problem of assuming all outflow PVCs/VT originate from the RVOT. Some studies are beneficial for procedural planning—differentiating RVOT from CC helps with access planning, for example. However, while differentiation of left versus right‐sided origin is important, understanding when you are dealing with a complex substrate/region, associated with lower success rates, may be of incremental importance.
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