Clinical implications of a unique delta wave pattern in patients with left-sided Wolff–Parkinson–White

Catheter ablation of accessory pathways (AP) is a recommended treatment for patients with ventricular pre-excitation.1,2 Multicentre trials have demonstrated overall acute success rates of ∼95% with low complication rates.3–6 Multiple algorithms have been developed to identify AP location by pre-excitation pattern on electrocardiogram (ECG), with left-sided AP being the most common (∼40–60%) and most accurately identified by algorithm,7–10 with some left-sided AP requiring advanced diagnostics.11,12 While more recent algorithms have focused on precordial leads for localization,10 negative delta waves in lead II have traditionally been associated with subepicardial AP requiring ablation within the coronary sinus (CS).7 In evaluation of our contemporary institutional experience with left-sided manifest AP, we identified a unique pre-excitation morphology with prominent negative delta waves both in the inferior leads, as well as the left lateral precordial leads. The pathways were difficult to ablate and more distal along the CS body than suggested by the original Arruda algorithm.7 To highlight the challenges posed by these unique pathways, we compared them to our experience with other manifest left-sided AP, noting differences in procedural variables and outcomes. We conducted a retrospective analysis of all patients undergoing radio-frequency (RF) catheter ablation of left-sided manifest AP at Boston Children’s Hospital from 2013 to 2018, approved by our institutional review committee. Three index patients had the unique delta wave pattern along the left posterior to left lateral (LL) atrioventricular groove. Control patients included any manifest AP documented as ‘left lateral’, ‘left posterolateral (LPL)’, or ‘left posterior (LP).’ Patients with multiple AP, significant congenital heart disease (CHD), hypertrophic cardiomyopathy, and previous ablation and/or having undergone cryoablation were excluded from analysis. Five patients with minor CHD were included (two muscular VSD, two bicuspid aortic valve, and one dysplastic mitral valve). All patients underwent electrophysiology study with a three-dimensional electroanatomic mapping system (CARTO 3 System, Biosense Webster, Irvine, CA, USA) and fluoroscopy used intermittently per operator discretion. Accessory pathway mapping was performed during sinus rhythm, steady rate ventricular pacing, and/or supraventricular tachycardia. Accessory pathway was classified by anatomic location as LL, LPL, and LP. Coronary sinus angiography was performed per operator discretion. Left atrial access was obtained using trans-septal approach via the inferior vena cava. Non-irrigated RF ablation with a 4 mm tip electrode (temperature-controlled, target temperature of 70°C, and generator output up to 50 W) was used in most cases, and irrigated RF ablation with a 3.5 mm tip electrode (power-controlled, target power of 30 W) was used in a minority of cases. Test lesions were defined as limited RF applications (<10 s) at unsuccessful locations. Consolidation lesions were defined as applications after successful elimination of AP conduction. Acute success was defined as absence of latent pre-excitation during administration of adenosine in sinus rhythm 30 min after successful ablation lesion. Recurrence was defined as either post-procedural documented supraventricular tachycardia (SVT) or documented ventricular pre-excitation on 12-lead ECG. Coronary sinus angiography in LAO projection of patient with the unique delta wave morphology. Area of narrowing in the coronary sinus (arrow) corresponds to the area of successful ablation (inlay). Pre- and post-ablation electrocardiograms of unique pre-excitation pattern (left side) and conventional left-sided pre-excitation pattern (right side). Of the 104 total patients identified, 3 patients had left-sided AP ablations and abnormal ECG patterns characterized by deep Q waves in the inferior and lateral precordial leads, and 101 had left-sided AP ablations performed and 12-lead ECG without the unique delta wave morphology (79 LL, 12 LP, and 10 LPL). Baseline demographics of both groups are demonstrated in Table 1. Age, weight, and pathway characteristics at the time of electrophysiology study were similar between groups. Baseline demographic information and accessory pathway characteristics, comparing patients with a unique delta wave pattern vs. those without APERP, accessory pathway effective refractory period; SPPCL, shortest paced pre-excited cycle length. P < 0.05. Baseline demographic information and accessory pathway characteristics, comparing patients with a unique delta wave pattern vs. those without APERP, accessory pathway effective refractory period; SPPCL, shortest paced pre-excited cycle length. P < 0.05. Regarding ablation strategy, RF energy is needed to be applied for a longer time during the successful lesion before loss of pre-excitation in the index patients compared to controls (7 vs. 2.9 s, P = 0.004). Total number of RF lesions was higher in the index group, with a median of 14 lesions (range: 13–27) vs. 6 lesions (1–35) in controls (P = 0.02). When breaking down into test and consolidation lesions, there were no statistical differences between groups; however, a number of test lesions trended towards significance with more test lesions done in the index patients (12 vs. 2 lesions, P = 0.08). Total RF time was higher in the index group (550 vs. 240 s, P = 0.02), as was total case time (median total case time of 3.3 h vs. 2.1 h in the control group; P = 0.008). With a median follow-up of 1.2 years (0.2–2.5 years) in the index group and 0.4 years (0.1–1.2 years) in the controls, recurrence of the AP was observed in 1 out of the 3 index patients compared to 2 out of the 101 control patients (P = 0.09). Notably, CS abnormalities were observed in all three patients with the unique delta wave morphology (Figure 1). Selective CS angiography was performed in all three due to difficulty with catheter placement at the outset of the case prior to ablation. In each of these, there was a notable narrowing of the CS proper, right at the subsequent site of successful ablation. Coronary skin architecture was not systematically analysed in controls for comparison. In summary, evaluation of our contemporary institutional experience with manifest left-sided AP has unearthed a subset of abnormal AP within the CS body identifiable by pre-procedural ECG, comparable to pathways located within the proximal CS or CS diverticulum.7,10,13–15 These pathways are notoriously difficult to ablate and often have high recurrence rates.15 Given that these pathways run over a layer of myocardium that coats the CS, it can be difficult to deliver adequate energy to the desired location. Nonetheless, it is important to note that these unique pathways can be successfully ablated from an endocardial approach and correlate with discrete anatomical narrowing of the CS body. However, they do require a longer application of RF energy to achieve success, giving time for the ablation lesion to penetrate into the CS musculature. While our investigation has several limitations (retrospective design, proceduralist practice variation, and small sample size), the differences between the abnormal AP and other similar left-sided AP are stark. We feel this study provides enough of a contrast between these two groups that an encounter pre-operatively with an ECG with the described abnormal pattern should ready the operator for: A potentially longer and more arduous case. Utilization of CS angiography at case outset. Longer endocardial test lesions to allow the RF to penetrate the CS myocardium. None declared The data underlying this article will be shared on reasonable request to the corresponding author.