Quantitative UHF‐ECG Assessment of Pacing‐Induced Ventricular Activation: Comparison of LBBAP and RV Septal Pacing

ABSTRACT Background Left bundle branch area pacing (LBBAP) is increasingly used to achieve more physiological ventricular activation in patients requiring permanent pacing. However, conventional ECG provides only indirect timing and morphology markers of paced activation and does not directly quantify overall ventricular activation synchrony. Ultra‐high‐frequency ECG (UHF‐ECG) enables quantitative assessment of ventricular activation timing and dyssynchrony beyond QRS duration alone. Methods We report a descriptive two‐patient comparison of pacing‐induced ventricular activation in bradycardia patients with intrinsically narrow baseline QRS complexes who underwent dual‐chamber pacemaker implantation with either LBBAP or right ventricular septal pacing (RVSP). Paired pre‐implant and early post‐implant UHF‐ECG recordings were analyzed using ventricular activation maps and quantitative dyssynchrony indices, including ventricular electrical delay (VED) and mean ventricular depolarization time/dispersion (MeanVD). Conventional ECG metrics were assessed in parallel, including paced QRS duration, R‐wave peak time (RWPT), V6‐V1 interpeak interval, and global RWPT. Because systematic transition testing during decremental output pacing and/or programmed stimulation was not available, formal gold‐standard confirmation of LBB capture was not claimed; instead, RWPT‐based parameters, LBB score, and global RWPT were treated as supportive ECG‐based markers of LBB‐area engagement. Results In the LBBAP case, QRS duration increased modestly from 73.4 to 87.6 ms, while VED18 remained unchanged at ‐3 ms and MeanVD18 decreased slightly from 25 to 24 ms, indicating preservation of low dyssynchrony. RWPT(V6) was 87.6 ms, RWPT(I) 56.0 ms, RWPT(aVL) 54.8 ms, V6‐V1 interpeak interval 34.4 ms, global RWPT 143.6 ms, and simplified LBB score 4. In the RVSP case, QRS duration increased from 93.0 to 135.8 ms, VED16 increased from 2 to 37 ms, and MeanVD16 increased from 30 to 58 ms, indicating substantially greater pacing‐induced dyssynchrony. Conclusion UHF‐ECG provides reproducible, case‐level quantification of pacing‐induced ventricular activation and may help distinguish preservation of near‐physiological synchrony after LBBAP from dyssynchronous activation during RVSP. These observations are descriptive and hypothesis‐generating and should be confirmed in larger comparative cohorts.