Electrophysiological demonstration of nonselective His-Purkinje system capture with para-Hisian pacing

Permanent ventricular pacing has played a key role in the evolution of patients with bradyarrhythmias, and survival in this population has substantially improved. However, the adverse effects of conventional pacing have impaired the quality of life of those patients [[1], [2], [3], [4], [5], [6]]. Right ventricular (RV) apical pacing leads to loss of physiological activation of the muscle mass, dyssynchronous contraction, and ventricular remodeling similar to complete left bundle branch block (LBBB) [1,2,[7], [8], [9]]. These issues prompted the investigation of more physiological pacing sites.

Conduction disturbances such as LBBB lead to dyssynchronous ventricle activation due to late activation of the left ventricular (LV) lateral wall, which causes a disagreement between the pre-ejection periods in both ventricles, with the LV being the most delayed [10,11]. Nonphysiological apical RV pacing worsens this condition by increasing the contractile deficit and decreasing ventricular function indexes. Conduction system pacing has been proposed as an alternative, which consists of placing a lead precisely on the His bundle to generate a normal QRS complex with the same duration and spatial polarity of the native QRS [[12], [13], [14]]. However, selective His bundle pacing (SHBP) might not be the only way to activate the conduction system [15].

In patients with para-Hisian preexcitation syndrome, ventricular contraction results from an abnormal pattern of electrical activation, characterized by a slurring of the initial segment of the QRS complex on surface electrocardiogram (ECG) known as a delta wave. The final segment of the QRS complex, on the other hand, is narrow and has the same polarity of the normalized QRS. Because the conduction system is activated immediately after abnormal activation from the bundle of Kent, the final segment of the QRS complex is generated by ventricular activation through the intrinsic physiological conduction system. Consequently, the interval between the end of the intrinsicoid deflection, or peak R wave, and the final segment of the QRS complex (Rmax-QRSend) during preexcitation and after ablation of the bundle of Kent is the same, or during orthodromic tachycardia without antegrade conduction through the bundle of Kent.

In SHBP, the polarity and duration of the QRS complex and the Rmax-QRSend interval at baseline and after pacing are exactly the same. Based on the abnormal pattern of electrical activation in preexcitation syndrome, we raised the hypothesis that pacing from any site where an Rmax-QRSend interval similar to that of sinus beat is generated indicates that the His-Purkinje system was successfully captured, whereas pacing sites far away from the His-Purkinje system should generate a longer Rmax-QRSend interval with a very different morphology from that of the native beat.

Therefore, the objective of this study was to demonstrate that His-Purkinje system capture with para-Hisian pacing, which is a variant of nonselective His bundle pacing (NSHBP) [15], has the same effect as SHBP by comparing the post-pacing Rmax-QRSend interval, related to the final segment of the QRS complex.

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