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Left bundle branch area pacing (LBBAP) can effectively enhance cardiac contraction by engaging the conduction system. LBBAP, compared with right ventricular apex pacing, can reduce QRS duration and enhance left ventricular function. Consequently, LBBAP has been proposed as a viable alternative to cardiac resynchronization therapy (CRT).

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Deep Septal Pacing for Pacemaker-Induced Cardiomyopathy.

Pacing Clin Electrophysiol

January 2025

Servei de Cardiologia, Hospital Universitari de Bellvitge, L'Hospitalet de Llobregat, Barcelona, España.

Introduction: Right ventricular (RV) pacing can impair left ventricular function and cause heart failure, known as pacing-induced cardiomyopathy (PICM). Upgrade to cardiac resynchronization (CRT) is its usual treatment; recently left bundle branch area pacing (LBBAP) has emerged as a potential alternative. Deep septal pacing (DSP), a simplified alternative to LBBAP, is still able to achieve narrower paced QRS than during conventional RV pacing.

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Children with indications of pacing often require epicardial pacemakers with generators implanted in the abdominal wall due to small body size or challenging anatomy because of congenital heart diseases. However, left ventricle (LV) systolic dyssynchrony induced by epicardial pacing may result in adverse remodeling and LV dysfunction. Recently, distal His bundle pacing (dHBP) has been shown to restore normal ventricular function in adult patients with pacemaker induced ventricular dysfunction.

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The deleterious effects of long term right ventricular pacing are increasingly being recognized today. Current clinical practice favors the implantation of dual-chamber permanent pacemaker which maintains atrioventricular synchrony and is associated with better quality of life. However, despite the popular belief and common sense surrounding the superiority of dual-chamber pacing over single chamber pacing, the same has never been conclusively verified in clinical trials.

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The sympathetic nervous system modulates cardiac contractile and electrophysiological function and contributes to adverse remodelling following myocardial infarction (MI). Axonal modulation therapy (AMT), directed at the sympathetic chain, blocks efferent sympathetic outflow to the heart and is a strategy to transiently and controllably mitigate chronic MI-associated sympatho-excitation. In porcine models, we evaluated scalable AMT, directed at the paravertebral chain, in blocking reflex-mediated pacing-induced sympatho-excitation post-MI.

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