Narrowing the QRS, Expanding the Function: Left Bundle Branch Pacing in Dilated Cardiomyopathy.

IF 1.1 Q4 CARDIAC & CARDIOVASCULAR SYSTEMS
Journal of Cardiovascular Echography Pub Date : 2026-04-28 eCollection Date: 2026-01-01 DOI:10.4103/jcecho.jcecho_144_25
Fulvio Cacciapuoti, Ilaria Caso, Carlo Liguori, Salvatore Crispo, Antonio Torsi, Mario Volpicelli
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Abstract

Left bundle branch block (LBBB) is a key driver of electrical and mechanical dyssynchrony in heart failure with reduced ejection fraction (HFrEF). Conventional cardiac resynchronization therapy improves outcomes, yet up to one-third of patients is non-responders, partly due to nonphysiological ventricular activation. Left bundle branch pacing (LBBP) has emerged as a physiological alternative by directly recruiting the His-Purkinje system. We describe the case of a 62-year-old woman with nonischemic dilated cardiomyopathy, severely reduced left ventricular ejection fraction (30%), and complete LBBB (QRS 162 ms) who remained symptomatic despite maximally tolerated guideline-directed therapy. Multimodality imaging was central to decision-making: echocardiography demonstrated severe mechanical dyssynchrony and impaired strain, while cardiac magnetic resonance (CMR) excluded ischemic scar and revealed diffuse interstitial fibrosis, supporting the indication for physiological pacing. LBBP was successfully achieved, resulting in QRS narrowing to 118 ms and stable electrical parameters. At a 6-month follow-up, the patient showed marked symptomatic improvement (New York Heart Association I-II) and significant reverse remodeling, with left ventricular ejection fraction rising to 54%, global longitudinal strain improving from -8.2% to -18.8%, reduced mechanical dispersion, and regression of functional mitral regurgitation. This case highlights the value of advanced imaging for candidate selection and for quantifying structural and functional recovery. Emerging translational data suggest that LBBP may also favorably influence molecular remodeling, including connexin-mediated gap-junction coupling. LBBP represents a promising strategy for physiological resynchronization in HFrEF with LBBB and warrants further prospective evaluation.

扩张型心肌病左束支起搏的QRS变窄,功能扩展。
左束支传导阻滞(LBBB)是心力衰竭伴射血分数降低(HFrEF)的电和机械非同步化的关键驱动因素。传统的心脏再同步化治疗改善了结果,但多达三分之一的患者无反应,部分原因是非生理性心室激活。左束支起搏(LBBP)已成为一种直接招募His-Purkinje系统的生理替代方案。我们描述了一名62岁的非缺血性扩张型心肌病女性患者,左心室射血分数严重降低(30%),完全LBBB (QRS 162 ms),尽管在指南指导下进行了最大限度的耐受治疗,但仍有症状。多模态成像是决策的核心:超声心动图显示严重的机械不同步和受损的应变,而心脏磁共振(CMR)排除缺血性瘢痕并显示弥漫性间质纤维化,支持生理性起搏的指征。LBBP成功实现,QRS收窄至118 ms,电参数稳定。在6个月的随访中,患者表现出明显的症状改善(纽约心脏协会I-II)和明显的反向重构,左心室射血分数上升至54%,整体纵向应变从-8.2%改善至-18.8%,机械离散度降低,二尖瓣功能性返流消退。这个病例强调了先进的成像技术在选择候选人和量化结构和功能恢复方面的价值。新出现的翻译数据表明,LBBP也可能有利地影响分子重塑,包括连接蛋白介导的缝隙连接偶联。LBBP是HFrEF与LBBB生理再同步的一种有希望的策略,值得进一步的前瞻性评估。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Journal of Cardiovascular Echography
Journal of Cardiovascular Echography CARDIAC & CARDIOVASCULAR SYSTEMS-
CiteScore
1.40
自引率
12.50%
发文量
27
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