Cardiomyopathy Induced by Artificial Cardiac Pacing: To Whom, When, Why, and How? Insights on Heart Failure Development

ABSTRACT Coordinated and harmonic (synchronous) ventricular electrical activation is essential for better left ventricular systolic function. Intraventricular conduction abnormalities, such as left bundle branch block due to artificial cardiac pacing, lead to electromechanical “dyssynchronopathy” with deleterious structural and clinical consequences. The aim of this review was to describe and improve the understanding of all the processes connecting the several mechanisms involved in the development of artificially induced ventricular dyssynchrony by cardiac pacing, most known as pacing-induced cardiomyopathy (PiCM). The chronic effect of abnormal impulse conduction and nonphysiological ectopic activation by artificial cardiac pacing is suspected to affect metabolism and myocardial perfusion, triggering regional differences in the activation/contraction processes that cause electrical and structural remodeling due to damage, inflammation, and fibrosis of the cardiac tissue. The effect of artificial cardiac pacing on ventricular function and structure can be multifactorial, and biological factors underlying PiCM could affect the time and probability of developing the condition. PiCM has not been included in the traditional classification of cardiomyopathies, which can hinder detection. This article reviews the available evidence for pacing-induced cardiovascular disease, the current understanding of its pathophysiology, and reinforces the adverse effects of right ventricular pacing, especially right ventricular pacing burden (commonly measured in percentage) and its repercussion on ventricular contraction (reflected by the impact on left ventricular systolic function). These effects might be the main defining criteria and determining mechanisms of the pathophysiology and the clinical repercussion seen on patients.

【摘要】协调同步的心室电激活（synchronous ventricular electrical activation）对维持良好的左心室收缩功能至关重要。心室内传导异常（intraventricular conduction abnormalities）——如人工心脏起搏（artificial cardiac pacing）引发的左束支传导阻滞（left bundle branch block）——可导致机电‘失同步症（electromechanical dyssynchronopathy）’，并带来有害的结构与临床后果。本综述旨在阐述并深化对人工心脏起搏诱导的心室失同步（即学界公认的起搏诱导型心肌病（pacing-induced cardiomyopathy, PiCM））发生过程中所有相关机制的理解。人工心脏起搏引发的异常冲动传导与非生理性异位激活的慢性效应，可能影响心肌代谢与心肌灌注，触发激活-收缩过程的区域差异，进而通过心肌组织损伤、炎症与纤维化引发电重构与结构重构。人工心脏起搏对心室功能与结构的影响是多因素的，而PiCM的潜在生物学机制可能会影响该病的发生时间与患病概率。传统心肌病分类体系未纳入PiCM，这可能会阻碍该病的早期检出。本文综述了起搏诱导型心血管疾病的现有研究证据，阐述了当前对其病理生理学的认知，并强调了右心室起搏（right ventricular pacing）的不良影响——尤其是右心室起搏负荷（right ventricular pacing burden，通常以百分比量化）及其对心室收缩的影响（体现在对左心室收缩功能的影响上）。上述效应或为该病病理生理学与患者临床结局的核心判定标准与决定性机制。