Cardiac Stimulation Unit, Hospital São Lucas, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Rio Grande do Sul, Brazil.
Department of Electrophysiology, Hospital São Lucas, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Rio Grande do Sul, Brazil.
Braz J Cardiovasc Surg. 2023 Apr 23;38(2):278-288. doi: 10.21470/1678-9741-2021-0629.
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.
协调和和谐（同步）的心室电活动对于改善左心室收缩功能至关重要。室内传导异常，如人工心脏起搏引起的左束支传导阻滞，导致机电“不同步”，产生有害的结构和临床后果。本综述旨在描述和加深对由心脏起搏引起的人工诱导性心室不同步发展的所有连接机制的理解，这些机制通常被称为起搏诱导性心肌病（PiCM）。异常冲动传导和人工心脏起搏的非生理性异位激活的慢性作用被怀疑会影响代谢和心肌灌注，导致激活/收缩过程中的区域差异，从而由于心脏组织的损伤、炎症和纤维化导致电和结构重塑。人工心脏起搏对心室功能和结构的影响可能是多因素的，PiCM 的生物学因素可能会影响发病的时间和概率。PiCM 尚未包含在传统的心肌病分类中，这可能会阻碍其检测。本文综述了目前关于起搏诱导性心血管疾病的证据，以及对其病理生理学的现有理解，并强调了右心室起搏的不良影响，尤其是右心室起搏负担（通常以百分比衡量）及其对心室收缩的影响（反映在对左心室收缩功能的影响上）。这些影响可能是 PiCM 病理生理学和对患者临床影响的主要定义标准和决定机制。
