Mechanisms of stretch-induced electro-anatomical remodeling and atrial arrhythmogenesis

被引:1
|
作者
Medvedev, Roman Y. [1 ]
Afolabi, Saheed O. [1 ,2 ]
Turner, Daniel G. P. [1 ]
Glukhov, Alexey V. [1 ,3 ]
机构
[1] Univ Wisconsin, Sch Med & Publ Hlth, Dept Med, Madison, WI USA
[2] Univ Ilorin, Dept Pharmacol & Therapeut, Ilorin, Nigeria
[3] 8455 WIMR 2,1111 Highland Ave, Madison, WI 53705 USA
基金
美国国家卫生研究院;
关键词
Atrial fibrillation; Hypertension; Stretch; Atria; Cardiomyocyte; Fibrosis; Electro-anatomical remodeling; Calcium; CONTRACTION-EXCITATION FEEDBACK; ATTENUATES CARDIAC-HYPERTROPHY; HEART RHYTHM ASSOCIATION; OBSTRUCTIVE SLEEP-APNEA; RETICULUM CA2+ LEAK; CURRENT I-F; PULMONARY VEIN; VENTRICULAR MYOCYTES; ANGIOTENSIN-II; NITRIC-OXIDE;
D O I
10.1016/j.yjmcc.2024.05.011
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Atrial fibrillation (AF) is the most common cardiac rhythm disorder, often occurring in the setting of atrial distension and elevated myocardialstretch. While various mechano-electrochemical signal transduction pathways have been linked to AF development and progression, the underlying molecular mechanisms remain poorly understood, hampering AF therapies. In this review, we describe different aspects of stretch-induced electroanatomical remodeling as seen in animal models and in patients with AF. Specifically, we focus on cellular and molecular mechanisms that are responsible for mechano-electrochemical signal transduction and the development of ectopic beats triggering AF from pulmonary veins, the most common source of paroxysmal AF. Furthermore, we describe structural changes caused by stretch occurring before and shortly after the onset of AF as well as during AF progression, contributing to longstanding forms of AF. We also propose mechanical stretch as a new dimension to the concept "AF begets AF", in addition to underlying diseases. Finally, we discuss the mechanisms of these electro-anatomical alterations in a search for potential therapeutic strategies and the development of novel antiarrhythmic drugs targeted at the components of mechano-electrochemical signal transduction not only in cardiac myocytes, but also in cardiac non-myocyte cells.
引用
收藏
页码:11 / 24
页数:14
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