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Electroanatomic Remodeling of the Left Atrium in Paroxysmal and Persistent Atrial Fibrillation Patients Without Structural Heart Disease

医学 心脏病学 内科学 心房颤动 冠状窦 室上性心律失常 心脏病 肺静脉 心脏传导系统 窦性心律 中庭(建筑) 心电图
作者
A. Teh,Peter M. Kistler,Geoffrey Lee,Caroline Medi,Patrick M. Heck,Steven J. Spence,Paul Sparks,Joseph B. Morton,Jonathan M. Kalman
出处
期刊:Journal of Cardiovascular Electrophysiology [Wiley]
卷期号:23 (3): 232-238 被引量:164
标识
DOI:10.1111/j.1540-8167.2011.02178.x
摘要

Atrial Remodeling in Atrial Fibrillation. Introduction: The nature of the atrial substrate thought to contribute toward maintaining atrial fibrillation (AF) outside the pulmonary veins remains poorly defined. Therefore, our objective was to determine whether patients with paroxysmal and persistent AF have an abnormal electroanatomic substrate within the left atrium (LA). Methods and Results: Thirty‐one patients with AF (17 paroxysmal AF and 14 persistent AF) were compared with 15 age‐matched controls with left‐sided supraventricular tachycardia (SVT). High‐density 3‐dimensional electroanatomic maps were created and the LA was divided into 8 segments for regional analysis. Bipolar voltage, conduction, and effective refractory periods (ERPs) of the posterior LA, left atrial appendage (LAA), and distal coronary sinus (CSd) and percentage complex signals were assessed. In the majority of LA regions, compared with controls, AF patients had: (1) lower mean voltage and a higher percentage low voltage; (2) slower conduction; and (3) more prevalent complex signals. Many of these changes were more marked in the persistent than the paroxysmal AF group. Conclusions: Patients with AF have lower regional voltage, increased proportion of low voltage, slowed conduction, and increased proportion of complex signals compared to controls. Many of these changes are more pronounced in persistent AF patients, suggesting there may be a progressive nature to the changes. Differences occurred in the absence of structural heart disease. These substrate abnormalities provide further insight into the progressive nature of atrial remodeling and the mechanisms involved in maintenance of AF. (J Cardiovasc Electrophysiol, Vol. 23 p. 232‐238, March 2012.)

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