心房颤动与自主神经的相关性研究进展

心房颤动(房颤)是最常见的心律失常,其发病机制复杂,尚未完全研究清楚。大量研究表明,自主神经系统在房颤的发生、维持中发挥了重要作用,交感神经与副交感神经活动都是其最常见的触发机制。通过对自主神经功能的调节可以有效控制房颤。本文就自主神经张力异常、自主神经重构与房颤的关系及相关神经治疗做一综述,为房颤的临床治疗提供最新的理论基础。     

心脏自主神经活动在阵发性心房颤动发生和维持中的作用

心脏自主神经尤其是心迷走神经的功能活动与阵发性心房颤动（房颤）的发生和维持关系密切。据一些临床实验观察表明阵发性房颤与副交感神经的紧张性升高有关。Bettoni等对连续非选择的77例阵发性房颤患者的动态心电图检查结果进行分析发现：阵发性房颤的发作与自主神经紧张性的变化直接相关，首先是肾上腺素能神经紧张性升高，但很快转为以迷走神经紧张性升高为主；并且心率离散度的变化在有器质性与无器质性心脏病患者中差异无统计学意义。本文就阵发性房颤的发生和维持与心脏自主神经功能活动的关系作一综述。     

心房颤动的自主神经重构和电重构

实验发现快速起搏造成的犬心房颤动(简称房颤)模型存在心房不均一的神经萌出和去甲肾上腺素(NA)积聚[1],"自主神经重构"的概念由此而生.笔者对房颤的自主神经重构及其与房颤的发生和电重构的关系做一概述.     

自主神经重构与心房颤动关系研究的进展

心房颤动是临床最常见的快速性心律失常之一,大量研究发现,房颤的发生和维持与电重构,结构重构有关,近年来研究发现自主神经系统在房颤发生发展中具有重要作用,并提出自主神经重构是其可能机制。     

饮酒与心房颤动相关性的研究进展

随着人口老龄化和生活方式的改变,心房颤动(房颤)的发生率居高不下。近年来研究发现,饮酒是房颤的重要危险因素,饮酒可导致心房解剖重构和电重构,影响自主神经及房颤的其他危险因素,从而导致房颤的发生。此外,饮酒还影响房颤预后,增加了房颤发生不良事件的风险。本文将从饮酒与房颤发生的关系和相关机制以及饮酒对房颤预后的影响展开综述。     

糖尿病对心房颤动的作用

糖尿病是心房颤动(房颤)发生的主要危险因素之一。在糖尿病状态下,自主神经重构、电重构、电机械重构、结构重构是引起房颤的主要病理生理机制。该文阐述糖尿病与房颤的密切联系,讨论其主要的病理生理机制,并针对糖尿病引起的心房重构提出可能的上游治疗靶点。     

甲状腺机能亢进与心房颤动

心房颤动(简称房颤)是甲状腺机能亢进(简称甲亢)患者常见心律失常之一。血清甲状腺素水平长期升高使心房电生理特性、结构特性和自主神经分布发生改变,即出现电重构、结构重构和自主神经重构,这些可能是甲亢引起房颤发生并持续的主要原因。     

甲状腺机能亢进与心房颤动

心房颤动（简称房颤）是甲状腺机能亢进（简称甲亢）患者常见心律失常之一。血清甲状腺素水平长期升高使心房电生理特性、结构特性和自主神经分布发生改变，即出现电重构、结构重构和自主神经重构，这些可能是甲亢引起房颤发生并持续的主要原因。     

心脏自主神经作用于心房颤动的研究进展

心房颤动（房颤）是临床上最常见的心律失常之一。心脏自主神经在房颤的发生和维持中扮演了十分重要的角色。心脏内在和外在自主神经都对心脏节律和功能的调节具有重要意义,异常的自主神经激活可以导致房颤的发生。因此,在房颤研究中,自主神经调控已成为治疗房颤的研究热点。目前,较常用的心脏自主神经调控方法主要包括：去交感神经化,刺激迷走神经、消融心脏神经节从等。本文主要就心脏自主神经影响房颤的作用机制及心脏自主神经调控方法加以综述。     

炎症反应与心房颤动的研究进展

心房颤动（房颤）是临床上最常见的心律失常,常与心血管系统不良事件相关。房颤的核心机制是心房重构,包括电重构、结构重构和自主神经重构。炎症是机体应对损伤的一种修复反应,过度的炎症反应常导致各种疾病的发生。随着对房颤的深入研究,炎症反应在房颤发生、发展过程中的作用被广泛关注。炎症标志物可预测或诱发房颤,反之,房颤本身也可促进炎症反应的进一步发展。研究炎症反应标志物和开发新的抗炎药物将为房颤的诊治提供新的思路。     

Heart rate variability and early recurrence of atrial fibrillation after electrical cardioversion

OBJECTIVES: The study evaluated the role of the autonomic nervous system in atrial fibrillation (AF) recurrence. BACKGROUND: Early recurrence of AF after cardioversion (CV) is attributed to electrical remodeling. The possibility that an abnormal autonomic modulation might contribute to this phenomenon has not yet been adequately tested. METHODS: We analyzed short-term heart rate variability (HRV) in 93 patients with persistent AF and on chronic amiodarone treatment, after restoration of sinus rhythm by electrical CV. RESULTS: Two weeks later, 25 patients presented with AF. Spectral analysis of HRV revealed that patients wi     

心房颤动去神经治疗的临床效应

构成心脏自主神经系统的交感神经与迷走（副交感）神经在房颤（AF）的发生与维持中起着重要的作用,由此以心房神经丛（GP）消融为主的去神经治疗亦成为AF单独或辅助的介入疗法之一。然而GP消融带来的神经与心房重构现象也日益受到关注。     

Is the Atrial Neural Plexis a Therapeutic Target in Atrial Fibrillation?

Circumferential pulmonary vein isolation is the mainstay of atrial fibrillation (AF) ablation, but alternative approaches and techniques have been developed to improve the outcomes. One of these additional ablation targets are ganglionated plexi of the intrinsic cardiac autonomic system that contain a variety of sympathetic and parasympathetic neurons that communicate with the extrinsic cardiac autonomic nervous system. The ganglionated plexi of the heart do not serve as a simple relay station but could modulate the autonomic interaction between the extrinsic and intrinsic cardiac autonomic system. Intrinsic cardiac autonomic nerve activity is an invariable trigger of paroxysmal atrial tachyarrhythmia, including atrial fibrillation. Although multiple studies have shown that ganglionated plexi play an important role in initiating atrial fibrillation, there is no consensus on a standardized protocol for selecting target sites and determining how ganglionated plexi ablation can best be accomplished. Recent clinical trials have demonstrated the feasibility and efficacy of ganglionated plexi ablation in addition to pulmonary vein isolation, but novel technologies and strategies are necessary to improve the current ablation techniques in managing patients with atrial fibrillation. This review focuses on the relationship between atrial ganglionated plexi and atrial fibrillation and the potential benefits and limitations of ganglionated plexi ablation in the management of atrial fibrillation.     

Magnetism and cardiac arrhythmias

Low-level electromagnetic fields (EMFs) have been used to treat various neurologic disorders. In the present study, we applied micro Gauss (microG) levels of EMFs either to the vagosympathetic nerve trunks, dissected in the neck, or across the chest in anesthetized dogs. Based on theoretical and empiric grounds, we compared EMFs (2.87 microG at 0.043 Hz) delivered to the vagosympathetic trunks in an experimental set (n = 5) with a sham control group (n = 6). Over a period of 2 to 3 hours, heart rate decreased after an initial 5-minute EMF exposure. The maximal heart rate changes in the experimental versus control groups was 29% versus 12% (P = 0.03). The voltage applied to the autonomic nerves required to induce atrioventricular (AV) conduction block decreased by 60% in the experimental group versus a 5% increase in the control group (P = 0.005). This effect also lasted 2 to 3 hours. Another EMF setting (amplitude 0.34 microG, frequency 2 kHz) applied for 5 minutes to the vagosympathetic trunks was associated with a significant increase in the occurrence of atrial premature depolarizations (APDs), atrial tachycardia (AT), and atrial fibrillation (AF) in response to autonomic nerve stimulation compared with control states before EMF exposure. No atrial arrhythmias could be induced after propranolol and atropine, even at the highest voltage used to stimulate the autonomic nervous input to the heart (n = 11). Only 2 dogs showed no response to this EMF application. In 3 dogs in whom atrial pacing (cycle length = 250 ms) and autonomic nerve stimulation induced AF, an EMF (2.87 microG at 0.043 Hz) delivered for 35 minutes across the chest suppressed AF for up to 3 to 4 hours, after which the same protocol again induced AF. We conclude that in these preliminary experiments, specific low-level EMFs alter heart rate, AV conduction, and heart rhythm. These effects were mediated through the autonomic nervous system inputs to the heart based on adjunctive effect of autonomic nerve stimulation and the inhibitory action of autonomic blockers.     

Interrelationships between the autonomic nervous system and atrial fibrillation

Mechanisms responsible for atrial fibrillation are not completely understood but the autonomic nervous system is a potentially potent modulator of the initiation, maintenance, termination and ventricular rate determination of atrial fibrillation. Complex interactions exist between the parasympathetic and sympathetic nervous systems on the central, ganglionic, peripheral, tissue, cellular and subcellular levels that could be responsible for alterations in conduction and refractoriness properties of the heart as well as the presence and type of triggered activity, all of which could contribute to atrial fibrillation. These dynamic inter-relationships may also be altered dependent upon other neurohumoral modulators and cardiac mechanical effects from ventricular dysfunction and congestive heart failure. The clinical implications regarding the effects of the autonomic nervous system in atrial fibrillation are widespread. The effects of modulating ganglionic input into the atria may alter the presence or absence of atrial fibrillation as has been highlighted from ablation investigations. This article reviews what is known regarding the inter-relationships between the autonomic nervous system and atrial fibrillation and provides state of the art information at all levels of autonomic interactions.     

自主神经系统在心房颤动中的作用和联系

心房颤动（房颤）在临床上极为常见,目前心房颤动的机制尚未阐明,其中自主神经系统在房颤的发生、维持、终止和决定室性心律上是一个潜在的强大的调节因素。存在于中枢、神经节、外周组织、细胞和亚细胞水平的交感和副交感系统的复杂相互作用都能够改变心脏的传导性和不应期,较为重要的是分布于心脏的自主神经的调节作用能引起心房节律的改变以及影响触发活动的产生和类型,所有这些变化都能引发和维持房颤。本文就心脏自主神经系统在房颤发生发展过程中的可能的作用机制及相互联系作一综述,为基础研究和临床实践中对房颤的机制研究和治疗提供参考依据和理论基础。     

Statins and prevention of atrial fibrillation in patients with heart failure

Statins are highly effective and widely used lipid-lowering agents in clinical practice, that also display a number of pleiotropic properties beyond cholesterol lowering. Several trials have demonstrated that they reduce cardiovascular morbidity and mortality in both primary and secondary prevention. Atrial fibrillation (AF) and heart failure (HF) represent 2 world-wide epidemics. Recent evidence suggests that statins may have beneficial effects on cardiovascular outcomes in patients with HF, and specifically in the prevention of AF. The anti-arrhythmic mechanisms of statins regarding AF prevention in HF patients are not fully understood but are possibly related to their pleiotropic effects including anti-inflammatory, antioxidant, atrial remodeling attenuation, ion channel stabilization, and autonomic nervous system regulation.     

Diabetes Mellitus and Atrial Remodeling: Mechanisms and Potential Upstream Therapies

Atrial fibrillation (AF) is the most common cardiac arrhythmia in clinical practice, and its prevalence has increasing substantially over the last decades. Recent data suggest that there is an increased risk of AF among the patients with diabetes mellitus (DM). However, the potential molecular mechanisms regarding DM‐related AF and diabetic atrial remodeling are not fully understood. In this comprehensive review, we would like to summarize the potential relationship between diabetes and atrial remodeling, including structural, electrical, and autonomic remodeling. Also, some upstream therapies, such as thiazolidinediones, probucol, ACEI/ARBs, may play an important role in the prevention and treatment of AF. Therefore, large prospective randomized, controlled trials and further experimental studies should be challengingly continued.     

心房电重构与房颤关系的基础研究

目的检查观测心房电生理改变与房颤（AF）发生和持续的关系,探讨心房电重构与房颤的内在联系。方法健康成年杂种犬14只（雌雄不拘,体重10．0～12．5kg）,随机分为2组：对照组（A组）和起搏组（B组）。右侧开胸将电极置于右心房,以400次／min的频率快速起搏右心房（A组只手术不起搏）,分别于实验开始及起搏6h后对每只犬进行电生理检查,测定心房有效不应期（AERP）。起搏开始及起搏后测定burst刺激诱发房颤的频率和持续时间。结果A组在整个时间内AERP无变化,B组心房快速起搏后,AERP明显缩短。A、B两组起搏前房颤的频率和持续时间差异无统计学意义。A组起搏前、后房颤的频率和持续时间无变化,B组心房快速起搏后房颤的频率增多,持续时间延长。结论快速心房起搏可以引起心房有效不应期缩短,即心房电重构。心房电重构造成的心房有效不应期等电生理变化促进了房颤的发生和维持,是心房电重构与房颤关系的基础。