心脏自主神经网络调控及与心房颤动发生的关系

心脏自主神经调节网络包括外源与内源自主神经系统,其中神经丛是内源性和外源性心脏自主神经系统的协调中枢,这种网络调控一直处于一种动态平衡中,任何一个环节失衡都将导致心脏电生理的改变,从而诱发心房颤动(简称房颤)。自主神经网络的调控对房颤的发生起到关键作用。现研究表明能通过刺激和消融的方式调节自主神经网络系统,降低房颤的发生率。这是目前有效可行的预防房颤的方法,但也存在外周静脉神经生长因子浓度升高以及交感活性过度激活等问题。     

腺苷酸激活蛋白激酶在心房颤动发生和维持中的作用

腺苷酸激活蛋白激酶是细胞能量感受器,受上游激酶激活,调节葡萄糖和脂肪酸的代谢,参与维持代谢应激下能量平衡和氧化还原稳态,与心脏能量代谢密切相关。心房颤动(简称房颤)的发生和维持与心房电重构、结构重构、自主神经系统、能量代谢障碍以及炎症反应等有关。近来研究发现腺苷酸激活蛋白激酶在房颤的发生和维持中发挥作用,其机制研究为房颤的治疗提供新方向。     

心房颤动的神经机制及治疗研究进展

心房颤动(房颤)是临床最常见的心律失常.自主神经系统在房颤的发生及维持中起着重要作用.心脏受内外在自主神经的调节.外在自主神经中的交感神经纤维主要来源于椎旁神经节,特别是星状神经节,星状神经节与胸腔内的多条神经和结构相连,是心脏交感神经支配的最重要来源.心脏内在的自主神经是一个由轴突和神经节丛组成的网络,包含各种交感和...     

心脏内在自主神经系统在心房颤动发生机制中的作用

心房颤动(房颤)是临床最常见的快速性心律失常,也是患者致残和致死的重要原因.尽管目前房颤的治疗领域已经取得了很大进展,但是房颤发生机制仍然存在较大争议.应该认识到,最佳的治疗方案应该建立在对机制的充分理解上.近年来,关于房颤发生机制的研究层出不穷,但是这些研究大多局限于肺静脉特殊的解剖特点和电生理性质,得出的结论也仅能解释房颤的某一个方面.本文总结房颤研究领域的主要研究成果,阐述房颤发生的可能机制,并重点介绍心脏内在自主神经系统在房颤发生和维持中的重要作用.     

心房颤动自主神经机制与神经节消融

心房颤动（房颤）的发生机制,除了局灶学说和多发子波折返学说,大量的基础和临床研究证实,心脏内源性自主神经系统在房颤的发生和维持中起着重要作用,针对于心脏自主神经的神经节消融为治疗房颤提供了新的发展方向。     

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。     

心房颤动中心脏自主神经评价手段的研究进展

心脏受自主神经支配,自主神经系统包括心脏外在自主神经和固有自主神经系统,两者均包含交感成分和副交感成分,在心房颤动(房颤)的发生发展中均起重要作用。本文通过回顾文献,总结近年来用于评价心脏自主神经的手段,其中一些方法已经用来预测房颤的产生和发展,未来也可以通过这些方法进一步研究房颤的发病机制。     

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。     

生长因子与心房颤动的研究进展

心房颤动（简称房颤）是临床最常见的恶性心律失常之一。临床和基础研究都证实,心房肌存在电重构和结构重构,这是心房颤动自身维持的机制,也是心房颤动发生发展过程的特点。持续性房性心动过速发生最初几小时内,心肌组织即发生电生理改变;而心房结构重构则是一个缓慢的过程,指心房组织、细胞乃至亚细胞水平的形态和结构的改变,     

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。     

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.     

Ganglionated plexi as neuromodulation targets for atrial fibrillation

The autonomic nervous system plays an important role in the genesis of atrial fibrillation and is one of the candidate targets for atrial fibrillation therapy. This review focuses on the role of the autonomic nervous system in atrial fibrillation development and discusses the results of the ganglionated plexi catheter and surgical ablation in preclinical and clinical studies. The heart is innervated by the extrinsic and intrinsic autonomic nervous systems. The intrinsic autonomic nervous system consists of multiple ganglionated plexi and axons, which innervate the neighboring atrial myocardium and control their electrophysiological properties. Abnormal autonomic innervation has been observed in an animal model of atrial fibrillation and in humans. Direct recordings of autonomic nerve activity in canine models showed that atrial tachyarrhythmia episodes were invariably preceded by intrinsic cardiac autonomic nerve activity, thus supporting the importance of intrinsic cardiac autonomic nerve activity as the triggers for atrial tachyarrhythmia. Targeting ganglionated plexi with catheter ablation improves the outcomes of paroxysmal atrial fibrillation ablation in addition to pulmonary vein antrum isolation. Ablation of ganglionated plexi alone without pulmonary vein isolation is also useful in controlling paroxysmal atrial fibrillation in some patients. However, surgical ganglionated plexi ablation in patients with a large left atrium, persistent atrial fibrillation, and/or a history of prior catheter ablation does not result in additional benefits. These different outcomes suggest that ganglionated plexi ablation is effective in managing patients with paroxysmal atrial fibrillation, but its effects in patients with persistent atrial fibrillation and advanced atrial diseases might be limited.     

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.     

心率与心房颤动关系的研究进展

心房颤动（简称“房颤”）是临床上最常见的心律失常,其发病率随年龄增长而增加。心房重构是房颤的核心机制,包括电重构、结构重构及自主神经重构。自主神经功能障碍在房颤的发生、发展中起着重要的作用,而心率可以间接反映自主神经功能。心率与房颤发生的关系以及房颤射频消融术后心率变化与房颤复发关系复杂,且一直在研究中。     

心脏交感神经活动评估方法的研究进展

心脏自主神经系统是调节心脏功能活动的重要结构,自主神经活动异常是心力衰竭、心房颤动及缺血性心脏病等多种心血管疾病的重要发病机制之一,评估自主神经活动成为心血管基础和临床研究领域的重要课题.近年来,心脏交感神经活动评估方法经过长足的探索,目前可经皮肤连续24 h以上、无创地记录患者即刻心脏交感神经活动,具备广阔的临床应用...     

The role of autonomic denervation during catheter ablation of atrial fibrillation

PURPOSE OF REVIEW: To analyse recent experimental and clinical studies and show that all the pathological events occurring in the myocardium during atrial fibrillation are caused by changes in the autonomic nervous system. The current methods of radiofrequency ablation focus on damaging healthy myocardial tissue involved in the dysregulation caused by autonomic nervous system hyperactivity. Radiofrequency ablation should instead be targeted at compromised nerves and autonomic ganglia (ganglionated plexi). RECENT FINDINGS: Experimental data show that electrical stimulation of the autonomic nervous system may facilitate the induction of atrial fibrillation. The active role of pulmonary veins in atrial fibrillation results from the high density of adrenergic and cholinergic nerves around pulmonary veins. The areas most suitable for autonomic nervous system modification procedures are located in the immediate vicinity of the pulmonary vein-left atrial junction. The first clinical results of radiofrequency ablation of ganglionated plexi resulting in autonomic denervation are encouraging, and show this as a promising approach. There remain many debatable points; the most important of which is the best approach for locating clusters of ganglionated plexi. SUMMARY: Recent experimental and clinical findings have provided new insights into the causes of atrial fibrillation and allowed a re-evaluation of its treatment.     

Cardiac Arrhythmias and the Autonomic Nervous System

Cardiac Arrhythmias and the Autonomic Nervous System. The multiple facets of cardiac arrhythmias and their relationship with the autonomic nervous system can be investigated by studying the spontaneous heart rate behavior through ambulatory ECG recordins, an approach that complements the limitations of invasive electrophysiologic investigations. Information obtained from heart rate behavior is more reliable in the absence of structural heart disease and ventricular hypertrophy/failure, during which compensatory mechanisms involving the autonomic nervous system tend to limit reflex changes in heart rate. Thus, in such situations, less marked sinus rhythm variations preceding the arrhythmia onset do not imply a more limited influence of the autonomic nervous system, and the sensitivity of the electrophysiologic substrate may otherwise vary. These two factors may combine to form the basis of the adrenergic paradox¹¹ that implies that the more marked the autonomic nervous system dependence of tachyarrhythmias, the less obvious its evidence. Assessment of the QT interval dynamicity may also allow one to evaluate the modulation of autonomic neural effects on the ventricular tissues. Finally, it may be difficult to distinguish clearly autonomic nervous system dependence from rate dependence: the latter frequently conditions the behavior of the trigger whereas the former mainly concerns the electrophysiologic substrate. There are many examples of the importance of the autonomic nervous system as a determinant of cardiac arrhythmias. In the atrium, either limb of the autonomic nervous system, particularly the parasympathetic limb, can generate atrial fibrillation. The absence of structural heart disease defines pure electrophysiologic substrates responsible for benign forms of ventricular tachycardia as welt as potentially lethal tachyarrhythmias of the long QT syndrome and its variants. In both, the role of the autonomic nervous system is essential, although the therapeutic consequences are crucial only in the latter. In the presence of heart disease and, in particular, heart failure, the autonomic nervous system behavior is more difficult to assess than in the absence of structural heart disease. This does not mean that its role is less crucial. In this situation the beneficial effects of beta blockers may be as important as in normal hearts although physicians should be more cautious when heart failure is present.     

70例持续性房颤患者心率变异性临床分析

目的 探讨持续性房颤患者心率变异性（HRV）变化,分析其在基础心脏疾病伴房颤疾病中的临床意义.方法 70例持续性心房颤动患者作为房颤组,70例为正常对照组.行24h动态心电图检查,检测心率变异性时域指标.进一步将70例房颤患者分为孤立性房颤10例,冠心病伴房颤21例,高血压性心脏病伴房颤25例,心衰伴房颤14例.所有房颤患者均进行24h动态心电图监测,观察24h HRV时域分析指标.结果 房颤患者HRV时域分析较正常对照组下降（P＜0.01）.冠心病、高血压性心脏病、慢性心衰伴房颤患者HRV时域分析指标较孤立性房颤患者明显降低（P＜0.01）.结论 冠心病、高血压性心脏病、慢性心衰、伴房颤患者HRV降低,即自主神经对心脏的调节能力减弱.HRV可作为冠心病、高血压性心脏病、心衰伴房颤患者的无创性预测指标.     

Clinical approach to paroxysmal atrial fibrillation

In addition to the role of the electrophysiological substrate, paroxysmal atrial fibrillation depends on the modulation of the atrial tissues by the autonomic nervous system. Experimentally, models of atrial fibrillation can be based on either adrenergic or vagal stimulations that provoke the arrhythmia by disturbing in a different way conduction and refractory periods of the atrium. Clinically, the role of the autonomic nervous system can be suspected from the clinical history, and paroxysmal attacks can typically be observed either at daytime or at night, at exercise or at rest. Careful attention should be paid to the changes of heart rate that occur in the minutes or tens of minutes prior to the attacks, and the trend of acceleration or slowing of cardiac frequency observed in Holter tracings provides reliable indications of the state of the vago-sympathetic balance in these patients. During the attacks, the electrocardiographic aspect of atrial flutter alternating with a pattern of atrial fibrillation is typical of vagally dependent arrhythmias, whereas atrial tachycardia is more frequently observed at the onset of adrenergic atrial fibrillation. When the paroxysmal forms of arrhythmia are resistant to usual pure antiarrhythmic therapy including type IA agents and flecainide or encainide, one should take into account the role of the autonomic nervous system. Propafenone, or beta-blockers combined with type I drugs, are very effective every time an adrenergic factor is involved, but prevent the beneficial role of other agents if a vagal mechanism is predominant.(ABSTRACT TRUNCATED AT 250 WORDS)     

Heart rate variability and the onset of tachyarrhythmias.

The autonomic nervous system plays an important role in the genesis of cardiac arrhythmias but the precise definition of this role is quite complex. The fluctuations of the heart rate may provide useful information about the balance of the autonomic nervous system. However, one obvious limitation is represented by extrapolating to the ventricle events which occur at the sinus node level. It has been clearly documented that atrial fibrillation of vagal origin is preceded by a progressive decrease in heart rate. On the other hand, ventricular arrhythmias of adrenergic origin are preceded by progressive heart rate acceleration and by diminution of vagally mediated short term changes. The absolute value in heart rate is less important than the actual trend in allowing inferences on the relative sympathetic or vagal predominance. A better understanding of the changes in the autonomic balance will provide a key for the mechanisms underlying several clinical events.