心房颤动发病炎症机制的研究进展

<正>心房颤动(AF)是一种常见的心律失常,指规则有序的心房电活动丧失,代之以快速且无序的颤动波,是严重的心房电活动紊乱,有一定的心脏性猝死风险,主要表现为心慌、心悸等不适,引起多种并发症,脑栓塞疾病危害最大,造成患者认知功能下降、抑郁,往往需要反复住院治疗,大大降低了生活质量,给社会带来巨大经济负担,AF也是导致心力衰竭及脑血管疾病等相关疾病的主要原因之一,增加死亡风险^[1]。     

心房颤动心房结构重构发病机制的研究进展

心房结构重构在心房颤动 (房颤 )的发生和维持中起着重要作用 ,因而阐明其发生机制将对房颤的预防和治疗带来新的契机。本文就现阶段针对心房结构重构的分子发生机制的研究新进展作一综述。     

心房颤动的炎症机制研究进展

心房颤动的病理生理机制仍不完全清楚.以往的研究重点在心房颤动的电生理特性,近年来的研究提示心房结构重塑是其先决条件.心房纤维化不仅与心肌细胞和成纤维细胞的激活有关,也与白细胞激活有关.白细胞聚集活化并释放活性氧、细胞因子和生长因子,随后细胞外基质沉积增加,这导致心房病理性重构,提示炎症机制可能为心房颤动的重要发病机制.该文就心房颤动的炎症机制相关研究进展进行综述.     

心房颤动重构机制研究进展

心房颤动是最常见快速型心律失常性疾病。目前心房颤动发生机制研究分神经、重构、压力、炎症机制等临床方面和基因、分子生物学水平上的进展。其中重构机制是适应性代偿作用,又是心房颤动发生和维持的重要因素。现主要综述电生理、形态结构、功能上的重构与心房颤动的关系。     

心房颤动致心房重构分子机制研究进展

心房颤动是临床上一种常见的心律失常,心房颤动致心房重构是近年来研究发现的一个重要的电生理现象。心房颤动本身能够导致心房电生理、功能和结构的改变。本文综述了心房颤动致心房快速的电生理变化和缓慢的蛋白质表达及其分子改变机制。通过对心房电生理重构、离子重构和蛋白质重构和超微结构及其功能变化等不同方面的全面阐述,探讨了心房重构的分子机制研究进展。防治心房颤动新的策略将取决于心房重构机制更好的理解。     

低强度迷走神经刺激在心房颤动治疗中的研究进展

心房颤动（房颤）是临床上最常见的心律失常之一,心房炎症和心脏自主神经重构是房颤触发和维持的重要机制,主要表现为心房的炎症因子水平升高、星状神经节或心脏表面神经节丛的神经放电增加。研究表明,低强度迷走神经刺激能够抑制星状神经节或心脏表面神经节丛放电及心房炎症,从而降低房颤负荷。但目前临床上仍缺乏个体化的低强度迷走神经刺激治疗方案,深入探索低强度迷走神经刺激的保护机制有助于该治疗方式的进一步发展。     

心房颤动发病机制的相关研究进展

心房颤动（atrial fibrillation,AF）是老年人群中最为常见的心律失常,研究表明其发病机制与衰老、遗传突变、炎症反应、氧化应激、钙稳态异常、代谢异常等有关,越来越多的证据表明上述机制在心房电重构和结构重塑的演变中起着重要作用。在这篇综述中,我们讨论了房颤发生发展可能的分子机制,其中涉及多个典型的炎症途径,以及抗炎治疗、纠正代谢异常等方法 对房颤的防治潜力。     

心房颤动中心房重构的分子机制研究进展

<正>心房颤动是临床最常见的持续性心律失常,发病率随着年龄增加呈升高趋势[1],其并发症能够引起严重的致残致死事件。目前认为心房颤动是多种机制共同作用的结果,其发生有其触发因素和维持机制,包括自发异位起搏和多发子波折返。心房颤动时心房发生电重构和结构重构,随着病程的进展,左心房结构改变和功能受损[2],引起左心功能下降,严重时诱发心力衰竭。同时心房不规律的收缩及血流状态的改变可以引起左心房附壁血栓形成,导致栓塞事件。而慢性     

Calpains与心房颤动的关系

心房颤动(简称房颤)的发生发展是一个十分复杂的过程，有多种机制参与其中。大量研究表明，钙超载是房颤发病的主要机制之一。calpains是一类钙离子依赖性的中性蛋白酶，广泛存在于机体的各组织中，参与多种生理病理过程。近年来研究表明，calpains激活后能够部分降解收缩蛋白，引起心肌收缩功能下降，并影响心肌细胞结构和通道蛋白水平，与房颤心房电重构和结构重构有关。     

心房颤动致心房离子重构机制的研究进展

心房颤动(atrial fibrillation)是临床上常见且目前仍难以防治的心律失常，是许多疾病的临床表现之一，其总体发病率几乎达1％，且随年龄增加而发病率增高。心房颤动致心房重构是近年来心房颤动动物实验和临床研究发现的一个重要电生理现象。本文探讨心房颤动所致心房电生理参数改变及其离子重构机制的研究进展。     

Monogenic atrial fibrillation as pathophysiological paradigms

Atrial fibrillation (AF) is the most common cardiac rhythm abnormality and represents a major burden, both to patients and to health-care systems. In recent years, increasing evidence from population-based studies has demonstrated that AF is a heritable condition. Although familial forms of AF have been recognized for many years, they represent a rare subtype of the arrhythmia. However, despite their limited prevalence, the identification of mutations in monogenic AF kindreds has provided valuable insights into the molecular pathways underlying the arrhythmia and a framework for investigating AF encountered in the general population. In contrast to these rare families, the typical forms of AF occurring in the community are likely to be multigenic and have significant environmental influences. Recently, genome-wide association studies have uncovered common sequence variants that confer increased susceptibility to the arrhythmia. In the future, the elucidation of the genetic substrate underlying both familial and more typical forms of AF will hopefully lead to the development of novel diagnostic tools as well as more targeted rhythm control strategies. In this article, we will focus on monogenic forms of AF and also provide an overview of case-control association studies for AF.     

Targets and endpoints in ablation therapy for atrial fibrillation in the light of pathophysiological mechanisms

Atrial fibrillation (AF), an important public health problem is a complex and multifactorial arrhythmia. Non-pharmacological treatment for symptomatic patients is of increasing importance. The different catheter ablation techniques in AF treatment developed during recent years, all based on different pathophysiological insights, are discussed. The non-standardized use of different follow-up methods after ablation make interpretation and comparison of results difficult.     

Basic mechanisms of atrial fibrillation

The mechanism of AF remains controversial as support still exists for multiple wavelets, "mother rotor," and focal sources. These mechanisms need not be mutually exclusive. For example, the mother rotor hypothesis may not be distinct form the focal AF, if the rotor is of small size (ie, microre-entry). With the development of several animal models to study AF, along with improving technologies and mapping techniques, a further understanding of the pathophysiology of AF is being gained. Each animal model has unique electrophysiological and structural abnormalities, and one may not be able to generalize from one model to the next. It is likely that there is not one mechanism for all AF, but that there are substrate-specific mechanisms, and that AF may be comprised of several different mechanisms.     

The mechanisms of atrial fibrillation

In this article we have reviewed the mechanisms of atrial fibrillation (AF) with special emphasis on the thoracic veins. Based on a number of features, the thoracic veins are highly arrhythmogenic. The pulmonary vein (PV)-left atrial (LA) junction has discontinuous myocardial fibers separated by fibrotic tissues. The PV muscle sleeve is highly anisotropic. The vein of Marshall (VOM) in humans has multiple small muscle bundles separated by fibrosis and fat. Insulated muscle fibers can promote reentrant excitation, automaticity, and triggered activity. The PV muscle sleeves contain periodic acid-Schiff (PAS)-positive large pale cells that are morphologically reminiscent of Purkinje cells. These special cells could be the sources of focal discharge. Antiarrhythmic drugs have significant effects on PV muscle sleeves both at baseline and during AF. Both class I and III drugs have effects on wavefront traveling from PV to LA and from LA to PV. Separating the thoracic veins and the LA with ablation techniques also prevents PV-LA interaction. By reducing PV-LA interaction, pharmacological therapy and PV isolation reduce the activation rate in PV, intracellular calcium accumulation, and triggered activity. Therefore, thoracic vein isolation is an important technique in AF control. We conclude that thoracic veins are important in the generation and maintenance of AF.     

Diabetes mellitus and atrial fibrillation: perspectives on epidemiological and pathophysiological links

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, which is also associated with a substantial risk of mortality and morbidity from stroke, thromboembolism, heart failure and hospitalisations. On a epidemiological basis, diabetes mellitus is commonly associated with AF. Nonetheless, AF is also associated with vascular disease and hypertension, which are themselves intimately linked to diabetes. Indeed, the precise pathophysiological and clinical relationships between AF and diabetes mellitus are not completely understood. What we do know is that both diabetes and AF are individually bad for our patients, and the presence of both requires aggressive management strategies.     

Initiating mechanisms of paroxysmal atrial fibrillation.

BACKGROUND: The understanding of the onset mechanisms of paroxysmal atrial fibrillation (AF) may help to develop preventive therapy. Specific heart rate (HR) patterns and autonomic changes immediately before the onset of paroxysmal AF are not fully investigated. We undertook the present study to assess HR and heart rate variability (HRV) changes before the onset of AF using 24-h Holter electrocardiographic analysis in patients without antiarrhythmic medication. METHODS AND RESULTS: In 27 patients, 48 episodes of AF, lasting more than 30s and preceded by sinus rhythm for more than 1h were analysed. The hour preceding AF was divided in 5- and 30 min blocks. HR was also analysed in the last 15 beats. In 21% of the episodes, HR decreased >or=5% in the last 5 min (defined as deceleration); it increased >or=5% in 37% (defined as acceleration). HR, standard deviation (SD) and SD corrected for RR interval changed significantly in the last 5 min in the total group. Acceleration and deceleration were already visible over 30-min blocks in both these subgroups; changes in SD were only seen in the accelerators. The number of atrial premature beats (PACs) increased before AF, most clearly in the accelerators. Spectral HRV analysis revealed no additional information. CONCLUSIONS: Changes in HR, SD, and an increased number of PACs herald AF from at least 30 min before onset, more pronounced in accelerators. Spectral HRV parameters are not useful to foresee AF onset. This has possible implications for device therapy.