心房颤动、结构重构与肾素-血管紧张素-醛固酮系统关系

心房颤动是临床上最常见的心律失常之一,有较高的发病率、致残率,严重影响患者的生活质量。但是关于心房颤动的发病机制至今并未完全明确,目前对其结构重构的发生机制研究较多,包括钙离子超载、心肌局部肾素-血管紧张素系统激活、基质金属蛋白酶改变、缝隙连接蛋白改变等。同时,针对导致心房颤动结构重构的可能机制,出现了一些新的预防和治疗心房颤动策略。现就心房颤动结构重构的发病机制研究及相应治疗进展做一综述。     

心房颤动与血清尿酸水平的相关性研究进展

心房颤动是一种临床最常见的心律失常,随着年龄增加其发病率和患病率也逐渐上升。近年许多研究表明血清尿酸水平升高与心房颤动的发生、维持和复发相关,且对心房颤动患者血栓栓塞与左房血栓形成产生影响。其机制可能与炎症反应和氧化应激相关。     

脂肪因子与心房颤动和心肌纤维化的关系

心房颤动是最常见心律失常之一。结构重构在心房颤动中的作用和意义已被广泛关注。而近年来的研究表明,脂肪组织可分泌多种脂肪因子如抵抗素、内脂素、瘦素、趋化素、脂联素等。它们可以通过改变动作电位形态、离子的分布、炎症反应或是通过一定的通路对心房颤动产生影响,进而参与心肌纤维化的发生和发展过程,构成促纤维化和抑纤维化的复杂调节网络,影响心血管疾病的发展和转归。现通过总结分析,阐述几种脂肪因子与心房颤动的关系。     

心房颤动最新研究进展

心房颤动是临床上最常见的心律失常之一 ,心房颤动中的多子折返波一旦起动 ,会形成一系列的心肌细胞结构和电生理的改变 ,这就是结构和电生理重构。在结构重构中心房肌的纤维化是心房颤动发生的结构基础 ,已证实细胞间信号调控激酶 2(Erk 2 )、缝隙连接 (GJ)、间隙连接蛋白 40 (Cx40 )有显著的改变 ,在心房纤颤发生及维持过程中起了一定的作用。电重构是指心房颤动的心房肌纤维在持续性心房颤动中有效不应期进行性下降 ,钙超载机制是电重构中最重要的机制 ,以此为基础出现的一系列离子通道 ,包括L Ca2 通道、K 通道、Na 通道 ,以及一系列的钙调蛋白的改变 ,最终的结果是使心房肌纤维的有效不应期进行性延长 ,使心房颤动得以维持。了解心房颤动的重构机制对临床心房颤动治疗的用药有很大的指导意义。     

钙信号调节异常在房颤电重构过程中的作用

心房颤动（AF）是一种多因素导致的疾病,持续性AF后期不可避免要有结构上出现相应的改变,故在早期电重构期进行针对性的治疗很有必要。本文主要从AF电重构产生的生理基础、AF患者钙信号的改变及AF药物治疗的新思想方面做一综述。     

心房纤维化与基质消融

心房颤动的发生源于心脏电生理改变和心房结构重构的共同作用。心房纤维化将影响心房有效不应期、动作电位时程和细胞膜离子通道表达,因而是心房颤动的易损基质;另一方面,心房颤动又会导致心房纤维化,改变心房组织构成及功能,进而促进心房颤动的发生与维持。因此,针对心房颤动基质射频导管消融成为了治疗心房颤动的重要手段。现就心房纤维化与基质消融的研究进展做一综述。     

心房颤动患者心房纤维化研究进展

心房颤动的发生和维持与心房重构有关。心房纤维化是心房颤动患者心房结构重构最突出的表现,目前被认为是发生心房颤动的结构基础,是心房颤动发生、维持的一个重要因素。现综述心房颤动患者心房纤维化及其发生机制。通过对心房颤动患者心房纤维化结构改变及肾素-血管紧张素系统、转化生长因子、基质金属蛋白酶等在心房纤维化的发生和心房颤动发生、维持中的作用等的全面阐述,,探讨了心房颤动患者心房纤维化的研究进展。防治心房颤动新的策略取决于对心房纤维化机制更好的理解。     

心房颤动与自身免疫性疾病相关性的研究进展

心房颤动是一种常见的心律失常,心房颤动的发生与心房重构及炎症反应密切相关.自身免疫性疾病是一种全身性免疫炎症性疾病,可并发包括心房颤动在内的各种心血管疾病.近年来,大量关于自身免疫性疾病与心房颤动发生关系的研究结果表明,自身免疫性疾病与心房颤动的发生具有明显的相关性.本文就心房颤动与自身免疫性疾病相关性的研究进展进行了...     

非瓣膜性心房颤动与血栓栓塞

心房颤动是最常见的心律失常 ,并且是缺血性脑卒中最重要的危险因素之一 ,本文对非瓣膜性心房颤动与血栓栓塞的流行病学 ;非瓣膜性心房颤动发生血栓栓塞的血液学改变、危险因素以及预防作一综述。     

心房纤维化与结缔组织生长因子

心房纤维化为心房颤动的发生和维持提供了一种病理基础,而结缔组织生长因子(CTGF)是心脏中介导细胞外基质生成的重要介质,与心脏纤维化关系密切。所以开发能抑制CTGF产生和激活的药物将会有可能逆转纤维化,为心房颤动的治疗提供新的途径。     

Atrial fibrillation: molecular biology bases

BACKGROUND: Atrial fibrillation is the most frequent form of sustained arrhythmia. In most cases the arrhythmia is acquired, in rarer cases it may occur as a familial disease with a autosomal dominant pattern of inheritance. Recent advances in molecular biology and genetics have had a major impact on our understanding of the mechanisms responsible for the initiation, maintenance and chronification of the arrhythmia. Recently, the chromosomal locus for familial atrial fibrillation has been mapped to chromosome 10q22-q23, however, so far the causative gene has not been identified. ATRIAL REMODELING: Atrial fibrillation itself modifies atrial electrical properties in a way that promotes the occurrence and maintenance of the arrhythmia, in other words "atrial fibrillation begets atrial fibrillation". The principle stimulus for atrial remodeling is the rapid atrial rate. PERSPECTIVES: It is hoped that the results of future studies will not only further improve our understanding of the mechanisms underlying atrial fibrillation but may also help to develop new therapeutic strategies.     

Effects of operation on left atrial size and the occurence of atrial fibrillation in patients with hypertrophic subaortic stenosis

The relation between left atrial size and atrial fibrillation was examined in 37 patients who had left ventriculomyotomy and myectomy at the National Heart and Lung Institute. Atrial fibrillation was present in 11 of 27 (41%) patients with an echocardiographically measured left atrial dimension greater than 45 mm. No patient with a left atrial dimension less than 45 mm had atrial fibrillation pre or postoperatively. Eleven of 13 patients less than 40 years of age with an abnormal preoperative left atrial dimension had a 10% or greater reduction in left atrial dimension postoperatively. A group of 21 patients 40 years of age or older had an abnormal left atrial dimension preoperatively, and no significant change postoperatively. These results indicate that left ventriculomyotomy and myectomy can produce a significant decrease in left atrial size in younger patients with idiopathic hypertrophic subaortic stenosis. It is hoped that the decrease in atrial size may reduce the risk of atrial fibrillation in these patients.     

Molecular genetic studies in atrial fibrillation

Atrial fibrillation is a complex disease. Its etiologies are diverse and genetic factors may also contribute to this disease. With the advent of modern molecular biology technology, it is now possible to explore the genetic components in the pathogenesis of atrial fibrillation. Past molecular genetic studies on atrial fibrillation in the literature can be divided into linkage analysis studies and association studies. The subjects for linkage analysis studies are pedigrees of probands with Mendelian hereditary atrial fibrillation. The first locus identified for autosomal dominant atrial fibrillation locates at 10q22-q24. However, the exact gene is still unknown. Another linkage analysis study in Chinese revealed that LQT1 gene (I(Ks) alpha-subunit) was the responsible gene. A missense mutation in the I(Ks) alpha-subunit results in a gain of function, which is important in causing atrial fibrillation. The third known locus for familial atrial fibrillation locates at 6q14-16. The responsible gene remains still unknown. The other type of studies takes the case-control design (association studies) and the subjects have multigenic atrial fibrillation. In a study in a Japanese population, it was reported that the angiotensin-converting enzyme insertion/deletion polymorphism was not associated with atrial fibrillation. On the other hand, researchers in Taiwan reported that a nonsynonymous single nucleotide polymorphism of the LQT5 gene (I(Ks) beta-subunit) is associated with atrial fibrillation. In summary, there is growing evidence showing that genetic factors are important in the pathogenesis of atrial fibrillation. We expect that more genes responsible for or contributing to atrial fibrillation will be identified in the future and these will elucidate the molecular mechanisms of atrial fibrillation.     

左心耳封堵术对于房颤患者防治卒中的作用

心房颤动（Atrial fibrillation,AF),简称房颤,是最常见的持续性心律失常。随着人口的普遍老龄化,人群中房颤患病率呈显著上升趋势。预计到2050年房颤患病人口将在目前患病人数水平上增加一倍。而对于房颤患者,卒中的预防是房颤治疗的首要目标。据统计,房颤患者发生卒中的风险约为窦性心律失常人群的5倍。目前,对于房颤患者的卒中治疗预防主要是应用口服抗凝药物。最新研究表明,左心耳封堵术对于房颤患者的卒中预防有着显著疗效。本文将综述左心耳封堵术对于房颤患者防治卒中的作用,为临床应用提供依据。     

Paroxysmal atrial fibrillation in the wolff-parkinson-white syndrome

Eighty-eight patients with preexcitation were studied to determine how 30 patients with documented spontaneous paroxysmal atrial fibrillation differed from 58 patients without this arrhythmia. Inducible reentrant tachycardia was present in 23 (77 percent) of the 30 patients with, versus 28 (48 percent) of the 58 patients without, atrial fibrillation (p < 0.025). Heart disease was present in 13 (43 percent) of the 30 patients with, versus 15 (26 percent) of the 58 patients without, atrial fibrillation (not significant). Inducible reentrant tachycardia or heart disease, or both, were present in 29 (97 percent) of the 30 patients with, versus 34 (59 percent) of the 58 patients without, atrial fibrillation (p < 0.0005).Of 51 patients with inducible reentrant tachycardia, 23 patients with atrial fibrillation did not differ from 28 patients without this arrhythmia with respect to clinical features and atrial, sinus nodal, or anomalous pathway properties, or cycle length of induced reentrant tachycardia. Spontaneous degeneration of induced reentrant tachycardia to atrial fibrillation was observed in 6 (26 percent) of 23 patients with, versus none of 28 patients without, atrial fibrillation (p < 0.025).In summary, patients with preexcitation and documented spontaneous paroxysmal atrial fibrillation almost always have inducible reentrant tachycardia or heart disease, or both. It is likely that in many patients with inducible reentrant tachycardia, spontaneously occurring reentrant tachycardia relates to induction of atrial fibrillation. However, it is unclear why some patients with inducible reentrant tachycardia have atrial fibrillation and others do not. In many patients with organic heart disease, atrial fibrillation could relate to hemodynamic changes.     

肾素-血管紧张素-醛固酮系统基因多态性与心房颤动

心房颤动(房颤)的病因多认为是由心脏的组织结构及电活动的改变引起,近年来研究表明遗传因素也可能参与了房颤的发生:家族性房颤的遗传背景已较明确;非家族性房颤遗传因素的相关研究也取得了进展,其中肾素-血管紧张素-醛固酮系统基因多态性与房颤的相关性研究就取得了部分进展.有研究认为血管紧张素原基因多态性及血管紧张素转换酶基因多态性与房颤的发病有关,但也有相反观点;而血管紧张素受体基因多态性则多认为与房颤的发病无关;肾素和醛固酮合酶的基因多态性与房颤的相关性问题尚无明确报道.     

Changing axis deviation with changing bundle branch block and new-onset of atrial fibrillation during acute myocardial infarction

Paroxysmal atrial fibrillation is considered a frequent complication of acute myocardial infarction.It has been rarely reported alternating right and left bundle branch block associated with atrial fibrillation. It has also been rarely reported changing axis deviation with left bundle branch block also during atrial fibrillation and acute myocardial infarction. We present a case of changing axis deviation with changing bundle branch block and new-onset of atrial fibrillation in a 96-year-old Italian man with acute myocardial infarction.     

L型钙通道与心房重构

近年来的研究表明心房颤动引起 L 型钙通道变化,后者可能是引起以电重构、缝隙连接及收缩功能重构为主要形式的心房重构的中心环节。相应的药物干预可能是心房颤动治疗的新靶点。     

缝隙连接蛋白及其与心房颤动关系研究进展

心房颤动的发生和维持与缝隙连接蛋白密切相关。近年来发现心房颤动的伴随症状如心房纤维化、心房扩大、炎症以及遗传因素均可独立于心房颤动之外使缝隙连接蛋白发生改变,从而促进心房颤动的发生与维持。对心房颤动伴随症状的治疗有望成为心房颤动治疗的新靶点。