炎症、氧化应激与心房颤动

许多证据表明心房颤动中存在炎症和氧化应激,炎症和氧化应激可导致心房重构,包括电重构和结构重构,提示炎症和氧化应激可能在心房颤动的发生和维持中起着一定作用。抗炎和抗氧化治疗可减少心房颤动的发生和复发,这为干预心房颤动的发生和复发提供了新思路。     

心房颤动相关的生物学标记物

心房颤动是一种常见的心律失常,不仅严重损害心脏功能,而且明显增加缺血性脑卒中的发生。因此,预测心房颤动的发生至关重要。近年研究发现,炎症、氧化应激、纤维化、心房肌结构重构和电重构与心房颤动的发生密切相关;相应的生物学标记物可以预测心房颤动的发生和预后。     

抗痛风药物与心房颤动关系的研究进展

心房颤动是临床最常见的心律失常,炎症、氧化应激可能参与心房颤动发生的病理生理学机制,而嘌呤代谢反映体内氧化应激程度。抗痛风治疗基于抑制炎症和降低尿酸水平等药物,似乎可作为减少心房颤动发生的潜在策略。     

炎症反应与心房颤动的关系

心房颤动发病机制复杂,心房重构起着至关重要的作用,而心房重构又包括结构重构和电重构。心房重构的病理生理机制与炎症反应密切相关,二者的联系复杂多样,一些潜在的疾病以及内环境改变都可能影响到这些途径,从而导致心房颤动的发生。炎症标志物也与心房颤动的发生、维持、复发、心房颤动负荷以及血栓形成有关。在这种情况下,是否应该给予心房颤动患者具体的抗炎干预措施目前尚存在争议。现对近几年的炎症反应与心房颤动关系的相关研究进行简要概括,同时提出炎症标志物在心房颤动中的预测作用。此外,纳入心房颤动患者实施抗炎干预的部分研究现状。     

尿酸与心房颤动

心房颤动(AF)是最常见的心律失常,而我国人群中高尿酸血症(HUA)患病率高达13%,多项研究提示HUA是AF新发、复发的危险因素。一方面,HUA可能通过氧化应激、炎症、细胞内尿酸的聚积从而导致心房电重构、机械重构的发生,进而促进AF的发生;另一方面,低尿酸血症亦可导致AF,血清尿酸水平与AF之间似乎呈现J型曲线关系。     

脂肪因子在心房颤动诊治中的研究进展

脂肪细胞分泌的脂肪因子参与胰岛素抵抗、肥胖、代谢综合征,在许多心血管疾病的发生发展过程中起到重要作用。包括新型脂肪因子在内的多种脂肪因子与心房颤动的关系已引起了广泛关注,大量研究显示各种脂肪因子通过炎症反应和氧化应激、心房重构以及交感神经激活等作用,参与心房颤动的发生与发展,甚至可作为预测预后的因子,为心房颤动的发生以及防治提供新的思路。     

炎症、氧化应激与心房颤动

心房颤动（atrial fibrillation，AF）是最常见的心律失常之一。目前认为，其发生机制与开口于心房的大静脉肌袖有快速发放冲动灶和心房内引起多发子波折返等相关。而AF的维持机制与心房的电生理重构、组织结构重构和离子通道重构等相关。然而，上述发生机制和维持机制的触发和危险因素尚众说纷纭。本文就炎症和氧化应激与AF的发生、复发、持续和治疗等关系作一简述。     

高尿酸血症和心房颤动的相关性研究进展

尿酸是氧化损伤和炎性反应的生物标志物,高尿酸血症与心房颤动有关。高尿酸血症可能通过炎性反应和氧化应激参与了心房重构。该文介绍高尿酸血症与心房颤动的发生、进展及复发之间的相关性,并探讨降尿酸治疗对心房颤动的影响,为心房颤动的上游治疗提供思路。     

衰老与心房颤动

衰老与心房颤动(AF)发生密切相关,主要参与AF的结构重构和电重构.衰老通过细胞肥大、纤维化、肺静脉和左房大小、淀粉样变参与结构重构;通过调节离子电流、缝隙连接蛋白参与结构重构;另外通过氧化应激、炎症过程、性激素变化、交感神经的变化导致AF.     

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。     

Le r?le des médicaments non anti-arythmiques dans la prévention de la fibrillation auriculaire

After cardioversion of atrial fibrillation, structural and electrophysiologic remodelling of the atria is implicated in the arrhythmia recurrences despite antiarrhythmic drug treatment. Strategies targeting this substrate have therefore been proposed. In this view, Renin angiotensin system inhibition and drugs targeting inflammation and oxidative injury are the most promising strategies up to now. We discuss here the rationale and evidence which are behind these therapeutic approaches.     

What Do We Currently Know About Metabolic Syndrome and Atrial Fibrillation?

Metabolic syndrome represents a cluster of atherogenic risk factors including hypertension, insulin resistance, obesity, and dyslipidemia. Considering that all of these risk factors could influence the development of atrial fibrillation, an association between atrial fibrillation and the metabolic syndrome has been suggested. Additionally, oxidative stress and inflammation have been involved in the pathogenesis of both metabolic syndrome and atrial fibrillation. The mechanisms that relate metabolic syndrome to the increased risk of atrial fibrillation occurrence are not completely understood. Metabolic syndrome and atrial fibrillation are associated with increased cardiovascular morbidity and mortality. Because atrial fibrillation is the most common arrhythmia, and along with the prevalence of metabolic syndrome constantly increasing, it would be very important to determine the relationship between these 2 entities, especially due to the fact that the risk factors of metabolic syndrome are mainly correctable. This review focused on the available evidence supporting the association between metabolic syndrome components and metabolic syndrome as a clinical entity with atrial fibrillation.     

氧化应激与心房颤动关系研究进展

研究已证实氧化应激参与高血压、心力衰竭等疾病的发病过程,其与心房颤动的关系成为近年来研究热点之一。现综述氧化应激与心房颤动关系研究最新进展。     

Structural remodelling during chronic atrial fibrillation: act of programmed cell survival

Atrial fibrillation is the most common cardiac arrhythmia with an overall prevalence of almost 1%. Increasing prevalence and associated risks such as stroke and mortality have increased the need for better and more reliable therapeutic treatment. This has stimulated research to elucidate the pathophysiological mechanisms underlying atrial fibrillation. Atrial fibrillation is primarily characterised by electrical remodelling and functional deterioration. Both phenomena are reversible but after prolonged duration of atrial fibrillation, a discrepancy occurs between rapid electrical remodelling and slow recovery of contractile function. Recent studies have indicated that morphological remodelling might underlie this incongruity. In experimental models of lone atrial fibrillation, the remodelling involves cellular changes that are reminiscent of dedifferentiation and are characterised by cellular volume increase, myolysis, glycogen accumulation, mitochondrial changes and chromatin redistribution. The absence of clear signs of degeneration in these models points towards cardiomyocyte adaptation or a mechanism of programmed cell survival. In patients with atrial fibrillation cardiomyocyte degeneration does occur along with dedifferentiation which might be the result of underlying cardiac pathologies or longer duration of atrial fibrillation. In this review we focus on structural remodelling during atrial fibrillation. The different aspects of histological and ultrastructural changes as well as their role in atrial dysfunction and cardiomyocyte survival are discussed. We briefly describe the underlying molecular remodelling. and possible mechanisms responsible for remodelling involving calcium overload and stretch are presented.     

氧化应激在心房颤动发生维持中的作用

心房颤动（房颤）是临床上最常见的慢性心律失常。房颤使心房发生电重构及结构重构,然而心房重构发生的同时也加重房颤的发生及维持。有多项研究证实,氧化应激产物如活性氧能够影响房颤时心房电重构及结构重构,而房颤本身又使心房肌的氧化应激产物增加。房颤时心房氧化应激作用的机制可能与离子通道功能失调、NADPH氧化酶途径及线粒体损伤等有关。在一些近期的研究中也发现具有抗氧化作用的药物如他汀类、肾素-血管紧张素-醛固酮系统阻断剂可能通过防止心房重构,减少房颤发生。     

心房重构的机制及临床意义

心房颤动时心房一方面发生电重构,主要表现为L型钙离子通道功能下降和心房的不应期缩短;另一方面出现组织结构重构,主要表现为细胞间质的纤维化、心房的淀粉样变性。针对心房重构的一些药物在临床应用并取得一定疗效,为心房颤动的治疗提供了新的思路。     

老年性心房颤动心房电重构与钙离子机制研究进展

心房颤动是一种十分常见的心律失常,随年龄增长发病率增加。在心房颤动的发生机制中,心房电重构起着重要作用。本文就心房电重构的离子分子基础、钙离子机制在心房电重构发生和维持中的作用以及老龄对心房电重构影响的现阶段研究进展予以综述。     

Enhancement of cardiac oxidative stress by tachycardia and its critical role in cardiac hypertrophy and fibrosis

OBJECTIVE: To examine the mechanism and significance of tachycardia-induced cardiac damage, using azelnidipine, a relatively new dihydropyridine calcium channel blocker which does not increase heart rate. METHODS: Comparing azelnidipine and amlodipine, we examined the cardiac effects and the direct effects on a sinus node/atrial preparation in stroke-prone spontaneously hypertensive rats (spSHRs). By pacing the right atrium, we examined the effect of tachycardia per se on cardiac oxidative stress. Using apocynin, a reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, we investigated the role of oxidative stress in cardiac remodelling. RESULTS: Azelnidipine suppressed cardiac hypertrophy, fibrosis, NADPH oxidase and superoxide in spSHRs more potently than amlodipine, and was associated with lower heart rates than amlodipine. Azelnidipine caused a greater reduction than amlodipine in the beat rate of the sinus node/atrial preparation of spSHRs. A 10 or 20% increase in heart rate, independent of blood pressure or sympathetic nerve activity, significantly enhanced cardiac NADPH oxidase activity, superoxide and activated mitogen-activated protein kinases. Reduction of cardiac oxidative stress by apocynin led to the suppression of cardiac hypertrophy, inflammation and fibrosis in spSHRs, beyond its hypotensive effect. CONCLUSIONS: Our work provided evidence that the increase in heart rate per se, independent of sympathetic nerve activity, enhances cardiac oxidative stress and activates mitogen-activated protein kinases, which seem to be responsible for cardiac remodelling. Azelnidipine, without causing an increase in heart rate, has the potential to be useful for the treatment of cardiac remodelling.