糖尿病致心房颤动机制与钙信号的关系

糖尿病是心房颤动的独立危险因素,但其致心房颤动的机制尚不清楚。研究表明,钙信号的调控异常在心房颤动的发生中发挥重要作用,甚至可以成为心房颤动治疗的新靶点,而糖尿病可能通过氧化应激影响钙信号的性状,因此"高糖-氧化应激——调控钙信号"可能是糖尿病致心房颤动的重要机制之一,现就糖尿病致心房颤动机制与钙信号的关系做一综述。     

高尿酸血症与心房颤动的关系

心房颤动是临床上最常见的持续性心律失常,可能导致心力衰竭、血栓栓塞等并发症.心房颤动的发生、发展可能与心房重构、炎性反应及氧化应激有关.人体内血尿酸不仅与心房氧化应激程度密切相关,还与炎性标志物水平相关,因此血尿酸水平与多种心血管疾病密切相关.近年来,越来越多的研究表明,血尿酸水平升高和心房颤动的发生风险密切相关,其可能机制一方面是高尿酸血症可以使高血压、肾功能衰竭等疾病发生风险增加,而后者是心房颤动发生的重要危险因素;另一方面氧化应激和炎性反应参与了心房颤动的发生,这可能是高尿酸血症和心房颤动联系的中间环节.     

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。     

高尿酸血症与心房颤动的研究进展

近年来研究发现高尿酸血症是阵发性心房颤动、持续性心房颤动以及心血管外科手术后心房颤动的危险因素。炎症和氧化应激参与心房颤动的发生、发展,尿酸参与氧化应激和炎症反应,成为高尿酸血症参与心房颤动发生的重要机制。此外,尿酸转运蛋白在细胞内尿酸浓度的调节中发挥关键作用。因此深入研究尿酸水平增高导致心房颤动发生发展的机制,并探索抑制心房颤动发生的关键靶点,进而寻找合适的药物进行干预治疗,具有重要的科学意义。     

心脏瓣膜术后氧化应激水平变化与新发心房颤动的关系

目的探讨心脏瓣膜术后氧化应激水平变化与新发心房颤动的关系。方法连续入选2015年4月至2016年8月于阜外医院拟行心脏瓣膜手术且无心房颤动的患者122例。收集患者术前基线资料,测量术前、术后血浆中氧化应激指标丙二醛加成产物水平,分析其变化与新发心房/ml比(75. 30±2. 86)ng/ml,P<0. 01]。术后新发心房颤动的患者丙二醛加成产物较无新发心房颤动的患者上升更高[分别上升(24. 29±3. 66)ng/ml和(9. 24±1. 80)ng/ml,P<0. 01]。回归分析证实,循环丙二醛加成产物上升与术后新发心房颤动显著相关(OR:1. 04,95%CI:1. 02～1. 07,P<0. 01)。结论心脏瓣膜术后氧化应激水平上升与新发心房颤动显著相关。     

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。     

心房颤动与炎症和氧化应激

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。     

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。     

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。     

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.     

热休克蛋白60与心房颤动的关系

目的探索心房颤动(简称房颤)与氧化应激的关系。方法以住院行心脏换瓣手术的病人作为研究对象,按患者心律分为房颤组(n=22)和对照组(n=20),对照组为窦性心律。所有研究对象的心房肌组织样本,均作病理形态学观察,并用免疫组织化学法检测其热休克蛋白60(HSP60)表达;用乳胶增强免疫比浊法测定其血清C-反应蛋白(CRP)水平。结果房颤病人的心肌细胞肥大与间质纤维化程度都比对照组明显。HSP60表达阳性率房颤组高于对照组(68.2%vs 25.0%),灰度值房颤组低于对照组(157.69±16.00 vs 178.69±28.63)。血清CRP含量房颤组高于对照组(20.72±17.92 mg/L vs 6.80±6.26 mg/L,P均<0.05)。结论氧化应激与房颤关系密切。     

气道阻塞性睡眠障碍与心房颤动的机制与治疗进展

摘要 心房颤动（AF）是临床最常见的心律失常，同时增加了心血管疾病的发病率和死亡率。 气道阻塞性睡眠呼吸暂停（OSA）是一种常见的呼吸系统疾病，它是 AF 发生的独立危险因素。 目前认为 OSA 患者 AF 发生的病理生理机制如下：缺氧，胸腔内压改变，交感神迷走神经失衡，心房重塑，氧化应激，炎症及神经体液因子的激活。研究表明 OSA 能降低 AF 患者药物转律、电转律及导管消融的成功率。持续气道正压通气（CPAP）能有效预防通气障碍、减少交感神经激活和房颤复发的频率。本文揭示了 OSA 与 AF 之间的关系，主要介绍了OSA 在 AF 发生中的生理机制及现有的治疗方案。     

血尿酸与心房颤动研究进展

心房颤动(房颤)是临床上最常见的心律失常之一,同时也增加了心血管疾病和脑卒中的患病风险。既往研究表明氧化应激与房颤的发生发展、预后及复发均存在相关性,尿酸作为一种氧化应激标志物,由于具有安全、廉价及方便的检测特性,它可以更好地帮助临床医师对发生房颤的高危人群进行早期诊断、疗效判断和预后评估,在临床上具有较好的应用前景。     

The relationship between personality, socio-economic factors, acute life stress and the development, spontaneous conversion and recurrences of acute lone atrial fibrillation.

AIMS: The present study was designed to establish the relationship between personality factors, socio-economic factors and acute life stress with development, spontaneous cardioversion and recurrences of acute lone atrial fibrillation. METHODS: The study group consisted of 116 patients with lone atrial fibrillation cardioverted within 48h of the onset of arrhythmia; they underwent a series of cognitive tests to evaluate acute psychological stress and personality type. The socio-economic status and other covariates (alcohol consumption, smoking, and body mass index) were investigated. A control group, age- and sex-matched, was selected and compared. In the logistic regression analysis, the presence of spontaneous conversion to sinus rhythm was used as the dependent variable. Independent variables were indicator variables representing categories of stress, Type A behaviour pattern, coffee consumption and body mass index. Variables considered for logistic analysis were only those with independent prognostic value. RESULTS: Type A behaviour pattern was found in 23 (20%) patients with atrial fibrillation and in 11 (9%) controls (P<0.001). The mean score among patients with atrial fibrillation was 8+/-2.7, while in control subjects it was 5.5+/-2. The mean acute life stress score among patients with atrial fibrillation was 56+/-33, while in controls it was 34+/-27 (P<0.01). Spontaneous conversion of atrial fibrillation to sinus rhythm was observed in 72 patients (63%). In univariate analysis alcohol consumption, income, education and smoking habits did not affect spontaneous conversion. High coffee consumption (OR 0.3 95% CI 0.11-0.49; P<0.008) and high body mass index were associated with a significantly greater risk of atrial fibrillation (OR 1.5 95% CI 1.2-1.7). CONCLUSIONS: Type A behaviour pattern and acute life stress affect the development and spontaneous conversion of atrial fibrillation. Patients with acute stress showed the highest probability of spontaneous conversion followed by patients with Type A behaviour. Other socio-economic factors affect spontaneous conversion and recurrences of lone atrial fibrillation to a lesser extent.     

Structural remodeling in atrial fibrillation

Atrial fibrillation occurs and maintains itself in the context of a morphologically and functionally altered atrial substrate that can be induced by stressors such as underlying diseases (cardiac or noncardiac) or aging. The resultant structural remodeling is a slow process that progressively affects myocytes and the myocardial interstitium, and takes place from as early as the first days of atrial tachyarrhythmia. The left atrium, and particularly its posterior wall, is the location where remodeling is concentrated to the greatest extent. The mechanisms that underlie the remodeling process in atrial fibrillation have not yet been completely elucidated, although experimental and clinical investigations have indicated a number of signaling systems, inflammation, oxidative stress, atrial stretching and ischemia as factors involved in the cascade of events that leads to atrial fibrillation. The aim of this Review is to provide a comprehensive overview of the morphological changes that characterize the fibrillating atrial myocardium at histological and ultrastructural levels, and the established and hypothetical pathogenetic mechanisms involved in structural remodeling. This article also highlights the emerging therapies being developed to prevent progression of atrial fibrillation.