心房颤动的心房重构

心房颤动心房重构是指房颤后心房肌发生电生理、生化、解剖结构和收缩功能上改变(即电重构、生化重构、收缩功能重构、解剖重构),也称为心房心肌病。心房重构在房颤的发生、复发及维持方面起着明显作用,具有重要的临床意义。以下是国内外近几年来的一些研究结果。     

微小RNA-1与心房重构

心房重构在心房颤动(简称房颤)的发生、维持机制中起着关键作用,心房重构包括电重构和结构重构。微小RNA(miRNA)是一类由约22个核苷酸组成的非编码RNA,以mRNA为靶分子,通过切割降解mRNA或者抑制翻译来实现其重要的生物学调节功能。miRNA-1是心脏特异性的和含量最丰富的miRNA,参与了心脏重构的发生、发展。本文拟针对房颤患者miRNA-1与心房重构的关系作一综述。     

风心病房颤患者心房结构重构的研究

[目的]探讨心房颤动(房颤)结构重构的机制及其作用.[方法]通过HE染色和PAS染色观察风湿性心脏病患者心房组织病理改变并用TUNEL 法标记心房肌细胞凋亡PCD指数.[结果]房颤患者心房肌细胞数目减少,结缔组织增生,心肌细胞水肿等,其中房颤时间超过6个月患者变化更明显;房颤患者凋亡指数显著增高并与房颤持续时间成正相关.[结论]房颤患者存在的心房肌组织细胞学重构是房颤的发生和维持的主要原因.     

胺碘酮对心房颤动犬心房结构及基质金属蛋白酶-9表达的影响

目的 观察Ⅲ类抗心律失常药物乙胺碘呋酮(胺碘酮)对长期心房快速起搏诱发心房颤动(房颤)犬心房结构及基质金属蛋白酶-9(MMP-9)表达的影响,探寻胺碘酮对房颤犬心房结构重构的作用机制.方法 20只犬随机分为假手术组(n=6)、对照组(n=7)和胺碘酮组(n=7).对照组和胺碘酮组犬心房快速起搏6周(400次/min),建立房颤犬模型.胺碘酮组犬起搏后口服胺碘酮30 mg/(kg·d),直至起搏结束.超声评价各组犬起搏前后左心房、左心耳结构和功能;测定房颤诱发情况;Masson染色检测心房肌胶原容积分数(CVF);免疫组化法观察心房肌MMP-9蛋白表达情况.结果 胺碘酮能够有效防止心房快速起搏诱发房颤犬左心房、左心耳功能降低,使犬房颤诱发率和平均持续时间显著减少,降低房颤犬心房肌CVF值,有效抑制房颤犬心房肌MMP-9表达增加.结论 胺碘酮能够阻止长期心房快速起搏房颤犬心房结构的改变及心房纤维化,防止房颤犬心房结构重构,减少房颤发生.     

糖尿病NADPH氧化酶相关的氧化应激与房颤

正心房颤动(房颤)是我们目前临床工作中一种非常常见的心律失常,人群的发病率相对较高,约为1%-2%~([1])。房颤状态下心房组织的氧化应激增强,促进心房组织发生结构性重构和电学重构,继而对房颤的产生和持续起着一定作用~([2])。糖尿病是房颤发生的独立性危险因素之一,荟萃分析显示,糖尿病患者并发房颤的几率升高约34%~([3])。然而,糖尿病引起房颤发生的具体机制至今仍然不是十分清楚,糖尿病时机体会产生大量的活性氧(ROS),ROS参与了许多病理生理过程~([4]),可能是两者之间的关键     

糖尿病心房重构的研究进展

心房颤动(房颤)是临床上最常见的心律失常之一,其发生率随年龄增长而增加,可导致脑卒中[1-3]、心力衰竭 (心衰)[4],使患者病死率增加2倍.糖尿病是房颤发生的独立危险因素[5],但其机制尚不明确.心房结构重构、电重构、神经重构可能参与房颤的发生发展.结合本课题组的前期工作,对近年来糖尿病心房重构研究进展综述如下.     

心房颤动的结构重构

心房颤动(房颤)主要特征是心房的电重构和结构重构,这两种现象都具有可逆性,但在持续较长时间后,它们就会出现一定的差异,结构重构是造成上述差异性的主要原因.本文复习近年文献,对房颤结构重构综述如下.     

卡托普利在心房颤动复律后维持窦性心律中的作用及其对左房功能的影响

研究证实，很多心房颤动（房颤）的复发，是心房电重构的结果，而电重构的发生与肾素血管紧张素系统（RAS）激活密切相关。本文观察血管紧张素转换酶抑制剂卡托普利，在房颤转复后抑制RAS激活，长期维持窦性心律的有效性及其对左房功能的影响。     

血管紧张素受体拮抗剂对心房重构影响的研究

心房颤动（AF）是最常见的心律失常之一，研究显示AF是一种自我延续性心律失常，其中的主要机制是AF引起了心房电重构和结构重构。血管紧张素受体拮抗剂（ARB），目前已广泛应用于治疗冠心病、高血压、充血性心力衰竭等疾病，其对心脏血管重构影响的研究已被证实。本文就近年有关ARB对心房重构影响的研究进展概述如下。     

非甾体类抗炎药物对心房颤动的影响

心房纤颤(房颤)是最常见的心律失常之一,由其引起的缺血性脑卒中的发生率占脑卒中总发生率的20%~40%[1]。除器质性心脏病外,充血性心衰、儿茶酚胺的大量分泌都可作为引起房颤的诱因;另一方面,年龄、高血压、糖尿病、甲状腺功能异常、饮酒、慢性炎症可引起心房结构重构及电重构也增加房颤发生风险[2]。其中炎症一直被认为在房颤的发生和发展中发挥着重要作用[3]。因此,推断抗炎治疗     

超声心动图评价左心房重构的应用

目的 左心房重构是心房颤动和心力衰竭等心血管疾病的重要机制,也是疾病进展的主要病理生理学基础。本文主要对超声心动图在早期诊断左心房重构,并对其进行危险分层,及有效评价左心房重构逆转程度等方面的应用进行综述。     

迷走神经对心房电生理特性的调节在犬心房电重构中的变化

目的研究迷走神经对心房电生理特性的调节在心房电重构中的变化。方法成年杂种犬9只,麻醉后分离双侧颈部交感-迷走神经干。给予美托洛尔阻断交感神经的影响。在右心房（RA）、冠状静脉窦（CS）和右心室（RV）放置多极导管。消融希氏束完全阻断房室结并植入右室临时起搏器。通过RA导管进行600次／min的起搏30min构建急性心房电重构模型。在心房电重构前后测量基础状态（无迷走神经刺激）和迷走神经刺激下的心房有效不应期（ERP）和房颤易感窗口（VW）。结果在基础状态下,ERP在心房电重构后明显缩短（P〈0.05）。迷走神经刺激下,ERP在心房电重构后也明显缩短（P〈0.05）。基础状态下,在心房电重构前后均不能诱发房颤（VW接近0）。迷走神经刺激时,房颤易感窗口在心房电重构后明显增大（P〈0.05）。结论短期的心房电重构能够缩短心房的有效不应期。心房电重构伴随着迷走神经对心房电生理特性的调节发生改变,导致迷走神经介导性房颤的易感性增加。     

Risk of Complications of Atrial Fibrillation

Atrial fibrillation is associated with three major risk of complications: thromboembolism, hemodynamic compromise, and arrhythmogenesis. In patients with chronic atrial fibrillation the incidence of embolization is about 5% per year. The risk of embolism and in particular of stroke can be reduced by warfarine anticoagulation. Aspirin is generally less effective than warfarin, although it is probably more effective than placebo. The hemodynamic complications which may occur during atrial fibrillation are mainly due to the loss of effective atrial contraction, the irregular ventricular rhythm, and the possible excessively rapid ventricular rate. Sudden death is a recognized manifestation of Wolff-Parkinson-White syndrome and is considered to be precipitated by atrial fibrillation in the majority of patients. Torsades de pointes is perhaps the most widely recognized proarrhythmia associated with treatment of atrial fibrillation, especially with 1A antiarrhythmic drugs and sotalol. The chronic treatment with type 1C drugs in 3.5%–5% of patients may induce atrial flutter with 1:1 conduction with significant hemodynamic compromise.     

Antiarrhythmic drug therapy of atrial fibrillation: focus on new agents

The precise mechanisms of clinical effect of antiarrhythmic agents and the ideal "molecular targets" against arrhythmias, in particular atrial fibrillation, are poorly understood. Current antiarrhythmic drug development, particularly for drugs expected to be active against atrial fibrillation, has focused on drugs with multiple ionic mechanisms of action, in particular on those that block multiple potassium channels. Investigation of antiarrhythmic agents is complicated by the diversity of animal-disease models studied, by the potential multiple mechanisms of arrhythmias, and by the incompletely understood relationships between risks and benefits of antiarrhythmic drug therapy. Furthermore, rhythm control strategies in large groups of patients with atrial fibrillation have failed to show substantial clinical benefit. Nevertheless, drugs that block multiple potassium channels and appear to have relatively little organ toxicity, such as tedisamil, may represent an important new avenue in the therapeutic approach to highly symptomatic arrhythmias such as atrial fibrillation.     

血压变异性与慢性房颤血栓前状态的关系

目的探讨血压变异性与慢性房颤患者血栓前状态之间的相关性。方法入选对象分为房颤组（NHYA分级心功能正常的慢性房颤46例）和对照组（其他窦性心律患者51例）。对比两组之间24h平均收缩压变异性（24hSSD）和24h平均舒张压变异性（24hDSD）,以及血浆血管性假血友病因子（vWF）、血小板α颗粒膜蛋白-140（GMP-140）、纤维蛋白原和D-二聚体等血栓前状态指标的差异,并对各组血压变异性与血栓前状态的指标进行相关性分析。结果1．房颤组24hSSD和24hDSD均显著高于对照组。2-房颤组vWF和GMP-140均显著高于对照组。两组纤维蛋白原、D-二聚体无显著差异。3．房颤组24hSSD与vWF呈显著正相关（r=0．416,P〈0．05）,与GMP-140无显著相关性;24hDSD与vWF和GMP-140均呈显著正相关（r=0．432,P〈0．05和r=0．378,P〈0．05）;24hSSD、24hDSD与纤维蛋白原或D-二聚体均无显著相关性。4．对照组24hSSD和24hDSD与vWF、GMP-140、纤维蛋白原或D-二聚体均无显著相关性（P〉0．05）。结论血压变异增大的慢性房颤患者血管内皮损害和血小板激活更显著,提示房颤发生血栓性并发症的危险性可能随血压变异性的增大而增加。     

健康体检人群心房颤动发病相关影响因素分析

[目的] 探讨健康体检人群房颤发病的相关影响因素.[方法] 回顾性分析2013年6月至2016年6月来本院进行健康检查的11375例研究对象的临床资料,根据是否发生心房颤动将其分为心房颤动组(n=52)和非心房颤动组(n=11323).比较两组研究对象的临床资料,分析健康体检人群房颤发病的相关影响因素.[结果] 11375例健康体检者共计52例心房颤动患者,其中31例(59.61%)为阵发性心房颤动、16例(30.76%)为持续性心房颤动、5例(9.63%)为永久性心房颤动.心房颤动组年龄、心率均显著大于非心房颤动组,服用降压药物、糖尿病史所占比例显著高于非心房颤动组,心房颤动组体质量指数(BMI)、舒张压(DBP)、收缩压(SBP)与非心房颤动组比较,差异均具有统计学意义(均P<0.05).高心率、高BMI、高DBP、高SBP、卒中史为健康体检人群房颤发病的危险因素(均P<0.05).[结论] 高心率、高BMI、高DBP、高SBP、卒中史为健康体检人群房颤发病的危险因素,应加强对这类患者的监控,做到早发现、早治疗.     

Clinical utility of left atrial strain in predicting atrial fibrillation recurrence after catheter ablation: An up-to-date review

Rhythm control is the core part of the integrated management of atrial fibrillation (AF), especially in the early stages. Despite advances in catheter ablation (CA), the recurrence rate of AF after CA remains high. As a result, stratification and early management of AF recurrence after CA are critical. Currently, predictors of recurrence of AF after CA are mostly based on dysfunction caused by structural remodeling, apart from traditional risk factors. Atrial strain is a recently developed important parameter for detecting the deformability of atrial myocardium during the cardiac cycle prior to atrial remodeling. Although there is only preliminary evidence, atrial strain is still a promising parameter in predicting the recurrence of AF after CA at an early stage. This review focuses on the evaluation of atrial strain, the current applications of atrial strain in assessing atrial function, and predicting the recurrence of AF after CA. We summarize the contents related as follows: (1) CA for rhythm control in AF; (2) Evaluation methods of atrial strain; (3) Atrial strain in the remodeling and reverse remodeling of AF; and (4) Clinical applications of atrial strain in predicting the recurrence of AF after CA. Although there is accumulating evidence on the role of decreased atrial strain in the early prediction of AF recurrence, atrial strain is limited in clinical practice for lacking exact cut-off values and difficulty in distinguishing specific function phases of the atrium. More research is needed in the future to add strength to the early prediction value of atrial strain in AF recurrences.     

经颈静脉肝内门-腔静脉分流术的护理

目的 总结左心房肺静脉前庭电解剖隔离术治疗心房颤动的护理方法。方法对20例行左心房肺静脉前庭电解剖隔离术的心房颤动患者在手术前后实施相关护理措施及出院健康教育，总结护理要点。结果发生术后并发症6例，其中穿刺点血肿4例，尿路感染1例，心包积液1例。在治疗和精心护理后均治愈出院。结论左心房肺静脉前庭电解剖隔离术手术方法复杂、并发症发生率较高且严重，围手术期需要密切护理、及时发现并协助处理各种并发症。     

Novel pharmacological targets for the rhythm control management of atrial fibrillation

Atrial fibrillation (AF) is a growing clinical problem associated with increased morbidity and mortality. Development of safe and effective pharmacological treatments for AF is one of the greatest unmet medical needs facing our society. In spite of significant progress in non-pharmacological AF treatments (largely due to the use of catheter ablation techniques), anti-arrhythmic agents (AADs) remain first line therapy for rhythm control management of AF for most AF patients. When considering efficacy, safety and tolerability, currently available AADs for rhythm control of AF are less than optimal. Ion channel inhibition remains the principal strategy for termination of AF and prevention of its recurrence. Practical clinical experience indicates that multi-ion channel blockers are generally more optimal for rhythm control of AF compared to ion channel-selective blockers. Recent studies suggest that atrial-selective sodium channel block can lead to safe and effective suppression of AF and that concurrent inhibition of potassium ion channels may potentiate this effect. An important limitation of the ion channel block approach for AF treatment is that non-electrical factors (largely structural remodeling) may importantly determine the generation of AF, so that “upstream therapy”, aimed at preventing or reversing structural remodeling, may be required for effective rhythm control management. This review focuses on novel pharmacological targets for the rhythm control management of AF.     

血管紧张素Ⅱ及卡托普利对犬心房肌细胞外向钾通道电流的作用

目的 观察血管紧张素Ⅱ(AngⅡ)及卡托普利对犬心房肌细胞外向钾通道电流的作用,揭示其参与房性心律失常的细胞电生理机制.方法 健康成年杂种犬(普通级)10只,体质量(15-20)k,雌椎不拘,天津利群实验动物服务中心提供.急性分离单个犬心房肌细胞,采用伞细胞膜片钳方法 分别记录Ang Ⅱ及卡托普利灌流前后细胞膜快速延迟整流钾电流(Ikr)、缓慢延迟整流钾电流(Ikr)、超快速延迟整流钾电流(Ikr)及短暂外向钾电流(It0).采用pClamp 7.0 for windows及pClampfit7.0软件测量电流;数据用均数±标准差((-x)±s)表爪;应用SPSS 10.0统计软件进行统汁学分析,用药前后的比较采用自身配财t枪验,以P<0.05为差异有统计学意义.结果 0.5t mol/L Ang Ⅱ可增加,Ikr、Iks,抑制Ito[(19.54±2.41)pA/pF VS.(24.83±2.52)pA/pF,P=0.001;(20.69 4±2.29)pA/pF vs.(25.59±3.42)pA/pF,P=0.0003;(6.34±1.93)pA/pF vs.(3.71±1.50)pAZpF,P=0.001)],对Ikur无明显影响[(19.78±1.22)pA/pF vs.(20.39±1.50)pA/pF,P=0.258];5 mol/L卡托普利对,¨Iks Ikur 及均无明显作用[(19.11±4.91)pA/pF vs.(18.99±4.04)pA/pF,P=O.808;(20.76±2.89)pA/pF vs.(20.27±3.46)pA/pF,P=0.305;(18.50±3.78)pA/pF VS.(18.25±4.02)pA/pF,P=0.704;(7.31±1.99)pA/pF vs.(6.89±2.12)pA/pF,P=0.136)].结论 Ang II通过对外向钾电流的影响促进心房颤动时的心房屯重构,卡托普利作为血管紧张素转换酶抑制剂,可能通过抑制肾素.血管紧张素系统呆改善心房颤动时的心房电重构,对心房颤动有防治作用.