房颤药物治疗现状与展望

心房颤动是临床常见的心律失常之一,其发病率越来越高。自1909年人类认识心房颤动以来,心房颤动的治疗经历了仅着眼于转复心房颤动本身的Ⅰ类抗心律失常药物、直流电转复以及外科迷宫手术等单一治疗,发展到针对心房颤动的病理基础、离子通道、并发症预防等综合治疗。治疗方式、方法、途径与以往比较也发生了巨大变化。虽然近年来房颤的射频消融有了飞速发展,但药物治疗仍然是一线治疗,有时甚至是唯一可行的方法。     

快速心房颤动86例临床诊治分析

目的总结快速心房颤动的临床特点,治疗经验及并发症的预防。方法回顾性分析笔者所在医院2006～2010年经药物治疗快速心房颤动86例临床资料。结果本组86例患者根据不同病因及发病情况,分别选用相应的抗心律失常药物治疗。其中16例抗心律失常治疗后恢复窦性心律,68例患者药物治疗后心室率有效控制,2例未应用抗心律失常药物,心电图恢复正常。结论快速心房颤动可以并发于各种心脏病,亦可见于正常人。临床上根据不同病因及发病情况,进行正确的诊断,合理的治疗,积极预防并发症,能够取得满意的治疗效果。     

心房纤颤的临床药物治疗

心房颤动日益成为临床最常见的快速心律失常之一,由此引发的血液动力学异常、心衰加重、脑及重要脏器栓塞等并发症正成为临床医师经常要面对的难题。如何选择抗心律失常药物以及抗凝、抗栓药物与抗心律失常药物如何联合应用尤为重要,现就心房颤动的特点及药物治疗作简要概述。     

心房颤动的药物治疗研究进展

药物是心房颤动一线治疗的首选。由于传统的抗心律失常药物潜在的致心律失常作用和心外不良反应,使其在心房颤动的治疗中受到限制;抗凝治疗也存在明显的使用限制,因此使得新药的研发显得尤为重要。胺碘酮类似物、选择性心房离子通道阻滞剂、新的抗凝药物及非抗心律失常药物的联合应用,给心房颤动的药物治疗带来了新的希望。现就心房颤动药物治疗进展作简要概述。     

抗心律失常药的治疗矛盾

心律失常的药物治疗并不是一律都有效,常因药物的副作用而出现种种现象。 1.抗心律失常药物对生存的影响 用抗心律失常药长程治疗,尤其是奎尼丁治疗的心房颤动病例,其死亡率增加。心房颤动的率中预防试验表明,用Ⅰ类抗心律失常药(多为奎尼丁或普鲁卡因胺)治疗的心房颤动病例,其死亡率比对照高2.5倍。奎尼Ⅰ组死亡率增加的原因是发生扭转型室速或其他心律失常。也有报导心房颤动病人的预防卒中试验,Ⅰ类抗心律失常药治疗的心衰患者死亡率和心律失常死亡人数比不用抗心律失常药者增加3倍。由此可见,Ⅰ类抗心律失常药对心房颤动的治疗价值很     

抗心律失常药物的新靶点及新药研发

正常心脏功能依赖于适当而规律的心跳速率(心率).当心率太快或太慢时,心脏功能可能发生障碍,伴随着从轻度乃至危及生命并发症的可能.过去,依靠药物治疗心律失常很困难因为缺乏有效性同时又伴有高风险的并发症.一些最新进展为开发新型的、优越的心律失常治疗方法开辟了令人振奋的可能性.文章就药物治疗心房颤动及心室颤动两种常见心律失常的最新进展和前景进行综述.     

钙离子拮抗剂药物维拉帕米对老年阵发性心房颤动疗效的研究

心房颤动是一种常见的心律失常,在老年人中更为常见。房颤严重地危害人类健康．可以引起运动耐力下降、室性心律失常、心动过速性心肌病、血栓栓塞和心衰等并发症。本文通过观察钙离子拮抗剂药物维拉帕米对阵发性房颤患者治疗效果,以探讨维拉帕米在阵发性房颤中的治疗价值。     

心房颤动的抗血栓治疗

心房颤动是临床常见的心律失常,血栓栓塞为其严重并发症.本文主要就房颤并发血栓栓塞的发病机制、危险分层、治疗方法及进展,以及循证医学的证据做详细阐述.     

心房颤动的治疗学与展望

心房颤动是临床最常见的持续性心律失常,其治疗目前仍以药物为基础,近年来随着介入治疗的不断发展,从肺静脉口点消融、节段性消融、环肺静脉口的电隔离到心房基质改良的应用,以及外科改良迷宫术等新技术新方法的应用,已大大提高了心房房颤治疗的成功率并显著减少了并发症。现就心房颤动的治疗学进展进行综述。     

房颤的治疗体会

房颤是一种很常见的心律失常,可分为:缓慢性心房颤动、快速型心房颤动、速型心房颤动;阵发性房颤、持续性房颤、永久性房颤;粗波型房颤、细波型房颤。房颤治疗的目的是恢复心脏正常的节律性搏动,或控制合理的心室速率;预防血栓栓塞并发症的出现等。     

Drug-induced atrial fibrillation

Atrial fibrillation (AF) is a common cardiac arrhythmia that is associated with severe consequences, including symptoms, haemodynamic instability, increased cardiovascular mortality and stroke. While other arrhythmias such as torsades de pointes and sinus bradycardia are more typically thought of as drug induced, AF may also be precipitated by drug therapy, although ascribing causality to drug-associated AF is more difficult than with other drug-induced arrhythmias. Drug-induced AF is more likely to occur in patients with risk factors and co-morbidities that commonly co-exist with AF, such as advanced age, alcohol consumption, family history of AF, hypertension, thyroid dysfunction, sleep apnoea and heart disease. New-onset AF has been associated with cardiovascular drugs such as adenosine, dobutamine and milrinone. In addition, medications such as corticosteroids, ondansetron and antineoplastic agents such as paclitaxel, mitoxantrone and doxorubicin have been reported to induce AF. Whether bisphosphonate drugs are associated with new-onset AF remains controversial and requires further study. The potential contribution of specific drug therapy should be considered when patients present with new-onset AF.     

Risk of atrial fibrillation with high-dose corticosteroids

Atrial fibrillation (AF) is the most common sustained arrhythmia observed in clinical practice. Some drugs have been associated with the onset of AF, but knowledge about the role of drugs in the development of AF is scarce. High-dose corticosteroid therapy has been associated with the development of AF, but this is mainly based on case reports. Therefore, the authors review the available data in the international literature about the cause–effect relationship between corticosteroid therapy and the onset of AF.     

Risk of atrial fibrillation with high-dose corticosteroids

Atrial fibrillation (AF) is the most common sustained arrhythmia observed in clinical practice. Some drugs have been associated with the onset of AF, but knowledge about the role of drugs in the development of AF is scarce. High-dose corticosteroid therapy has been associated with the development of AF, but this is mainly based on case reports. Therefore, the authors review the available data in the international literature about the cause-effect relationship between corticosteroid therapy and the onset of AF.     

Update on pharmacologic approaches to prevent thromboembolism in atrial fibrillation: are thrombin and factor Xa inhibitors the ultimate answer?

Atrial fibrillation (AF) is the most common clinically relevant cardiac arrhythmia. Prevalence and incidence rates are rising with the advancing population age. A severe complication of untreated AF is thrombus formation in the left atrial appendage with consecutive peripheral thromboembolism. Thus, AF is a major contributor to thromboembolic events, especially in the elderly. Depending on the CHADS2 score for thromboembolic events that takes into account congestive heart failure, hypertension, age, diabetes mellitus and stroke as risk factors, oral anticoagulation therapy with vitamin K antagonists is currently the treatment of choice for the prevention of thromboembolism. However, due to drawbacks of current anticoagulation therapy new substances for oral therapy are currently evaluated in various clinical studies. This article provides an up to date overview of orally active compounds for the future treatment of AF. Emphasis lies on comparison of direct thrombin inhibitors with factor Xa inhibitors that are currently investigated in clinical phase III studies for the treatment of non-valvular AF. The direct thrombin inhibitor dabigatran will be compared with factor Xa inhibitors like rivaroxaban and apixaban. Other promising agents currently investigated in phase II trials such as direct factor Xa inhibitors DU-176b (edoxaban) and YM150, will also be discussed.     

环状RNA对房颤患者的影响及其作用机制研究

心房颤动（房颤）是心内科常见的心律失常,主要原因是心脏传导系统异常,严重者可诱发心力衰竭、心源性休克、卒中及血栓栓塞性疾病而危及生命。房颤的早期诊断和预测一直是困扰临床工作者的重要难题,如何尽早甄别和预测房颤为临床重要任务。近年来,随着分子生物学技术的不断发展,越来越多的研究证实环状RNA能够参与房颤的发生并促进疾病的进展。汇总环状RNA对房颤发病过程的影响及其机制,有望为房颤的预防及分子靶向治疗提供新的见解,为患者争取更大的临床获益。     

房颤的药物治疗进展

房颤（AF）的治疗策略包括节律控制和控制心室率同时联合抗凝治疗。药物治疗经济且效果肯定,仍是现阶段AF治疗的主要方案。本文综述近年AF药物治疗的主要进展。     

Prevention of atrial fibrillation complications with antiarrhythmic drugs: still an unmet need in clinical practice

Atrial fibrillation (AF) is the most common arrhythmia and is associated with substantial cardiovascular morbidity and mortality, with stroke being the most important complication. Present drugs used for the therapy of AF (antiarrhythmic drugs and anticoagulants) have major intrinsic limitations, including moderate efficacy and increased risks of life-threatening proarrhythmic effects and bleeding complications. There is great diversity in the pathophysiological substrate, clinical presentation and prognosis of AF. Therefore, assessing the risk of AF-associated stroke and choosing the most appropriate antithrombotic therapy, selecting in which patient to pursue a rhythm- versus a rate-control approach, and when to consider nonpharmacological therapies, such as catheter ablation, remain difficult decisions in most patients. Antiarrhythmic drugs like dronedarone have the potential to prevent AF-related complications like stroke and provides clinicians with a new option when choosing antiarrhythmic therapy. However, major concerns with dronedarone are its low efficacy for AF and lack of evidence for effectiveness in patients failing other antiarrhythmic agents. New oral anticoagulants like dabigatran have important safety advantages versus traditional vitamin-K antagonists in preventing stroke, but they do not arrest or prevent AF. Thus, there is still a clear unmet need for new and more effective antiarrhythmic drugs that prevent AF-related complications. Hopefully such new drugs will lead to improved patient management in the future.     

心房颤动发病机制及其治疗药物应用评价

心房颤动（AF）是临床常见的心律失常。近几十年来,随着人均寿命增加,AF发病率显著上升,且呈现出随年龄增长而增加的趋势。本综述同顾相关发病机制研究,重点分析各药物在AF治疗中的应用评价。     

ELECTROPHYSIOLOGICAL PROPERTIES OF THE FIBRILLATING ATRIUM: IMPLICATIONS FOR THERAPY

1. Atrial fibrillation (AF) is the most commonly occurring cardiac dysrhythmia and remains a challenge to medical therapy. Although the disorder has been recognized for over 100 years, surprisingly very little is understood about its pathophysiology. Over the past decade, a variety of experimental and animal models of AF have been developed and these have provided insights into the mechanism of AF. 2. The pathophysiology of AF is complex. Atrial fibrillation can be caused either by a single source of very rapid impulses or, in the majority of cases, by multiple random re-entering wavelets. The notion that AF may be initiated by a single rapid firing focus and the perpetuation of AF may be partly dependent on macro re-entry around the natural atrial orifices provides a new potential curative therapy for AF by radiofrequency ablation. 3. Shortening of atrial wavelength, either by slow atrial conduction velocities, short atrial refractory periods or both, seems to predispose to development of intra-atrial re-entry and, thus, AF. The functional mechanism by which anti-arrhythmic drugs terminate AF appears to be by prolonging the wavelength and decreasing the number of re-entry wavelets. These understandings are important for the future development of effective anti-arrhythmic agents against AF. 4. The presence of a short and variable excitable gap during AF may be potentially important for termination of AF by pacing. 5. New insights are being gained into the potential role and mechanism of electrical remodelling of the atrium due to AF. Repeated induction of AF by rapid atrial pacing leads to a shortening of atrial refractoriness with loss of rate adaptation, which favours the induction and maintenance of AF. These electrophysiological changes were assumed to occur during repeated AF and to facilitate the generation of multiple re-entrant wavelets. These data suggest that prompt restoration of sinus rhythm and new novel therapy that prevents or diminishes electrical remodelling may promote maintenance of sinus rhythm after successful cardioversion.     

ELECTRICAL REMODELLING OF CHRONIC ATRIAL FIBRILLATION

1. It is now recognized that atrial fibrillation (AF) is not a benign condition, as it is associated with a 40% increase in mortality and a doubling of the risk of stroke. 2. The development of AF leads to mechanical, electrophysiological and cellular changes in the atria that tend to sustain AF. This process is known as atrial remodelling. 3. The three electrophysiological elements in the atria that initiate and sustain AF are: (i) shortening of the refractory period and an increase in dispersion; (ii) slowing of conduction velocity; and (iii) the presence of triggerin. foci. 4. As AF is a heterogeneous disorder, therapeutic strategies include the use of devices (pacemakers and atrial defibrillators), radiofrequency ablation (focal ablation or the creation of linear lines) and drug therapy that may reverse a remodelle. atrium.