阵发性心房颤动经射频导管消融恢复窦性心律与药物控制心室率对生活质量影响的对比研究

目的比较阵发性心房颤动经射频导管消融恢复窦性心律与药物控制心室率对患者生活质量影响。方法 60例阵发性房颤患者,平均年龄(45．6±15．1)岁,其中30例经肺静脉导管消融治疗恢复窦性心律,其余30例给予β受体拮抗剂和／或钙离子通道拮抗剂和/或洋地黄类药物控制患者的心室率在静息状态下≤80次／min,平均随访时间(10±20)个月,根据SF-36生活质量评价方案对两组患者的生活质量进行评价。结果导管消融恢复窦性心律治疗组患者的生活质量评价积分高于药物控制心室率治疗组(P<0．05)。结论经肺静脉导管消融治疗阵发性心房颤动较药物控制心室率能显著改善患者的生活质量。     

抗心律失常药物治疗心房颤动的现状及研究进展(综述)

心房颤动是临床常见的心律失常。最近几年,房颤因其较高的发病率和死亡率,越来越多地受到人们的重视。目前,抗心律失常药物在转复及维持房颤患者窦性心律方面显得有些力不从心。虽然新的治疗手段如肺静脉消融等已经有所进展,但是对于很多心房颤动患者,药物治疗仍然很重要。这些非药物治疗方法由于其适应证较窄、并发症较高或医疗费用较昂贵等原因只能使部分患者受益;抗心律失常药物(antiarrhythmic drug,AAD)治疗仍有着不可替代的作用。心房颤动的药物治疗包括:(1)恢复和维持窦性心律,常用Ⅰ类和Ⅲ类抗心律失常药;(2)允许心房颤动存在,通过减慢房室结传导控制心室率,常用Ⅱ类、Ⅳ类和洋地黄类药物。     

导管射频消融术治疗心房颤动127例临床分析

【摘要】目的探讨导管射频消融术治疗心房颤动的有效性、安全性及术后复发的相关因素。方法回顾性分析127例心房颤动患者的临床资料,在三维标测系统指导下行环肺静脉消融,观察患者手术远期成功率及有无不良反应,并分析心房颤动术后复发的相关因素。结果127例患者术后12个月进行随访,共94例患者保持窦性心律,33例患者复发,单次消融成功率为74．02％（94／127）。复发患者中11例接受再次消融并成功,两次消融成功率82．68％（105／127）,其中持续性心房颤动成功率为56．52％（13／23）,阵发性心房颤动成功率为88．46％（92／104）。单因素分析显示：心房颤动类型、左房内径、病程、早期复发、体质量指数与心房颤动导管射频消融术后复发相关。多因素Logistic回归分析显示心房颤动类型和左房内径是预测其术后复发的独立危险因素（P〈0．05）。结论导管射频消融术治疗心房颤动具有较好的临床疗效,心房颤动类型、左房内径是心房颤动导管射频消融术后复发的临床预测指标。     

胺碘酮联合氯沙坦治疗房颤的临床研究

目的观察胺碘酮联合氯沙坦治疗心房颤动及维持窦性心律的疗效。方法将66例具有转复窦性心律指征的心房颤动患者随机分为两组,单用胺碘酮治疗组（n=32）和胺碘酮＋氯沙坦治疗组（n=34）,12个月后停用胺碘酮,共随访18个月,观察药物对两组患者窦性心律的维持率及心房重构的影响。结果随访第12月和第18月,窦性心律维持率：胺碘酮＋氯沙坦组均显著高于胺碘酮组（P〈0．05）。胺碘酮＋氯沙坦组转变为永久性心房颤动患者（7例）显著低于单用胺碘酮治疗组（13例）（P〈0．05）。结论胺碘酮联合氯沙坦能提高心房颤动复律后维持窦性心律的疗效。     

胺碘硐与索他洛尔治疗心房颤动的疗效比较分析

心房颤动（房颤）是临床上常见的心律失常，维持窦性心律可以明显提高患者的生活质量和运动耐量。而目前对于房颤转律和维持窦性心律以哪种药物疗效最佳尚有争议，我们于2005年1月-2006年1月对105例房颤患者随机分为胺碘酮组、索他洛尔组与对照组进行疗效对比，现报告如下。     

心房颤动非药物治疗的进展

心房颤动是当今心律失常研究的热点和治疗难点。抗心律失常药物转复房颤的疗效有限,心房颤动的非药物治疗包括外科手术和导管消融及植入式装置。外科手术向微创外科消融发展,但应用仍较局限;导管消融发展很快,随着对心房颤动发病机制研究的深入和环肺静脉线性消融及心房复杂破碎电位消融的开展,导管消融的成功率提高,并发症减少,有望成为心房颤动的一线治疗手段;植入起搏器等装置治疗房颤疗效并不肯定,目前尚不推荐。     

房颤导管消融研究再获新成果

上海市胸科医院刘旭教授等对心房颤动（房颤）及临床导管消融治疗技术策略进行了系统的研究，使环肺静脉消融电隔离成功率明显增加，消融术后严重肺静脉狭窄发生率显著降低，提高了我国房颤导管消融的研究和治疗水平。近日，相关研究成果获得了第八届上海医学科技奖一等奖。     

双极射频消融迷宫术在治疗风湿性心脏瓣膜病合并心房颤动中的疗效观察

目的 探讨风湿性心脏瓣膜病合并心房颤动患者在行瓣膜替换术的同时行双极射频消融迷宫术的疗效.方法 选取风湿性心脏瓣膜病合并心房颤动患者15例(治疗组),在行瓣膜替换术的同时行双极射频消融迷宫术治疗心房颤动.同期随机选择15例仅行心脏瓣膜替换术而未行双极射频消融迷宫术的患者作为对照组.对两组患者的治疗结果进行比较.结果 治疗组15例患者术后全部恢复窦性心律.随访6个月,14例维持窦性心律,1例偶发阵发性心房颤动.对照组13例术中心脏复跳后即为心房颤动心律,2例心脏复跳后为窦性心律,分别在术后1、2 d后转为心房颤动心律,应用胺碘酮均不能恢复窦性心律.两组术后左房内径、左室收缩末期内径、左室舒张末期内径、心胸比率均较术前显著降低(P＜0.01),左室射血分数较术前显著增加(P＜0.05).治疗组术后左房内径及心胸比率显著低于对照组术后[(31.06±2.28)mm比(36.16±2.23)mm,t=11.645,P=0.002;(50±9)%比(56±10)%,t=8.052,P=0.008].结论 风湿性心脏瓣膜病合并心房颤动患者在行瓣膜替换术的同时行双极射频消融迷宫术疗效较好,操作简便,耗时短.     

氯沙坦复合胺碘酮对阵发性心房颤动患者复律及复律后窦性心律维持的影响

目的 探讨氯沙坦复合胺碘酮对阵发性心房颤动患者的复律效果及复律后窦性心律维持的影响.方法 将76例阵发性心房颤动患者按随机数字表法分为对照组(39例,给予胺碘酮治疗)和观察组(37例,给予氯沙坦+胺碘酮治疗),比较两组治疗24h、3d和1周时心房颤动的转复情况.在心房颤动复律后,继续药物治疗并随访观察12个月,评价两组窦性心律的维持效果.结果 对照组治疗24 h、3 d和1周时心房颤动转复率分别为66.7%(26/39)、76.9%(30/39)和84.6%(33/39),观察组分别为67.6%(25/37)、81.1%(30/37)和94.6%(35/37),治疗1周时两组心房颤动转复率比较差异有统计学意义(P<0.05).治疗12个月时,对照组与观察组窦性心律的维持率分别为69.7%(23/33)和88.6%(31/35),左房内径分别为(38.6±1.0)mm和(31.3±9.1)mm,差异均有统计学意义(P<0.05).结论 氯沙坦复合胺碘酮对阵发性心房颤动患者的复律及复律后窦性心律维持均优于单用胺碘酮治疗,可能与氯沙坦抑制肾素-血管紧张素系统,降低心脏负荷,抑制心房电重构及结构重构有关.     

胺碘酮与厄贝沙坦联合治疗阵发性心房颤动的临床疗效观察

目的评价厄贝沙坦和胺碘酮联合治疗阵发性心房颤动维持窦性心律的长期疗效。方法将70例阵发性房颤患者分为胺碘酮组（I组n=36）。胺碘酮＋厄贝沙坦组（Ⅱ组,n=34）,治疗随访时间为2年。研究的一级终点为房颤复发。比较二组治疗后的窦性心律维持率以及治疗前、治疗后6、12 18及24个月的左心房内径。结果治疗12个月后,I组左心房内径大于Ⅱ组（P〈0.05）。治疗10个月后,I组窦性心律的维持率明显低于Ⅱ组（P〈0.05）,试验终点时,I组的窦性心律维持率为55.56%（20/36）。II组为79.41%（27/34）。QT间期延长,2组间差异无统计学意义（P〉0.05）。结论胺碘酮联合厄贝沙坦,治疗阵发性房颤维持窦性心律优于单用胺碘酮,并能抑制左心房的扩大。     

Biatrial pacing--new possibility in the non-pharmacologic treatment of drug-resistant paroxysmal atrial fibrillation

Biatrial pacing seems to be a possible non-pharmacological therapeutic choice in the prevention of drug-refractory, paroxysmal atrial fibrillation. Biatrial pacing using standard right atrial and coronary sinus left atrial pacing shows an antiarrhythmic effect, which mechanism is not well understood. Biatrial pacemaker was implanted in three patients suffering from drug refractory, symptomatic paroxysmal atrial fibrillation (lone and nonvalvular in 2 and in one case, respectively). Interatrial conduction disturbance (P > 120 ms) was found in three case. Bradycardia dependent arrhythmia development was not observed. Left atrial and right atrial premature beats dominated in 2 and in one case, respectively. P-wave duration was decreased by biatrial pacing in every patients. Atrial fibrillation has not been detected in two patients 1 day and 4 weeks after pacemaker implantation (follow up period: 9 and 5 months), however antiarrhythmic drugs has been withdrawn. In the number of left atrial premature beats a marked decrease was observed. Neither biatrial nor standard right atrial pacing nor combined medical and atrial pacing antiarrhythmic therapy were proven to be effective. In Hungary we were the first to implant and apply effectively biatrial pacemaker in the prevention of paroxysmal drug-refractory atrial fibrillation. However better identification the responding patients subgroup with atrial fibrillation is needed.     

射频消融治疗持续性心房颤动的长期疗效对比分析

目的:分析射频消融和抗心律失常药物治疗持续性心房颤动的长期疗效。方法:挑选本院收治的80例持续性心房颤动患者,随机分成观察组、对照组。对照组40例应用抗心律失常药物治疗,观察组40例采用射频消融治疗。对比两组疗效。结果:观察组有效率52.50%,对照组有效率17.50%,有统计学意义(P<0.05)。结论:采用射频消融治疗持续性心房颤动的效果,优于抗心律失常药物。     

伊布利特联合胺碘酮转复持续性房颤的有效性及安全性研究

目的研究伊布利特联合胺碘酮对转复持续性房颤的有效性及安全性。方法选取持续性房颤的患者75例,随机分为研究组(n=39)和对照组(n=36),研究组序贯给予胺碘酮300 mg和伊布利特静脉注射,对照组给予与胺碘酮相同剂量的安慰剂(5%葡萄糖注射液)和伊布利特静脉注射。比较两组的转复率、室性心律失常发生率、f波间期、QT间期和QTc间期的变化。结果研究组与对照组比较,持续性房颤转复成功率为76.9%和58.3%;室性心律失常的发生率分别为1例(2.5%)和17例(47.2%)。结论 (1)静脉应用伊布利特联合胺碘酮对转复持续性房颤的成功率明显优于单独应用伊布利特,联合用药更具有明显的有效性;(2)明显降低了单用伊布利特时室性心律失常的发生率,联合用药提高转复安全性。     

胺碘酮联用缬沙坦治疗阵发性房颤临床疗效观察

目的：观察口服胺碘酮联合应用血管紧张素II受体拮抗剂（ARB）缬沙坦在阵发性心房颤动复律后维持窦律的疗效。方法：将145例阵发性房颤分为胺碘酮组（I组，n=72），胺碘酮加缬沙坦组（Ⅱ组，n=73），疗效观察24个月。结果：治疗6个月后两组左心房内径无显著差异，但12个月后两组有显著差异（p〈0．05），窦性心律维持12个月后有显著差异（p〈0．05）。结论：胺碘酮与缬沙坦联合治疗阵发性房颤维持，窦性心律的疗效优于单用胺碘酮，并能延缓左心房扩大。     

Life-threatening ventricular tachycardia during flecainide treatment for symptomatic atrial fibrillation in a patient with a structural cardiac disorder

A 37-year-old man with symptomatic acute atrial fibrillation and a low-voltage electrocardiogram was treated with flecainide intravenously. Instead of conversion to sinus rhythm, he developed a wide-complex tachycardia suggestive of ventricular tachycardia. The patient recovered following electric cardioversion. First-choice therapy for symptomatic atrial fibrillation of recent onset (duration < 48 hours) is chemical conversion with a class IC antiarrhythmic drug (e.g. flecainide, propafenone). However, in patients with structural heart disorders, these drugs may induce ventricular tachycardia. A low-voltage electrocardiogram is suggestive of left ventricular damage. For these patients, electric cardioversion is a better alternative.     

Drug therapy of atrial fibrillation

The authors summarize the up-to-date knowledge relating to the pharmacological treatment of atrial fibrillation. They emphasize that drug treatment continues to be in the forefront of the therapy of the arrhythmia, which can now be considered to constitute a cardiovascular epidemic. In the era following the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AF-FIRM) trial, the strategy of pharmacological treatment will certainly change: in place of "rhythm control", which in recent decades has been overforced in patients identical with the elderly, cardiac patients with an impaired left ventricular function who were enrolled into AFFIRM, there will be a more frequent use of ventricular "rate control". Naturally, this does not mean that, in certain patient groups, an effort should not be made to restore and maintain the sinus rhythm. In cases involving congestive heart failure and structural heart disease complicated by a depressed left ventricular systolic function, atrial fibrillation is currently treated with antiarrhythmic drugs possessing low proarrhythmic activity that prolong refractory period (Class 3), and with the even safer mortality-reducing beta-receptor blockers. The classical antiarrhythmic drugs (quinidine, procainamide, disopyramide) are being increasingly forced into the background, and the areas of indication of the novel Na(+)-channel blocker antiarrhythmics (propafenone, flecainide) have also narrowed: they are administered only in the event of atrial fibrillation in patients with a structurally intact heart or left ventricular hypertrophy. After a brief survey of the more important aspects of ventricular rate control, and of the drugs available, the research trends aimed at the progression of the pharmacological treatment of atrial fibrillation are outlined. The clinical introduction of procedures based on myocardial gene therapy is now a realistic therapeutic approach as concerns atrial fibrillation too.     

Pathophysiology and clinical management of atrial flatter

The authors review the current knowledge relating to the pathophysiology and treatment of atrial flutter, the most common supraventricular macroreentrant tachycardia. After an account of the historical and epidemiological data, the atrial tachycardia classification system based on the up-to-date North American + European consensus is presented. The main electrophysiological and electrocardiographic features of right atrial isthmusdependent typical and reverse typical flutter are detailed, as are those of the nonisthmus dependent, atypical forms. The electrophysiological connection between the very frequently coexisting atrial flutter and atrial fibrillation, and also the transitional form (flitter), are discussed. Following the clinical presentation, an account is given of the drug and non-pharmacological therapeutic modalities. It is pointed out that the recently-developed drugs with Vaughan Williams class 3 antiarrhythmic action, which block potassium channels and prolong atrial refractory period, are now primarily used (e.g. ibutilide, dofetilide). Effective means of terminating atrial flutter include transthoracic direct-current cardioversion (pretreated with antiarrhythmic = hybrid therapy) and transoesophageal or intraatrial overdrive pacing. It is stressed that the efficiency of prevention of atrial flutter with the antiarrhythmic drugs currently used even today is poor. Accordingly, the optimum mode of treatment of atrial flutter, which is primarily a method of first choice in special cardiac centres, is curative radiofrequency catheter ablation.     

Diagnosis and treatment of haemodynamically significant fetal tachycardia--in 33 cases

INTRODUCTION: Fetal tachycardia may lead to an increased pre- and postnatal morbidity and mortality rate particularly if it is complicated by cardial decompensation and hydrops fetalis. AIM AND METHODS: In this study 33 fetal tachycardia cases diagnosed and treated between 1993 and 2004 in the fetal echocardiography unit of the I. Department of Obstetrics and Gynecology of the Semmelweis University, Budapest are reviewed. The data of postnatal care of the newborns delivered in the author's department from these pregnancies, and the follow up data provided by the National Institute of Cardiology are examined as well. RESULTS: Mean gestational age at diagnosis of fetal tachycardia was 30 weeks (21-41 weeks). The tachyarrhythmias were classified into atrial flutter (n = 8), supraventricular tachycardia (n = 18), arrhythmia absoluta (n = 5), parasystole (n = 1) and brady-tachyarrhythmia (n = 1). Six cases were complicated by hydrops fetalis, 13 cases by cardial dysfunction. Transplacental antiarrhythmic therapy was applied in 22 cases, in 8 cases the newborns were delivered because of advanced gestational age, in 3 cases tachyarrhythmia resolved spontaneously or therapy was not indicated. The drug of first choice for transplacental therapy was digoxin, which was combined with amiodarone or verapamil (n = 10). Transplacental therapy led to cardioversion in 13/22 cases. The outcome of the 33 examined pregnancies was live birth in 27 cases, in utero death in 3 cases and 3 newborns were delivered elsewhere. The postnatal documentation of 24 newborns out of the 27 born in the author's department is available. At the time of birth 15/24 newborns were in sinus rhythm--out of whom 5 developed tachyarrhythmia later during the neonatal period--, 9/24 were tachycardic. Out of the 14 cases of tachyarrhythmia detected in the neonatal period altogether 3 resolved spontaneously, in 7 cases antiarrhythmic therapy was successful, in 4 cases unsuccessful. In 2 of these latter cases electrical cardioversion led to sinus rhythm. Neurological disorder was not detected in any case. In the early postnatal period 2 in utero severely decompensated newborns died. The follow-up data of 10 children is available, the follow-up period ranges between 6 weeks and 5 and a half years. All 5 children with history of supraventricular tachycardia are in sinus rhythm, 3 of them after suspending antiarrhythmic treatment, while the other 2 still on antiarrhythmic medication. Four out of 5 children with history of atrial flutter are in sinus rhythm, 2 of them left antiarrhythmic therapy, and 2 of them still take antiarrhythmic agents after electrical cardioversion. The atrial flutter of a 3 month old child could not be controlled yet permanently, despite several drug combinations applied. CONCLUSIONS: Survival and late prognosis of tachycardic fetuses treated in utero is good. A prospective study of even more cases is required to establish uniform therapeutic guidelines and to provide appropriate follow-up data.