控制快速房性心律失常心室率即时疗效临床用药体会

目的　观察并比较静脉注射毛花甙C、艾司洛尔及地尔硫艹卓控制快速房性心律失常心室率的有效性。方法　将2001-03~2003-08中国医学科学院阜外心血管病医院94例快速房性心律失常(房颤、房扑、房速)患者随机分为3组,分别静脉用毛花甙C(29例)、艾司洛尔(30例)和地尔硫(35例)。结果　毛花甙C、艾司洛尔和地尔硫均能有效控制快速房性心律失常的心室率,心室率下降幅度分别为30 .4%、29.3%和27. 6%,总有效率分别为86%、83%和85%,平均用药有效时间分别为( 34. 3±21 .0 )min、( 10. 0±3. 9 )min和( 10 .0±3. 9 )min。结论　艾司洛尔、毛花甙C及地尔硫艹卓均能有效、迅速、安全控制快速房性心律失常的心室率。     

静脉注射地尔硫Zhuo与毛花甙C控制快速房性心律失常心室？…

目的 观察和比较静脉注射地尔硫Ｚｈｕｏ、毛花甙Ｃ控制快速心房颤动（房颤）和心房扑动（房扑）心室率的即时疗效及安全性。方法５４例快速房颤或房扑患,采用随机方式分且,分别静脉注射地尔硫Ｚｈｕｏ、毛花甙Ｃ。结果 地尔硫Ｚｈｕｏ、毛花甙Ｃ组控制房颤或房扑的快速心室总有效率分别为：９４％、７０％,心室率平均下降幅度分别为：３４％、２３％,平均起铲时间分别为：（７．１±４．２）分钟、（３２．８±２２．８）分     

地尔硫(艹卓)在急诊控制心房颤动快速心室率中的应用

目的观察比较静脉注射地尔硫(艹卓)、毛花甙C控制急诊心房颤动快速心室率即时疗效比较及安全性.方法71例急诊心房颤动伴快速心室率患者随机分成2组,分别静脉注射地尔硫(艹卓)或毛花甙C.结果地尔硫(艹卓)、毛花甙C二组控制心房颤动快速心室率总有效率为93.5%,72.9%;心室率平均下降幅度分别为36%、28%;平均起效时间为6.5±3.4min、24±16.5min.地尔硫(艹卓)组有2例出现一过性低血压,可自行恢复.结论静脉注射地尔硫(艹卓)10mg,10～15mg/h维持静脉滴注对心房颤动快速心室率的控制安全、迅速、有效.     

地尔硫在急诊控制心房颤动快速心室率中的应用

目的　观察比较静脉注射地尔硫、毛花甙 C控制急诊心房颤动快速心室率即时疗效比较及安全性。方法　 71例急诊心房颤动伴快速心室率患者随机分成 2组 ,分别静脉注射地尔硫或毛花甙 C。结果　地尔硫、毛花甙 C二组控制心房颤动快速心室率总有效率为 93 .5 % ,72 .9% ;心室率平均下降幅度分别为 3 6%、2 8% ;平均起效时间为 6.5± 3 .4min、2 4± 16.5 min,地尔硫组有 2例出现一过性低血压 ,可自行恢复。结论　静脉注射地尔硫 10 mg,10～ 15 mg/ h维持静脉滴注对心房颤动快速心室率的控制安全、迅速、有效。     

静脉注射艾司洛尔与毛花甙C控制快速房性心律失常心室率即时疗效的观察

目的观察并比较静脉注射艾司洛尔与毛花甙C控制快速房性心律失常心室率的有效性.方法24例快速房性心律失常(房颤、房扑、房速)患者随机分为二组,分别静脉用毛花甙C和艾司洛尔.结果毛花甙C和艾司洛尔控制快速房性心律失常心室率总有效率分别为85%和82%;心室率下降幅度分别为28.9%、24.7%;平均用药有效时间分别为(33.8±22.4)min、(9.8±4.8)min.结论艾司洛尔能有效、迅速、安全控制快速房性心律失常的心室率.     

胺碘酮和毛花甙C转复阵发性心房颤动及 心房扑动疗效的比较

目的对比胺碘酮和毛花甙C治疗阵发性心房颤动(房颤)及心房扑动(房扑)的疗效。方法阵发性房颤及房扑发作1～72h,随机分为胺碘酮组(30例)和毛花甙C组(28例),毛花甙C组静脉注射毛花甙C0.4～0.8mg;胺碘酮组静脉注射胺碘酮150或225mg后改为静脉滴注150～450mg,观察其复律情况,心室率的变化,QT间期及药物副作用。结果毛花甙C组,阵发性房颤24例,复律成功11例,阵发性房扑4例,复律成功2例。胺碘酮组,阵发性房颤25例,复律成功19例,阵发性房扑5例,复律成功3例。两组未复律者心室率均有明显控制,QT间期及副作用差异无显著性意义;毛花甙C组复律平均时间3.5h,胺碘酮组平均复律时间6.5h。结论阵发性房颤及房扑的复律胺碘酮疗效高于毛花甙C,二者心室率的控制及副作用无显著性差别,复律时间毛花甙C短于胺碘酮。     

静脉普罗帕酮和毛花甙C转复阵发性非瓣膜病心房颤动

目的　对比普罗帕酮和毛花甙C在转复阵发性非瓣膜病心房颤动 (房颤 )的作用。方法　房颤发作在 0 5～ 72小时的患者 ,随机分入普罗帕酮组和毛花甙C组。静脉推注毛花甙C 0 4～ 0 6mg或普罗帕酮 70～ 2 10mg ,观察房颤转复情况及心室率的变化。 结果　共 70例患者 ,阵发性房颤病程 ( 2 8 2± 4 2 0 )个月。毛花甙C组 3 4例 ,转复成功 15例 ( 4 4 1% ) ;普罗帕酮组 3 6例 ,转复成功 2 8例 ( 77 8% ) ;P <0 0 1。转复成功时间 :毛花甙C组 ( 86 1± 5 3 5 )分钟 ,普罗帕酮组 ( 4 7 6±3 7 7)分钟 ,P =0 0 5 ;未转复成功者的心室率下降情况 :毛花甙C组由 ( 12 4 6± 2 0 3 )次 /min降至( 93 1± 19 2 )次 /min ,普罗帕酮组由 ( 12 4 0± 3 2 1)次 /min降至 ( 118 6± 2 1 0 )次 /min ,P >0 1。结论　在阵发性房颤的转复中静脉普罗帕酮的成功率高于毛花甙C ,普罗帕酮转复时间较毛花甙C短 ,而毛花甙C在减慢心室率方面优于普罗帕酮。     

静脉地尔硫(卓)治疗老年人快速心室率房颤、房扑和室上速的临床观察

目的　观察静脉地尔硫艹卓 对老年人快速心室率的房颤、房扑及室上速的疗效与安全性。方法　 1 5例患者 (7例房颤、3例房扑、5例室上速 )静脉注射地尔硫艹卓 1 0～ 1 5mg,有反应者继以 1 0～ 1 5mg/ h浓度持续静点 6～ 1 2 h。结果　用药后心室率比用药前基础心率减少 >2 0 % ;转复为窦性心律或心室率 <1 0 0次 / min为治疗有反应 ,本组 1 5例患者 1 2例 (80 % )有反应 ;用药后心室率下降最大效应时间 1 1 min,心室率下降幅度 42± 1 6次 / min。结论　地尔硫艹卓 能安全地应用于快速心室率的房颤或房扑及室上速的老年人 ,并在大多数病人能迅速有效地达到心率的控制和中止室上速的发作 ,而且不会引起或加重心功能障碍。     

老年肺心病心衰伴快速房颤的临床疗效观察

目的:比较老年肺心病中重度心功能衰竭伴快速房颤的患者静脉注射地尔硫卓及西地兰控制心室率的临床疗效和安全性.方法:采用随机单盲方法,将60例老年肺心病合并中重度心功能衰竭伴快速房颤患者分为2组,分别给予地尔硫卓和西地兰静脉注射,观察控制心室率的有效率及临床症状和体征的变化.结果:地尔硫草组控制心室率有效率为93.6%,西...     

医院外使用地尔硫治疗快速心房颤动

目的 评价医院外静脉注射地尔硫(艹卓)治疗快速心房颤动(房颤)或心房扑动(房扑)的疗效。 方法 采用回顾性对照研究。地尔硫(艹卓)治疗组43例来自1999年全美辅助医疗机构的快速房颤或房扑患者,平均心室率≥150次/分,接受9个月地尔硫(艹卓)治疗,平均剂量19.8mg。对照组27例,从1998年起未用地尔硫(艹卓)治疗。剔除气管插管或电击复律史者。以转为窦性心率、心室率≤100次/分或     

Importance of right and left atrial dilation and linear ablation for perpetuation of sustained atrial fibrillation

INTRODUCTION: Atrial dilation associated with increasing atrial pressure plays an apparent role in the development of atrial fibrillation (AF). We characterized a new model of separate and biatrial dilation in the Langendorff-perfused rabbit heart. The aim of this study was to examine if sustained AF in this model (1) would be inducible by separate right atrial (RA) and left atrial (LA) dilation; (2) would be reproducibly inducible at the same pressure level; and (3) could be suppressed by RA, LA, or biatrial ablation. METHODS AND RESULTS: Intra-atrial pressure was increased stepwise in the RA (n = 13), LA (n = 12), or both atria (n = 25) until sustained AF could be induced or a pressure of 20 cm H2O was reached. The stimulation protocol was repeated once in RA and LA dilation (n = 9) and three times in biatrial dilation (n = 7). Then, RA orifices (superior and inferior caval veins, tricuspid valve annulus, and foramen ovale) or LA orifices (pulmonary veins, mitral valve annulus, and foramen ovale) were connected by radiofrequency (RF) lesions. Sustained AF was rendered inducible in 100% of hearts with biatrial dilation, but in only 92% of hearts with RA dilation and 67% with LA dilation. Inducibility of sustained AF was reproducible. Under biatrial dilation, not RA ablation (0/10 hearts; P = NS) but LA ablation (4/11 hearts; P < 0.05) and biatrial ablation (16/21; P < 0.01) reduced the inducibility of sustained AF. CONCLUSION: The inducibility of sustained AF due to increased intra-atrial pressure differs between the RA and LA. LA and biatrial lesions, not RA RF lesions, reduce the ability to perpetuate sustained AF.     

Atrial Electrograms and Activation Sequences in the Transition Between Atrial Fibrillation and Atrial Flutter

Transition Between Atrial Fibrillation and Flutter. Introduction: The eletrophysiologic mechanism of atrial fibrillation (AF) has a wide spectrum, and it seems that some atrial regions are essential for the occurrence of a particular type of AF. We focused on one type of AF: AF associated with typical atrial flutter (AFI), which was right atrial (RA) arrhythmia, and sought to investigate intra-atrial electrograms and activation sequences in the transition between AF and AFL.
Methods and Results: Intra-atrial electrograms and activation sequences in the R.A free wall and the septum were evaluated in the transition between AF and AFL in seven patients without organic heart disease (all men; mean age 57 ± 11 years). In five episodes of the conversion of AFL into AF, the AFL cycle length was shortened (from 211 ± 6 msec in stable AFL to 190 ± 15 msec before the conversion, P, 0.001). Interruption of the AFL wavefront and an abrupt activation sequential change induced by a premature atrial impulse resulted in fractionation and disorganization of the septal electrograms. During sustained AF, septal electrograms were persistently fractionated with disorganized activation sequences. However, the RA free-wall electrograms were organized, and the activation sequence was predominantly craniocaudal rather than caudocranial throughout AF. In 12 episodes of the conversion of AF into AFL, the AF cycle length measured in the RA free wall increased (from 165 ± 26 msec at the onset of AF to 180 ± 24 msec before the conversion, P, 0.001). AFL resumed when fractionated septal electrograms were separated and organized to the caudocranial direction, despite the RA free-wall electrograms remaining discrete and sharp with an isoelectric line.
Conclusion: Changes of the electrogram and activation sequence in the atrial septum played an important role in the transition between AF and AFL.     

Implantable Atrial Defibrillator and Detection of Atrial Flutter

The implantable atrial defibrillator (IAD) is designed to detect and treat atrial fibrillation (AF) with low energy synchronized shocks. A patient with a history of persistent AF was implanted with an IAD after ineffective treatment with procainamide and sotalol. Through four months of follow-up, the IAD performed appropriate detection and treatment of AF. During the fifth month, the patient was put on flecainide in an attempt to minimize the AF recurrence rate. On flecainide the patient experienced typical atrial flutter which required IAD reprogramming for appropriate detection and therapy delivery. This case report examines the optimization of the IAD to detect atrial flutter. Six months of follow-up after optimization the IAD has shown appropriate detection of both atrial flutter and AF. During the entire follow-up period the IAD had appropriate detection of sinus rhythm (no false positive detection, i.e. sinus rhythm as AF).     

The Spatial Dispersion of Atrial Refractoriness and Atrial Fibrillation Vulnerability

The local dispersion of conduction and refractoriness has been considered essential for induction of atrial arrhythmias. This study sought to determine whether a difference of refractoriness and vulnerability for induction of atrial fibrillation between trabeculated and smooth as well as high and low right atrium may contribute to initiation of atrial fibrillation in dogs.In 14 healthy mongrel dogs weighing 22.4 ± 1 kg, closed-chest endocardial programmed stimulation was performed from four distinct right atrial sites. Atrial refractory periods and vulnerability for induction of atrial fibrillation or premature atrial complexes were determined during a basic cycle length of 400 and 300 ms and an increasing pacing current strength.For a pacing cycle length of 300ms, atrial refractory periods were longer on the smooth, as compared to the trabeculated right atrium (102 ± 25 vs. 97 ± 17ms, p < 0.05), whereas for a pacing cycle length of 400ms, there was no significant difference. The duration of the vulnerability zone for induction of atrial fibrillation was longer on the smooth right atrium, for a cycle length of both 400 ms (40 ± 30 vs. 31 ± 22 ms; p < 0.05) and 300 ms (33 ± 25 vs. 23 ± 21 ms; p < 0.01). When comparing high and low right atrium, refractory periods were longer on the the low right atrium, for a cycle length of both 400 ms (111 ± 23 vs. 94 ± 24ms; p < 0.01) and 300 ms (104 ± 20 vs. 96 ± 23ms; p < 0.01). For a pacing cycle length of 300 ms, the duration of the atrial fibrillation vulnerability zone was longer for the high, as compared to the low right atrium (34 ± 22 vs. 22 ± 22, p < 0.01). Seven dogs with easily inducible episodes of atrial fibrillation demonstrated significantly shorter refractory periods as compared to 7 non-vulnerable dogs, regardless of pacing site and current strength.In conclusion, significant differences in refractoriness and vulnerability for induction of atrial fibrillation can be observed in the area of the crista terminalis in healthy dogs. Thus, local anatomic factors may play a role in the initiation of atrial fibrillation.     

Pharmacological Atrial Defibrillation via Temporarily Occluded Coronary Sinus: First clinical experience and implications for an implantable device

The aim of this paper is to report the first experience of pharmacological atrial defibrillation in humans via a temporarily occluded coronary sinus.Patients and methods: In 6 patients (3 women, 3 men; mean age 57.8y, min 31, max 71), with clinical recurrences of atrial fibrillation, an occlusive coronary venogram was carried out in order to establish the origin of the Vein of Marshall. Atrial fibrillation was then induced by atrial pacing in all the patients and after an adequate waiting period to assure that the atrial fibrillation episode was persistent and stable, a bolus of a very low dose of an antiarrhythmic drug was delivered in 3–4 seconds into the temporarily balloon occluded coronary sinus near the orifice of the vein of Marshall. For both the venogram and the pharmacological test a Baim-Turi (USCI-Bard, Billerica MA) or a Vueport (Cardima, Fremont CA) catheter was used.Results and comments: In five patients a single dose of 7mg of propafenone was immediately effective in restoring the sinus rhythm. In the remaining patient 2 doses of 7mg of propafenone failed to interrupt the arrhythmia, which was subsequently interrupted by a bolus of 0.1mg of ibutilide fumarate given after a waiting period of 20 minutes. Retroperfusion of the left atrium could account for these results; in fact the Vein of Marshall has no valvular apparatus in contrast with other coronary sinus tributary veins which are equipped with an uni- or bicuspidal valve.Conclusions: Pharmacological atrial defibrillation with a minimal dose of an antiarrhythmic drug delivered near the orifice of the Vein of Marshall via the temporarily occluded coronary sinus is feasible and effective. This new pharmacological atrial defibrillation can offer interesting opportunities in developing an implantable pharmacological atrial defibrillator.     

Atrial fibrillation: mechanistic insights from biatrial (and triatrial) mapping

Percutaneous radiofrequency ablation of pulmonary vein potentials has been shown to eliminate atrial fibrillation in a subset of patients characterized by frequent and repetitive paroxysms of atrial fibrillation. However, pulmonary vein disconnection has had only limited success at curing patients with persistent atrial fibrillation. In those patients, left atrial substrate modification and linear ablation strategies have had substantially higher success rates. Furthermore, in other patients, elimination of right atrial triggers (superior vena cava) or modification of right atrial substrate has been required for elimination of atrial fibrillation. Finally, the realization that the coronary sinus is a third atrial chamber that can both initiate and maintain atrial fibrillation has provided new understanding to the pathogenesis of atrial fibrillation. From a clinical perspective, only careful anatomic and mapping strategies specifically aimed at each subset of patients with atrial fibrillation will allow for pattern recognition and establish which mechanisms are responsible for initiation and maintenance of atrial fibrillation. Only the latter will allow for increased long-term success rates of ablation of atrial fibrillation.     

Transvenous atrial defibrillation--techniques and clinical applications.

Atrial fibrillation (AF) is the most common arrhythmia requiring treatment. The most desirable therapy may be restoration and maintenance of sinus rhythm. Limitations of the current methods for cardioversion of AF have prompted the development of transvenous atrial defibrillation (TADF) as an alternative and more effective technique for converting AF. Recent advances in the technique of TADF, particularly in the design and configuration of the electrodes, and the use of an optimal biphasic shock waveform have dramatically improved the efficacy of TADF for the termination of all types of AF. The reduction in voltage and energy requirements for cardioversion by TADF may allow the procedure to be performed with little or no sedation and the risk of general anesthesia may be avoided. Both experimental and clinical studies have demonstrated the feasibility, safety, and efficacy of using TADF as a new temporary or "permanent" mode of electrical therapy for AF. It has several potential applications, from acute termination of AF in the electrophysiology laboratory and in patients who have failed to respond to external cardioversion, to its use as an implantable device for treating recurrent AF. This article reviews the current technique and clinical applications of TADF for treatment of AF.     

Heterogeneous changes in electrophysiologic properties in the paroxysmal and chronically fibrillating human atrium

INTRODUCTION: The regional changes in atrial electrophysiologic properties related to atrial fibrillation (AF) in patients with paroxysmal AF (PAF) and chronic AF (CAF) remain unclear. The purpose of this study was to investigate the regional changes in atrial electrophysiology in patients with AF. METHODS AND RESULTS: We evaluated the atrial electrophysiology at different sites (high right atrium, low right atrium [LRA], and distal coronary sinus [DCS]) in 11 patients with CAF, 8 patients with PAF, and 10 controls. Patients with CAF had significantly prolonged interatrial conduction and corrected sinus node recovery time, and shortened atrial effective refractory period (ERP) with loss of rate-related adaptation in the DCS, but had paradoxic prolongation of atrial ERP in the LRA, as compared with patients with PAF and the controls. As a result, the spatial distribution of atrial ERP that was observed in the controls and in patients with PAF was reversed in patients with CAF, without an increase in the dispersion of atrial refractoriness. Patients with PAF showed intermediate changes in atrial conduction times and atrial refractoriness as compared with patients with CAF and controls. CONCLUSION: There was a regional heterogeneity on the changes of atrial electrophysiology in different parts of the atrium, and the "normal" spatial distribution of atrial refractoriness was reversed in patients with CAF. The electrophysiologic changes observed in patients with PAF appear to behave as if in transition from the control state to CAF, suggesting progressive changes in atrial electrophysiologic properties.     

左房异常与心房颤动的关系

目的探讨左房异常与心房颤动发生的关系。方法应用心电图和动态心电图进行,持续性房颤患者为A组,阵发性房颤、房扑患者为B组,仅有心电图P波增宽的患者为C组,A、B、C三组各40例。所有入选患者均经超声心动图检测左房大小,观察患者窦性心律时心电图P波时限、切迹和P波离散度,并分析与房颤发生的关系。结果房颤男性多于女性,年龄大于60岁者94例(占78.3%),三组中86.7%的患者存在器质性心脏病(104例)。心电图P波切迹明显、P波离散度大者快速房颤发生率高;超声心动图检测左房直径大者房颤发生率高,持续性房颤比阵发性房颤患者左房直径大(p<0.05)。结论左房扩大、房内阻滞及P波离散度增大的患者易发生房颤。     

Electrophysiologic Characteristics of a Dilated Atrium in Patients with Paroxysmal Atrial Fibrillation and Atrial Flutter

This study investigated the difference of atrial electrophysiologic characteristics between a normal and dilated atrium and compared them among patients with paroxysmal atrial fibrillation and flutter. Twenty-seven patients with paroxysmal atrial fibrillation and 28 patients with paroxysmal atrial flutter were divided into four subgroups, according to the presence of a normal atrium or bilateral atrial enlargement. Thirty patients without atrial arrhythmia (20 patients with normal atrium and 10 patients with bilateral atrial enlargement) were included in control group. The atrial refractoriness in patients with a dilated atrium was longer than those with normal atrial size. In patients with paroxysmal atrial fibrillation and patients of control group, the P-wave duration and interatrial conduction velocity with or without atrial enlargement were similar. However, in patients with paroxysmal atrial flutter, P-A_PCS (86 ± 10 ms vs. 73 ± 9 ms, p < 0.05) and P-A_DCS (109 ± 9 ms vs. 95 ± 9 ms, p < 0.05) in patients with a dilated atrium were longer than in patients with a normal atrium. The patients with paroxysmal atrial fibrillation or atrial flutter all demonstrated longer P-wave duration and interatrial conduction time than control group. Among the groups with a normal atrium or a dilated atrium, atrial refractoriness in patients with paroxysmal atrial flutter was shorter than that in control group. Moreover, in the patients with a normal atrium, the potential minimal wavelength in control group (6.6 ± 1.7) was longer than that of paroxysmal atrial fibrillation (5.3 ± 1.1), or atrial flutter (5.0 ± 1.2). These findings suggest that atrial electrophysiologic characteristics of a dilated atrium were different from those of normal atrium, and these changes were different between paroxysmal atrial fibrillation and flutter. Multiple factors are considered to be related to the genesis of atrial tachyarrhythmias.