贝那普利联用胺碘酮预防心房颤动复发改善左心房功能临床研究

目的:观察贝那普利在持续性心房颤动复律后维持窦性心律中的作用及其对左心房收缩功能的影响.方法:80例持续性心房颤动(持续超过7日)患者,药物或电复律后随机分为两组,Ⅰ组40例给予胺碘酮0.2 g每日1次;Ⅱ组40例给予贝那普利10 mg每日1次,胺碘酮0.2 g,每日1次;两组均连服6个月.分别于治疗后第1周、2周、1个月、2个月、4个月及6个月复查心电图或动态心电图,观察心房颤动复发情况;复律后次日及6个月后做UCG检查,观察左心房功能变化.结果:共71例完成治疗.随访6个月,心房颤动复发Ⅰ组34%(12/35),Ⅱ组为14%(5/36),两组比较差异有统计学意义(P＜0.05),Ⅱ组复律后次日及治疗6个月后,超声测量左心房内径由(43±12)mm缩小为(35±11)mm,治疗前与治疗6个月后比较差异有统计学意义(P＜0.01),而Ⅰ组上述指标比较差异无统计学意义(P＞0.05).结论:贝那普利加胺碘酮用于持续性心房颤动复律后维持窦性心律,较单用胺碘酮更有效,长期服用贝那普利可逆转左心房扩大,降低左心房压,有利于消除心房颤动复发的基础.     

胺碘酮单用与联合氯沙坦对阵发性心房颤动疗效比较

目的:评价氯沙坦联合胺碘酮对阵发性心房颤动(房颤)的疗效.方法:124例阵发性房颤随机分为Ⅰ组(胺碘酮)、Ⅰ组(胺碘酮+氯沙坦),观察房颤转复率、窦性心律维持率及左心房内径.结果:治疗后7 d房颤转复率Ⅰ组为84.48%,Ⅱ组为94.44%.随访1 a时窦性心律维持率Ⅰ组为70.24%,Ⅱ组为86.48%(P<0.05);左心房内径Ⅰ组为(38.25±1.52)mm,Ⅱ组为(35.12±1.46)mm(P<0.05).结论:氯沙坦联合胺碘酮对阵发性房颤的复律及复律后窦性心律的维持均优于单用胺碘酮,并能抑制左心房扩大.     

缬沙坦与胺碘酮联合对煤矿工人风湿性心脏病持续性心房纤颤转复的临床观察

目的研究煤矿工人风湿性心脏病持续性心房颤动（房颤）应用缬沙坦联合胺碘酮转复窦性心律的维持作用。方法选择住院的准备房颤复律且符合人选标准的风湿性心脏病（风心病）瓣膜置换术后持续性房颤煤矿工人51例。随机分为对照组（26例）和试验组（25例）。对照组给予胺碘酮,试验组给予缬沙坦加胺碘酮。试验起始时间是入选患者转复为窦性心律后,试验终点是转复后12个月。终点事件：症状或无症状性房颤复发。结果试验组窦性心律维持率显著高于对照组（60％与42．3％）。治疗12个月后,试验组左心房内经（LAD）显著小于对照组[（49．3±4．8）mm与（52．3±4．5）min,P〈0．05]。结论LAD是风心病持续房颤复发的危险因素。缬沙坦联合胺碘酮在煤矿工人风心病持续性房颤复律后维持窦性心律的效果优于单用胺碘酮,并能延缓左心房扩大,防止房颤复发。     

血管紧张素Ⅱ受体拮抗剂、胺碘酮联用在心房颤动复律后维持窦性心律的临床观察

目的:观察厄贝沙坦联用胺碘酮在持续性心房颤动转复后维持窦性心律的作用及对左心房功能的影响。方法:入选61例持续性心房颤动(持续超过7d)患者,药物或电复律后随机分为两组,Ⅰ组31例给予胺碘酮0.2g,1次/d;Ⅱ组30例给予厄贝沙坦150mg,1次/d,胺碘酮0.2g,1次/d。分别于治疗后第1周、第2周、1个月、2个月、4个月、6个月、12个月、18个月、24个月复查心电图及动态心电图,观察心房颤动复发情况;复律后次日及6个月、12个月、18个月、24个月做超声心动图检查,观察左心房功能变化。结果:Ⅱ组窦性心律维持率明显高于Ⅰ组,有显著性差异。结论:厄贝沙坦联用胺碘酮在持续性心房颤动转复后维持窦性心律方面,较单用胺碘酮更有效,长期服用厄贝沙坦可逆转左心房扩大,降低左心房压,有利于消除心房颤动复发的基础。     

缬沙坦在心房颤动复律后维持窦性心律中的作用及其对左心房的影响

目的:观察缬纱坦在心房颤动复律后维持窦性心律的有效性及其对左心房功能的影响。方法:66例持续性心房颤动患者恢复窦律后被随机分为2组,I组:复律当日始至6个月给予胺碘酮0.2g,1次/d;II组在胺碘酮治疗的基础上联用缬沙坦80mg,1次/d。结果:60例完成整个试验。6个月随访期间,I组30例中11例心房颤动复发(37%),II组30例中4例心房颤动复发(13%),两组比较P<0.05,差异有统计学意义。心房颤动复律后次日及6个月后对两组患者行心脏超声检查,前后比较提示缬沙坦治疗可使左房内径明显缩小,左房压力较治疗前减小。结论:用于持续性心房颤动复律后维持窦性心律,缬沙坦与胺碘酮联用较单用胺碘酮更有效。     

厄贝沙坦对胺碘酮治疗慢性心房颤动疗效的影响

目的 观察厄贝沙坦与胺碘酮联合运用在持续性心房颤动复律中的作用。方法持续性心房颤动患者128例,以入选时间顺序按自然数编号,单数者64例（A组）抗凝3周后以胺碘酮0.2g,3次／d,随后0.2g每日一次;双数者64例（B组）开始抗凝3周的同时给予厄贝沙坦150mg每日一次,3周后加用胺碘酮复律（剂量和服法同A组）,观察一个月后转复窦性心律的例数及已复律者在6个月时维持窦性心律的情况。结果 治疗1个月后,A组转窦性心律成功率54.60％,B组转窦性心律成功率76.56％。治疗6个月,A组维持窦性心律占74.29％;B组维持窦性心律占91.84％。B组转复成功率及中期（6月）维持窦性的情况均优于A组（P〈0.05）。结论 复律前短期服用厄贝沙坦能提高胺碘酮对持续性房颤的复律效果;中期使用厄贝沙坦能防止房颤的复发。     

厄贝沙坦与胺碘酮联用在心房颤动复律后维持窦性心律中的作用

目的 观察厄贝沙坦联用胺碘酮在心房颤动(房颤)复律后维持窦性心律的作用及对左房大小的影响.方法 选择住院的房颤复律的非瓣膜性持续性房颤患者83例,随机分为对照组(41例)和试验组(42例).对照组给予胺碘酮,试验组用胺碘酮+厄贝沙坦.入选患者转复为窦性心律后即为试验起始时间,试验终点为转复后12个月.终点事件:症状或无症状房颤首次复发.结果 试验组窦律维持率显著高于对照组(83.3%与61.0%,P＜0.05),而左心房内径(LAD)显著小于对照组[(36.9±1.2) mm 与(34.1±1.4) mm,P＜0.05].结论 厄贝沙坦联用胺碘酮复律后维持窦性心律较单用胺碘酮更有效,并可逆转左房扩大.     

胺碘酮联合血管紧张素Ⅱ受体拮抗剂在心房颤动复律后维持窦性心律临床观察

目的：观察胺碘酮联合应用血管紧张素Ⅱ受体拮抗剂（ARB）在心房颤动复律后维持窦性心律的疗效。方法：85例持续性心房颤动的患者,药物或电复律后随机分为两组,Ⅰ组43例,单纯口服胺碘酮,Ⅱ组42例口服胺碘酮联合应用血管紧张素Ⅱ受体拮抗剂,观察12个月。结果：79例完成治疗。Ⅱ组窦性心律维持率明显高于Ⅰ组,有统计学差异。结论：胺碘酮联合应用血管紧张素Ⅱ受体拮抗剂较单用胺碘酮更有效。     

厄贝沙坦联合胺碘酮治疗持续性心房颤动患者临床疗效观察

目的 对比分析胺碘酮、胺碘酮联合厄贝沙坦在治疗持续性非瓣膜性心房颤动转复后窦性心律维持的时间及对左心房重构的影响.方法 选择因持续性非瓣膜性房颤就诊的患者86例,将患者随机分为两组：A组44例为胺碘酮治疗组;B组42例为厄贝沙坦与胺碘酮联合治疗组.A、B组均服用胺碘酮,第1周600 mg/d,第2周400 mg/d,第3周200 mg/d,持续至试验结束或房颤复发;A组如同时伴有高血压病（〉140/90 mm Hg,1 mm Hg=0.133 kpa）,加用钙离子拮抗剂;B组在此基础上常规加用厄贝沙坦,根据患者血压情况选择（40～80 mg/d）.比较两组疗效.结果 治疗1年后B组（73%）患者窦性心律维持率高于A组（54%）;B组患者左心房内径为（35.1±1.2）mm,优于A组的（37.3±1.6）mm.结论胺碘酮联用厄贝沙坦在治疗持续性非瓣膜性心房颤动转复、窦性心律维持时间、改善心脏功能方面,优于单用胺碘酮.     

缬沙坦联合稳心颗粒防治阵发型房颤的作用研究

目的:比较缬沙坦联合稳心颗粒与胺碘酮对阵发性房颤患者房颤复发预防的效果。方法:87例阵发性房颤,随机分为缬沙坦+稳心颗粒组(A组,n=44)和胺碘酮组(B组,n=43),随访时间为2年,初级终点为房颤复发。比较两组治疗后窦性心律维持率以及6、12、18、24个月的左心房内径。结果:A组窦性心律维持率明显高于B组,B组左心房内径大于A组。结论:缬沙坦联合稳心颗粒治疗阵发性房颤对预防房颤复发优于胺碘硐,并可抑制左心房扩大。     

Atrial Pressure and Experimental Atrial Fibrillation

SIDERIS, D.A., et al .: Atrial Pressure and Experimental Atrial Fibrillation . A possible profibrillatory effect on the atria of an elevated atrial pressure and the site of atrial stimulation was examined. In 15 anesthetized dogs, right or left atrial or biatrial pacing was applied at a high rate (300–600/min) for 5 seconds at double threshold intensity under a wide range of atrial pressures achieved by venous or arterial transfusion or bleeding. Induction of atrial fibrillation in 236 of 1,971 pacing runs was associated with a significantly higher (P < 0.001) atrial pressure (21.6 ± 12.2 mmHg, mean ± SD) than maintenance of sinus rhythm (16.8 ± 11.1 mmHg in 1,735 of 1,971 pacing runs). Stimulation of the right atrium resulted in atrial fibrillation more frequently than left atrial or biatrial stimulation, with biatrial stimulation less frequent than right or left atrial stimulation. The induction of atrial fibrillation was related to the atrial pressure and to the site of stimulation but not to the pacing rate or the prepacing heart rate. The prepacing heart rate, associated with failure to induce sustained atrial fibrillation, was higher than that associated with atrial fibrillation in 12 of 15 experiments (significantly in 6) and not significantly lower in 3 of 15. Atrial fibrillation lasting 1 minute or more was more frequently associated with simultaneous stimulation of both atria than of either atrium alone. Thus, an elevated atrial pressure may facilitate the induction of atrial fibrillation. The site of stimulation also plays an important role for both the induction and maintenance of atrial fibrillation in this model.     

Persistent Atrial Standstill with Atrial Inexcitability

Electrophysiologic studies including His bundle recording, atrial, and ventricular stimulation, were performed in three symptomatic patients with persistent atrial standstill of unknown etiology. The rhythm was junctional in two cases and ventricular in one. In two cases, evidence suggestive of associated impairment of the His bundle conduction system was found. The atria were inexcitable at multiple sites and no retrograde conduction to the right atrium could be elicited by ventricular pacing. Follow-up in the three cases, respectively for 48, 42 and 12 months after pacemaker implantation, revealed no return of spontaneous atrial electrical activity.     

Atrial Septal Versus Atrial Appendage Pacing:

HERMIDA, J.-S., et al. : Atrial Septal Versus Atrial Appendage Pacing: Feasibility and Effects on Atrial Conduction, Interatrial Synchronization, and Atrioventricular Sequence. Atrial septal (Se-P) and atrial appendage pacing (Ap-P) were compared in a randomized, controlled study to assess the feasibility, the reliability, and the effects of Se-P on atrial conduction, interatrial synchronization, and the AV sequence. The main baseline characteristics of the patients were comparable in both groups. There was no difference in feasibility or reliability between the two techniques. Compared to Ap-P   (n = 28)   , Se-P   (n = 28)   decreased the P wave duration, left atrial electromechanical delay (LAEMD), and interatrial interval (−1.6% vs   +28%, P < 0.001; −3%   vs   + 30%, P < 0.001; −130%   vs   + 78%, P < 0.001   ); it induced a smaller increase of the right AEMD, a slight reversal of the timing of the atrial systoles and a shortening of the PR interval (−13% vs   + 25%, P < 0.001   ) and of the interval separating atrial systoles from ventricular activation. Finally, the shortening of the PR interval was smaller during high Se-P versus low Se-P. Se-P avoids the undesirable prolongation of the atrial, interatrial, and AV conductions observed during Ap-P. In addition, Se-P creates a slight reversal of the timing of the atrial systoles and induces a shortening of PR interval, the extent of which could depend on the height of the pacing site on the septum. (PACE 2003; 26[Pt. I]:26–35)     

Familial Atrial Standstill with Coexistent Atrial Flutter

A child with familial atrial staudstill and a ventricular pacemaker had syncope due to atrial flutter that was treated bv His-bundle ablation. Bradycardia protection alone may be insufficient in patients with atrial standstill.     

Atrial and Ventricular Pressures in Atrial Flutter

The hemodynamic effects of atrial flutter (AF) are unknown. The purpose of the present study was to investigate the changes in atrial and ventricular pressures after induction of AF. In 23 patients with paroxysmal AF (age 59 ± 9 years), a hemodynamic study was performed both during sinus rhythm and after induction of the tachyarrhythmia. During AF, 13 patients showed a fixed 2:1 AV conduction and 10 patients showed variable conduction. Mean right and left atrial pressures increased (P < 0.001) and right and left ventricular end-diastolic pressures decreased (P < 0.001) after induction of AF. Roth the increase in mean atrial pressures and the decrease in ventricular end-diastolic pressures were present either in the patients with fixed 2:1 AV (heart rate: 133 ± 15 beats/min) or in those with variable conduction (heart rate 96 ± 15 beats/min), but were more marked in the former. AF produces an impairment of atrial function, as evidenced by the increase in mean atrial pressures and reduction in ventricular end-diastolic pressures in the absence of an elevated heart rate. The mechanisms responsible for the increase in mean atrial pressures are unknown; however, atrial contractions against closed AV valves seem to play an important role.     

Atrial Refractory Periods after Atrial Premature Beats in Patients with Paroxysmal Atrial Fibrillation

To study the effects of an atrial premature beat on atrial refractory periods, we investigated 11 patients (group A) who were the control group, 12 patients suffering from paroxysmal atrial fibrillation (group B), and 10 patients (group C) without arrhythmias but with cardiopathy or cardiomyopathy. At every eighth complex of a constant atrial electrostimulated rhythm a fixed premature extrastimulus was introduced, and effective and functional refractory periods (ERP and FRP) were measured in three different sites of the right atrium, before and after introduction of this extrastimulus. Average ERP and FRP shortened respectively in group A, from 220.28 ± 25.68 msec and 281.17 ± 28.15 msec before extrastimulation, to 190.58 ± 22.74 msec and 245.88 ± 19.86 msec after; in group B, from 219.44 ± 27.38 msec and 284 ± 30.06 msec to 191.66 ± 28.72 msec and 253.23 ± 34.01 msec; and in group C from 229.03 ± 29.65 msec and 289.67 ± 51.62 msec to 194.19 ± 24.6 msec and 237.74 ± 39.59 msec. The average dispersions of ERP and FRP in group A were, respectively: 41.81 ± 21.36 msec and 36.36 ± 18.04 msec before extrastimulation, 28.18 ± 18.14 msec and 35.45 ± 15.72 msec after. In group B: 26.66 ± 19.46 msec and 41.66 ± 16.96 msec versus 45.83 ± 23.91 msec and 45 ± 34.77 msec and in group C: 27 ±11.59 msec and 45 ± 29.15 msec versus 29 ± 18.52 and 27 ± 18.88. It is concluded that an atrial premature beat tends to shorten the dispersion of atrial refractory periods when patients are free of arrhythmias, and to lengthen them when paroxysmal atrial fibrillation are documented.     

Left Atrial Voltage during Atrial Fibrillation in Paroxysmal and Persistent Atrial Fibrillation Patients

Background: Left atrial (LA) endocardial voltage characteristics assessed during atrial fibrillation (AF) have not been previously compared in different AF types. This study was aimed at investigating the LA voltages and volumes in patients with paroxysmal and persistent AF. Methods: LA electroanatomic voltage maps acquired during AF were compared between consecutive patients without major structural heart disease undergoing first catheter ablation for paroxysmal AF (n = 100) or persistent AF (n = 100). The groups were comparable in baseline clinical characteristics. Results: Patients with persistent AF presented with lower median LA voltage (median 0.41, interquartile range [IQR] 0.31–0.51 mV versus median 0.99, IQR 0.47–1.56 mV; P < 0.001), and maximum LA voltage (4.07 ± 1.76 vs 6.42 ± 2.16 mV; P < 0.001). They also had a higher proportion of the LA points exhibiting voltage <0.2 mV (30 ± 20 vs 12 ± 11%; P < 0.001) and voltage 0.2–1.0 mV (55 ± 15 vs 42 ± 19%; P < 0.001). They further displayed higher LA volume/body surface area (75 ± 16 vs 58 ± 13 mL/m²; P < 0.001). In the multivariate regression model, both LA voltage (P < 10^?9) and LA volume (P < 10^?5) were significant determinants of AF type. Conclusion: Patients with persistent AF had significantly lower LA voltage compared with patients with paroxysmal AF even after adjustment for differences in indexed LA volume. LA voltage represents an independent covariate of clinical manifestation of AF. (PACE 2010; 541–548)     

Comparison of Arrhythmogenicity of Atrial Pacing at Several Right Atrial Pacing Sites: Evaluation of Canine Atrial Electrograms During Atrial Pacing and Arrhythmogenicity for Atrial Fibrillation

The changes in the duration of atrial electrograms and the appearance of AF during atrial pacing were compared among five atrial pacing sites in dogs to clarify the arrhythmogenicity of atrial pacing at different atrial pacing sites. In seven mongrel dogs (15–20 kg), the right atrial surface was exposed by right thoracotomy. Atrial electrograms were recorded via bipolar electrodes with an interelectrode distance of 1.2 mm at four right atrial sites: (1) the high right atrium (HRA), (2) the mid-right atrium (MRA), (3) the low right atrium (LRA), and (4) the center of the pectinate muscle (PM). The duration of the atrial electrograms at these four recording sites were measured during atrial pacing with fixed cycle lengths of 200, 150, and 120 ms delivered at five atrial sites: (1) the HRA, (2) the inferior vena cava (IVC), (3) the right atrial appendage (RAA), (4) Bachman's bundle (BB), and (5) the atrial septum (AS). In each dog, the atrial pacing with the 120-ms cycle length was performed five times at each pacing site to evaluate the in-ducibility of AF. When AF was induced, the atrial recording site which first showed a fragmented atrial electrogram was considered the initiation site of the AF. AF was induced during 9 of 35 episodes of atrial pacing at the HRA site, 11 of 35 at the IVC site, 5 of 35 at the RAA site. 3 of 35 at the BB site, and none at the AS site. The initiation site of AF was in the HRA site in 11 of 28 episodes of induced AF, in the MRA site in 9 of 28, and in the LRA site in 8 of 28. At each recording site, the shorter the paced cycle length, the longer the duration of the atrial electrogram regardless of the pacing site. During the atrial pacing with the 200-ms cycle length, the HRA pacing resulted in the shortest duration of the atrial electrogram at each recording site in comparison with the other pacing sites. However, during atrial pacing at the two shorter paced cycle lengths, the duration of the atrial electrogram was shorter during the pacing at the BB or AS sites in comparison with the other three pacing sites, i.e., the HRA, IVC, and RAA sites. These results were the same for all atrial recording sites, but the prolongation of the atrial electrogram was most prominent at the HRA and MRA recording sites, which are most likely initiation sites of the induced AF. In the canine atria, (1) the initiation sites of AF were likely to be the HRA, MRA, or LRA sites in comparison with the PM site; and (2) the atrial pacing at the BB or AS sites was considered less arrhythmogenic for AF than the pacing at the HRA, LRA, or RAA sites.     

Right Atrial Separation Procedure for Eliminating Chronic Atrial Fibrillation Associated with Atrial Septal Defect

Chronic atrial fibrillation (AF) had been documented in a patient with atrial septal defect for 7 years. A right atrial separation procedure was performed for ablation of chronic AF, concomitant with repair of the atrial septal defect, and followed by atrial electrophysiological mapping. A horizontal transectional incision extending to the borders of the atrial septum and the tricuspid annulus was made. Cryolesions of the atrial isthmus between the margin of the upper incision and the tricuspid valve annulus were created at -60†C for 2 minutes at a time. After the operation, the patient had restored normal sinus rhythm during a subsequent follow-up period of 48 months.