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。     

起搏器植入术中测试右心房A波振幅的价值

目的探讨阵发性房颤患者在房颤发作时植入心房电极的价值。方法 96例患者分为两组,84例窦性心律组和12例阵发性房颤组。两组均于窦性心律时或术中房颤发作时测试其右心房A波振幅。房颤组随访术后恢复窦性心律时的右心房A波振幅,并对窦性心律时和房颤发作时的右心房A波振幅进行对比分析。结果窦性心律组术中的右心房A波振幅为(2.6~9.5)m V(3.52±1.44)m V。阵发性房颤组术中房颤时右心房A波振幅为(1.3~3.1)m V(2.78±0.49)m V,两者差异无统计学意义(p0.05)。阵发性房颤组术后转复窦性心律即刻、术后3个月、术后6个月、术后1年测得的心房A波振幅分别为(1.8~4.5)m V(3.08±0.59)m V、(2.8~4.6)m V(3.19±0.49)m V、(2.7~4.8)m V(3.16±0.55)m V、(2.6~5.2)m V(3.13±0.69)m V,它们和房颤发作时测得的心房A波振幅差异无统计学意义(p0.05)。术后窦性心律时心房感知功能及起搏功能均良好。结论阵发性房颤发作时植入右房电极是可行的,右房A波振幅可作为植入的感知参数。     

胺碘酮和毛花甙C转复阵发性心房颤动及心房扑动的临床疗效

目的比较胺碘酮和毛花甙C对阵发性心房颤动(房颤)及心房扑动(房扑)的治疗效果差异。方法选取在该院住院治疗的病发阵发性房颤及房扑的患者72例,随机分为胺碘酮治疗组和毛花甙C治疗组。两组患者分别给予胺碘酮静脉滴注治疗和毛花甙C静脉滴注治疗,比较两组患者给药后的治疗效果及副作用发生情况。结果胺碘酮组复律成功26例(72.2%),毛花甙C治疗组16例(44.4%)。两组比较胺碘酮的治疗有效率较毛花甙C明显偏高(P<0.05)。两组患者给药后心室率均出现明显下降,但两组治疗后差异不显著(P>0.05)。毛花甙C治疗组的不良反应总发生率为25%,较胺碘酮组(8.3%)明显偏高(P<0.05)。结论胺碘酮对治疗阵发性房颤及房扑的成功率高,转复律疗效高于毛花甙C,且治疗安全,副作用少。可作为阵发性房颤和房扑患者复律治疗的一线药物。     

阵发性房颤患者房颤发作时心房电极植入的可行性

目的　探讨阵发性房颤患者在房颤发作时植入心房电极的方法和可靠性。方法　对 10例房颤发作时植入心房电极的患者与同期窦律下植入心房电极患者的植入时间、术中以及术后心房电极的感知、起搏功能进行对比随访观察。结果　阵发房颤患者恢复窦性心律后测定心房感知和起搏功能良好 ,房颤发作时所测得的房颤波振幅与窦性心律时所测心房波振幅有相关性 ,其手术时间和X线曝光时间与窦律下植入起搏器的患者无明显差异。结论　房颤发作时植入心房电极临床上是可行的     

右室起搏电极晚期穿孔拔除1例

患者,男,61岁,体质指数18.5,无糖尿病、冠心病病史.因病态窦房结综合征置入圣犹达公司2402L型单腔心脏起搏器,经左侧锁骨下静脉置入右室被动固定电极导线(圣犹达1646T)于右室心尖部(图1a).术中测得电极参数:阈值0.4V、R波8.1mV、阻抗730Ω.术后30 d复诊时无不适,由程控仪测:阚值0.6V、R波7.9 mV、阻抗390 Ω;心电监护:起搏感知功能正常.     

永久性心脏起搏器植入术中发生心房纤颤时心房电极导线定位经验

目的:研究永久性心脏起搏器植入术中心房纤颤(房颤)发作时以右心房波振幅最大处为右心房电极导线固定位置的可行性。方法:22例房颤发作时植入右心房电极导线的患者术中,测试右心房波振幅,术后随访恢复窦性心律(窦律)时测试右心房波振幅、起搏阈值,2者进行对比分析。结果:房颤心律时,所测得的右心房振幅与转为窦律后所测得的右心房波振幅有较好相关性,2者差异无统计学意义[(2.4±1.0)mv比(2.7±1.2)mv,P>0.05]。房颤时术中右心房波振幅平均(2.4±1.0)mv(1.6～3.7mv)者,在房颤转为窦律后所测定的心房感知和起搏功能良好。结论:在房颤发作时,右心房波振幅作为永久心脏起搏器合适的感知及起搏参数,有一定的临床实用价值。     

左室功能正常的患者阵发性心房颤动或扑动经复律成功后的复发

连续145例阵发性房颤或房扑患者(59±13岁,23～79岁),均经超声心动图证实左室功能正常并适于静脉药物及电复律治疗。阵发性房颤或房扑经心电图证实,其病程短于6个月,发作间歇证实为窦性心律。转复窦律后,抗心律失常药物由经治医师自行决定。初用药物包括氟卡胺、普罗帕酮、索他洛尔、奎尼丁、吡二丙胺。32例复     

静脉注射胺碘酮转复器质性心脏病并阵发性房颤的疗效观察

目的对比胺碘酮和普罗帕酮(心律平)转复器质性心脏病并阵发性心房颤动的疗效.方法将阵发性房颤发作1 h～ 72 h病人8例, 随机分为胺碘酮组40例和心律平组41例,心律平组静脉注射心律平70 mg;胺碘酮组静脉注射胺碘酮150 mg后改为静脉输注150 mg～450 mg,观察其复律情况及药物副反应.结果心律平组阵发性房颤41例,复律成功28例.胺碘酮组阵发性房颤40例,复律成功31例.两组未复律者心室率均有明显控制, 胺碘酮组副反应发生例数少于心律平组.结论静脉应用胺碘酮治疗并发器质性心脏病的快速房颤是有效且较安全的方法.     

45例阵发性房颤患者静脉注射胺碘酮转复的临床分析

目的:评估静脉注射胺碘酮转复阵发性房颤的疗效及安全性。方法:45例阵发性房颤(发作时间≤7 d)患者,均患有器质性心脏病,采用胺碘酮负荷量150 mg,稀释后10 min静脉注射,继之以1 mg/min静脉滴注维持;必要时15 min后重复负荷量150 mg;6 h后以0.5 mg/min维持,转复后逐渐过渡到口服胺碘酮长期维持。结果:24 h内45例心室率均有效控制,37例复律成功,转复成功率82%;转复后出现长RR间期2例,窦性心动过缓2例,无动脉血栓栓塞及尖端扭转性室速发生。结论:静脉注射胺碘酮转复有器质性心脏病合并阵发性房颤患者安全有效,转复治疗中积极防治并发症至关重要。     

伊布利特转复心房颤动和心房扑动的疗效观察

目的观察和比较伊布利特和普罗帕酮终止心房颤动(房颤)/心房扑动(房扑)的疗效及其不良反应。方法 268例发作持续时间<90 d的房颤/房扑患者,随机分组,分别静脉应用(1～2次,每次10 min推注)伊布利特(1.0 mg和1.0 mg)和普罗帕酮(70.0 mg和70.0 mg)。结果伊布利特转复房颤/房扑的成功率分别为67.6%(46/68)和92.4%(61/66),普罗帕酮转复房颤/房扑的成功率分别为32.5%(26/80)和29.6%(16/54)。伊布利特组平均转复时间(27±13)min,转复窦性心律时平均使用量为(1.5±0.4)mg。普罗帕酮组平均转复时间(39±7)min,转复窦性心律时平均使用量为(134.1±6.4)mg。房颤的转复率与左心房直径呈负相关,左心房直径<4.0 cm患者的转复率明显高了左心房直径≥4.0 cm患者的转复率;房扑持续时间可作为房扑终止的预测因子。扑动波周长延长是伊布利特终止房扑的主要特征。结论伊布利特作为一种Ⅲ类的抗心律失常药,在监测的条件下,能迅速、安全、有效地终止房颤/房扑。     

Bipolar atrial sensing thresholds in sinus rhythm and atrial tachyarrhythmias. A comparative analysis in patients with DDDR pacemakers.

Automatic mode switching (AMS) function in dual chamber pacemakers depends on adequate detection of atrial tachyarrhythmias. There are few data on showing how intra-operative atrial signal amplititude during sinus rhythm can predict atrial tachyarrhythmias after pacemaker implantation. In 43 patients undergoing DDDR pacemaker implantation and atrioventricular nodal ablation for the treatment of drug-refractory paroxysmal atrial fibrillation, atrial sensing thresholds during sinus rhythm and during induced atrial tachyarrhythmias (24-48 h after device implantation) were analysed. Five different DDDR pacemaker systems were implanted (Chorus 7034, Ela Medical n = 13; Meta DDDR 1254, Telectronics Pacing Systems n = 12; Vigor DR 1230, Guidant n = 6; Trilogy DR 2364, Pacesetter, n = 2; Kappa DR 401, Medtronic USA n = 10). Every patient received a steroid-eluting, screwing, bipolar atrial lead (Medtronic, Capsure-Fix 4068). The mean P wave amplitude during implantation was 3.91 +/- 1.14 mV. The mean atrial sensing threshold during sinus rhythm and during all modes of induced atrial tachyarrhythmias was 3.35 +/- 1.0 mV, and 1.52 +/- 0.92 mV, respectively (P < 0.001). Atrial fibrillation was induced in 36 patients. The mean sensing threshold during sinus rhythm in this patient group was 3.39 +/- 1.01 mV, the mean sensing threshold during atrial fibrillation was 1.27 +/- 0.56 mV, reflecting a 63% reduction of sensing threshold compared with sinus rhythm (P < 0.001). Atrial flutter was induced in seven patients. The mean sensing threshold during sinus rhythm was 2.92 +/- 1.19 mV, the mean sensing threshold during atrial flutter was 2.79 +/- 1.26 mV, reflecting a reduction of 5% (ns) compared with sinus rhythm. Atrial sensing thresholds during sinus rhythm were significantly correlated with sensing thresholds during atrial tachyarrhythmias (r = 0.44; P < 0.002), but there were significant variations in intra-individual results. The reduction of atrial sensing thresholds between sinus rhythm and induced atrial tachyarrhythmias ranged from 30% to 82%. CONCLUSION: Bipolar atrial sensing thresholds during sinus rhythm are correlated with sensing thresholds during atrial tachyarrhythmias, but there is a large degree of variance in individual patients. A 4:1 to 5:1 atrial sensing safety margin based on sensing threshold during sinus rhythm is a predictor for adequate postoperative detection of atrial tachyarrhythmias and the function of AMS devices.     

Placement of atrial pacing leads during atrial fibrillation. Feasibility and subsequent lead performance.

AIMS: To assess the feasibility of placing permanent atrial pacing leads during atrial fibrillation (AF) and whether such leads function satisfactorily. METHODS AND RESULTS: Prospective study of 17 consecutive patients in whom permanent atrial leads were positioned during an episode of paroxysmal AF. Fluoroscopic position ('figure of 8' or side-to-side movement and anterior position in RAO projection), lead impedance (> 300 but < 1000 ohms) and intracardiac electrogram (average peak to peak amplitude > 1 mV) were used to define an acceptable lead position. At 8 weeks post implant we measured: pulse duration pacing threshold at 5 V; lead impedance at 5 V and 0.5 ms; intracardiac electrogram (EGM) signal amplitude. At the end of the study we reviewed patients to establish whether AF had become permanent. In all patients, follow-up demonstrated satisfactory lead function. All leads had impedances between 300 and 1000 ohms. Pacing thresholds were all < 0.1 ms at 5 V. Mean atrial EGM amplitude seen in sinus rhythm was 3.3 mV (range 1.2-8.4); in patients where all follow-up was in AF in was 2.1 mV (range 1.5-2.5). Nine patients (53%) developed permanent AF. CONCLUSION: Placing atrial leads during AF is feasible using the technique described. However, some patients progress to chronic AF, eliminating the benefits of atrial pacing.     

Paroxysmal A trial Fibrillation:

Classification of Atrial Fibrillation. Introduction: Clinical aspects of paroxysmal atrial fibrillation are heterogeneous. The attacks of atrial fibrillation may differ in their duration frequency and presence and severity of symptoms. Therefore, a proposal for a clinical classification of paroxysmal atrial fibrillation may be helpful. We tested a new classification system in a cohort of 51 consecutive hospitalized patients with paroxysmal atrial fibrillation. Methods and Results: Paroxysmal atrial fibrillation was subdivided into three classes. Class I included a first attack of symptomatic atrial fibrillation either with spontaneous termination (IA) or requiring cardioversion because of poor tolerance (IB). Class II included recurrent attacks in untreated patients within three subgroups: IIA with no symptoms, IIB with < 1 symptomatic attack per 3-month period, and IIC > with 1 symptomatic attack per 3-month period. Class III included recurrent atrial fibrillation unresponsive to one or more antiarrhythmic agents for prevention of recurrences. Class III also consisted of three subgroups: IIIA with no or mild symptoms, IIIB with < 1 symptomatic attack per 3-month period, and IIIC with > 1 symptomatic attack per 3-month period. The criteria for paroxysmal atrial fibrillation (episode > 2 minutes and < 7 days in duration) were fulfilled by 51 patients (29 men, 22 women; mean age 61 ± 14 years). Structural heart disease was present in 31 patients; the atrial fibrillation was idiopathic in 18 (35%). All 51 patients could be classified within the three classes and their subgroups: 14 patients (27%) in Class I, 13 (25%) in Class II, and 24 (47%) in Class III. The incidences of idiopathic atrial fibrillation were 21%, 30%, and 45% of the patients in Classes I, II, and III, respectively. Conclusions: Based on this new classification system, all hospitalized patients with paroxysmal atrial fibrillation could be classified. This classification may be useful to delineate better the clinical subgroups of patients with paroxysmal atrial fibrillation, to characterize better the patient population in future studies, and to improve treatment strategies.     

Optimum lead positioning for recording bipolar atrial electrocardiograms during sinus rhythm and atrial fibrillation

Background: To date, Holter monitoring has been predominantly utilized in the investigation and monitoring of ventricular arrhythmias and myocardial ischemia. Whether currently employed lead configurations are optimal for recording atrial electrocardiograms (ECGs) is unknown. Hypothesis: This study was undertaken to determine which conventional and novel lead configurations are optimal for recording atrial electrical activity during sinus rhythm and atrial fibrillation. Methods: Recordings were performed on eight healthy volunteers in sinus rhythm and four patients in atrial fibrillation. Each subject had 10 ECGs of three bipolar and three augmented unipolar leads recorded during supine rest, while rising to upright, and during standing rest, yielding a total of 60 leads (30 bipolar leads). Each tracing was inspected by two observers, and parameters such as P-wave amplitude and duration, whether the P-wave onset was clearly seen, atrial fibrillatory-wave amplitude, and amplitude of noise during standing were scored. Results: Leads recording interiorly and leftward orientated bipoles provided the best registration of sinus P waves. The Pwave amplitude in the standard bipolar C5 lead (0.12 d? 0.02 mV) was, however, inferior to others such as recordings between Cl and C6 positions (P-wave amplitude 0.16 d? 0.02 mV) or from below the right clavicle to the left upper quadrant of the abdomen (0.16 d? 0.01 mV). Optimal recording of fibrillatory waves was from different leads, such as a bipole from below the left clavicle to a low C1 position (fibrillatory wave amplitude 0.27 d? 0.03 mV). Conclusion: When Holter recordings are performed for the investigation of atrial arrhythmias, nonstandard lead configurations provide superior recording of atrial electrical activity. We advocate the use of electrodes positioned from C1 to C6, from below the left clavicle to a low C1 position, and a vertically orientated lead from the manubium to the twelfth vertebra or the xiphisternum.     

Feasibility of Atrial Sensing Via a Free-Floating Single-Pass Defibrillation Lead for Dual-Chamber Defibrillators

Background: Detection and misclassification of rapidly conducted atrial fibrillation (AF) and marked sinus tachycardia by implantable cardioverter defibrillators (ICD) can result in the delivery of inappropriate therapies. Continuous atrial sensing may improve the differentiation between supraventricular and ventricular tachycardia. The present approach is to implant a separate atrial pacing lead connected to a dual-chamber defibrillator. We hypothesized that a free-floating single-pass defibrillation lead reliably senses the atrial electrical activity. The aim of the study was to assess during implantation the efficacy of a custom-built free-floating single-pass defibrillation lead and to record sinus rhythm (SR), induced AF, and atrial flutter (Afl). Methods: The free-floating single-pass defibrillation lead (Biotronik, Berlin, Germany) had an atrial bipole with 10 mm spacing and a distance between the atrial bipole and the electrode tip of 13.5, 15 or 17-cm. The lead was temporarily implanted in 15 patients during an ICD implantation. Fifteen seconds recordings were made during SR and after the induction of AF and Afl as well as during induced ventricular fibrillation. The amplitude and the time that the amplitude was less than 0.3 mV were assessed. Results: The amplitude during SR (2.1 ± 1.4 mV) was significantly higher compared with the amplitudes for Afl (1.3 ± 0.5 mV; p < 0.02) and AF (0.7 ± 0.5 mV; p < 0.001). Low amplitudes were not observed during SR and rarely during Afl (1.6 ± 3.1%), but they were observed 19.9 ± 15.9% of the time during AF (p < 0.05). The correlation coefficients between SR and AF amplitudes were r = 0.25, between SR and Afl amplitudes r = 0.31, and between AF and Afl amplitudes r = 0.41. During the ventricular fibrillation conversion test 9 patients were in continuous SR. The P-wave amplitude before the induction of ventricular fibrillation was 2.1 ± 1.4 mV. The signal during ventricular fibrillation decreased to 1.1 ± 0.7 mV and increased immediately after the termination of ventricular fibrillation to 1.6 ± 0.8 mV. Conclusions: The recorded unfiltered signals indicate that SR as well as AF and Afl can immediately be detected after the implantation of the new free-floating single-pass defibrillation lead. High signal amplitude during SR did not predict high amplitude during AF or Afl. During induced ventricular fibrillation the P-wave amplitude decreased intermittently.     

VVI起搏术后心房颤动与心钠素和室房逆传的关系

长期心脏起搏的患者,有部分并发心房颤动,尤其是VVI起搏者。本文主要阐述VVI起搏术后心房颤动与血心钠素和室房逆传的关系,为选择适当的起搏器和起搏方式以及临床干预措施提供理论依据,从而减少起搏术后心房颤动的发生。     

Electrophysiological determinants of atrial fibrillation in sinus node dysfunction despite atrial pacing.

AIMS: The effectiveness of atrial pacing in reducing the incidence of atrial fibrillation in patients with sinus node dysfunction is incomplete, and the correlation between electrophysiological atrial properties and the effect of permanent atrial pacing has been poorly investigated. Accordingly, the aim of the present study was to correlate electrophysiological data, in terms of atrial refractoriness, conduction parameters, and propensity to atrial fibrillation induction, and the likelihood of atrial fibrillation after DDD device implantation. METHODS AND RESULTS: The authors reviewed electrophysiological data of 41 patients with sinus node dysfunction (mean age 70 +/- 8 years, who were investigated free of anti-arrhythmic treatments before pacemaker implantation. At a drive cycle length of 600 ms, effective and functional refractory periods, S1-A1 and S2-A2 latency, A1 and A2 width, and latent vulnerability index (effective refractory period [ERP] A2), were measured. Atrial fibrillation induction was tested with up to three extrastimuli in 34 patients. Induction of sustained atrial fibrillation (> 1 min) was considered as the end-point. P-wave duration on the surface ECG in lead II/V1 was also measured. Minimal atrial rate was programmed between 60 and 75 bpm (mean: 64 +/- 4 bpm). After implantation, the patients were followed-up for 28 +/- 17 months, and ECG-documented occurrence of atrial fibrillation was determined. Electrophysiological characteristics of patients with (n = 12) or without (n = 29) paroxysmal atrial fibrillation before implantation were similar. When comparing patients with (n = 11) or without (n = 30) post-pacing atrial fibrillation occurrence, no differences were found in age, underlying heart disease, left atrial size, minimal pacing rate, and follow-up duration. Additionally, between the two former groups, there was no significant difference in terms of effective refractory periods (233 +/- 47 ms vs 239 +/- 25 ms), functional refractory periods (280 +/- 48 ms vs 272 +/- 21 ms), S1-A1 (44 +/- 20 ms vs 37 +/- 13 ms) and S2-A2 latency (77 +/- 28 ms vs 66 +/- 22 ms), and A1 duration (60 +/- 23 ms vs 53 +/- 16 ms). In contrast, in patients with post-pacing atrial fibrillation occurrence, the P wave was more prolonged (116 +/- 22 ms vs 98 +/- 13 ms; P < 0.01), A2 was longer (116 +/- 41 ms vs 87 +/- 27 ms; P < 0.01), effective refractory periods/A2 was lower (2.1 +/- 0.4 cm vs 3.1 +/- 1.4 cm; P < 0.05), and rate of atrial fibrillation induction was higher (8/11 patients vs 8/23 patients; P < 0.05). Electrophysiological characteristics of patients free of post-pacing atrial fibrillation with associated (n = 6) or unassociated (n = 24) paroxysmal atrial fibrillation history before implantation were quite similar. In patients with post-pacing atrial fibrillation with associated (n = 6) or unassociated atrial fibrillation history (n = 5) before implantation, effective refractory periods was statistically different (207 +/- 23 ms vs 264 +/- 46 ms; P < 0.05). Values of effective refractory periods < 220 ms were significantly more frequent in patients with post-pacing atrial fibrillation than in patients without (4/11 patients vs 2/30 patients; P < 0.05). When comparing patients with post-pacing atrial fibrillation with effective refractory periods > or = 220 ms (n = 7) and < 220 ms (n = 4), A2 duration was remarkably prolonged (145 +/- 42 ms vs 90 +/- 11 ms; P < 0.05) in those with effective refractory periods > or = 220 ms. By contrast, between the two groups, effective refractory periods/A2 were identical (2.08 +/- 0.6 cm vs 2.15 +/- 0.3 cm; P = n.s.). CONCLUSION: Prolonged atrial refractoriness, lesser degrees of conduction disturbance and a lower rate of atrial fibrillation induction seem to be predictive of stable sinus rhythm. In contrast, patients with persistence of atrial fibrillation despite pacing have a more abnormal and inhomogeneous atrial substrate, as well as a higher rate of atrial fibrillation induction. Prolonged P wave, shortened refractoriness, or remarkably abnormal conduction disturbances in the presence of prolonged refractoriness limit the effectiveness of standard atrial pacing in atrial fibrillation prevention. Identification of predictive criteria of failure of single-site atrial pacing may be used to consider dual-site atrial pacing in such patients with sinus node dysfunction.     

慢性心房颤动伴晕厥患者心电图回顾性分析

目的 回顾性分析19例慢性心房颤动（房颤）伴晕厥患者的心电图及动态心电图资料，探讨心电图特点，以及与临床转归的重要关系。方法 分析两年来入组患者的心电资料及晕厥发作时的相关心电图。结果 全组19例患者，16例晕厥系房颤伴缓慢心室率引起，平时就有房颤伴二度房室阻滞的心电图表现；2例晕厥为突发室颤所致；1例晕厥原因不明。心率缓慢组脑梗死的发生率明显增多。结论 本文资料显示，房颤伴心室率缓慢的患者有较高的晕厥及脑梗死的发生危险，房颤是室颤发生的重要原因之一，提示房颤不是一种良性心律失常。