双房同步起搏预防和治疗房性快速性心律失常

目的 观察双房同步起搏技术对伴有房间传导阻滞的阵发性快速性房性心律失常的疗效。方法 病态窦房结综合征合并房间传导阻滞的阵发性快速性房性心律失常患者7例，男4例、女3例，年龄58～78岁。其中4例行双房起搏(AAT)，3例行双房右室三腔起搏(DDD)，经穿刺左锁骨下静脉插入右房、右室和冠状静脉窦起搏电极导线，分别用于起搏右房、右室和左房。结果 起搏器及电极导线均顺利植入，未发生任何并发症。冠状静脉窦电极顶端距冠状静脉窦口2．5—3．5cm，P波振幅为1．6—5．5mV、阻抗624—808Ω,、单极起搏阈值0．5—0．7V。随访2—31个月，7例均健在，房性心律失常的临床发作得到明显控制。结论：双房同步起搏技术是房间传导阻滞合并快速房性心律失常的有效预防和治疗方法。     

双房同步起搏治疗房性快速性心律失常

双房起搏是心脏起搏技术的一项最新进展 ,可用于治疗由房间传导阻滞引起的房间折返性房性快速性心律失常。在常规右房、右室双腔起搏的基础上 ,植入冠状窦电极起搏左房 ,建立双房右室三心腔起搏系统 ,实现双房电活动的同步化 ,消除房间传导阻滞和房间折返 ,防治由房间传导阻滞引起的房性快速性心律失常。     

双房同步起搏治疗房性快速性心律失常

双房起搏是心脏起搏技术的一项最新进展,可用于治疗由房间传导阻滞引起的房间折返性房性快速性心律失常。在常规右房、右室双腔起搏的 基础上,植入冠状窦电极起搏左房,建立双房右室三心腔起搏系统,实现双房电活动的同步化,消除房间传导阻滞和房间折返,防治由房间传导阻滞引起的房性快速性心律失常。     

双房同步起搏临床应用中的若干重要问题探讨

双房同步起搏治疗病窦综合征伴房间传导阻滞导致的阵发性心房颤动 (简称房颤 )已应用于临床。通过对 6例安置双房同步起搏器病人术前及术后 1～ 2年的随访来探讨实际应用中若干需要重视的问题。结果 :①术前P波时限和离散度分别在 110～ 15 0ms和 10～ 5 0ms之间 ,双房同步起搏后则分别为 80～ 12 0ms和 10～ 30ms。② 1例房颤发作消失、3例控制、2例无效。③冠状窦电极脱位 3例。结论 :①严格掌握双房同步起搏的指征是确保疗效的关键 ,P波时限和离散度同时延长且延长越多 ,越适于双房同步起搏。②程控为双极AAT模式才能真正实现双房同步 ,合并房室阻滞的病人应选用具有DDTA功能的起搏器。③双房同步起搏体表心电图表现为P波时限短、负向或正负双向 ,PR间期相应缩短。④Medtronic 5 86 6 38M型适配器串联连接双房电极 ,心房电极总阻抗是右房和冠状窦电极阻抗之和 ,不应误认为电极脱位 ,需相应提高起搏电压以维持有效起搏。⑤冠状窦专用电极头端两个弯度必须均进入窦内 ,以深处为佳 ,导管缝扎固定须谨慎。     

左室电极导线的随访观察

行心脏再同步治疗(CRT)101例,随访29.5±19.5个月。左室电极导线脱位4例(占4.0%),其中2例轻度脱位,提高起搏阈值可起搏左室;1例脱至冠状窦,另1例为3根电极导线均脱到右房,此2例均重新置入。左室电极导线起搏阈值术后随时间延长呈逐渐增高的趋势,阻抗的变化趋势是逐渐降低。     

四腔起搏治疗充血性心力衰竭伴房间和室内传导延迟的一年随访

研究四腔起搏治疗充血性心力衰竭 (CHF)伴房间和室内传导阻滞的可行性及有效性。患者男性、70岁 ,反复发作CHF 5年 ,心功能进行性恶化伴房间和室内传导阻滞、阵发心房颤动 (AF)、NYHA分级Ⅳ级。采用Medtronic公司生产普通心房 (45 2 3)、心室电极 (40 2 3)和两根冠状窦电极 (2 188)和法国Ela公司生产的BrioDR 2 12型双腔起搏器。两根冠状窦电极分别经冠状窦进入心后侧静脉和心中静脉开口处 ,起搏左室和左房 ;右房、右室电极置于常规位置。起搏方式 :DDTAV。结果 :术后随访一年 ,不用药亦无房性心律失常发生 ,胸闷、憋气症状明显改善。术后二个月 6min步行距离明显延长 (2 0 0→ 710m)。术后一年各项活动基本不受限。超声心动图 (UCG)提示 :左室各壁运动呈向心性同步收缩。左室舒张末径缩小 (75 .8→ 6 4.4mm) ,左室射血分数增加 (0 .2 9→ 0 .33)。二尖瓣返流量减少(5 .0 6→ 3 .6 2m/s) ,NYHA分级Ⅰ～Ⅱ级。结论 :四心腔起搏治疗严重CHF伴房间和室内传导阻滞患者是可行的、安全的 ,近期疗效显著。双房同步起搏有助于预防AF复发 ,双室同步起搏使心功能明显改善     

双房三腔心脏起搏治疗慢-快综合征

目的　为治疗病窦综合征合并快速性房性心律失常 (慢 -快综合征 ) ,予 5例患者植入三腔(双房同步 )心脏起搏器。方法　经左锁骨下静脉穿刺 ,依次植入冠状静脉窦、右心室、右心房起搏电极导线 ,经测试各参数满意后 ,经 Y型转接器将冠状静脉窦电极与右心房电极组成新的心房双极电极。植入后分别进行 DDD和双房 AAT起搏。结果　随访 1个月～ 1年 ,所有患者症状基本缓解 ,心律失常得到控制 ,除 1例患者冠状窦电极脱位 ,经重新调整固定外 ,未出现其他并发症。结论　证明三腔心脏起搏器不仅能治疗缓慢性心律失常而且能有效地防治因房间传导阻滞引起的快速性房性心律失常 ,该型起搏器植入术有一定的技术难度 ,但合并症少、安全、具有一定的治疗效果。     

双房三腔心脏起搏治疗慢一快综合征

目的 为治疗病窦综合征合并快速性房性心律失常（慢一快综合征），予5例患者植入三腔（双房同步）心脏起搏器。方法 经左锁骨下静脉穿刺，依法植入冠状静脉窦、右心室、右心房起搏电极导线，经测试各参数满意后，经Y型转接器将冠状静脉窦电极与右心房电极组成新的心房双极电极。植入后分别进行DDD和双房AAT起搏。结果 随访1个月～1年，所有患者症状基本缓解，心律失常得到控制，除1例患者冠状窦电极脱位，经重新调整固定外，未出现其他并发症。结论 证明三腔心脏起搏器不仅能治疗缓慢性心律失常而且能有效地防治因房间传导阻滞引起的快速性房性心律失常，该型起搏器植入术有一定的技术难度，但合并症少、安全、具有一定的治疗效果。     

三腔心脏起搏器临床应用研究

目的 为治疗快速性房性心律失常(房性心动过速、心房扑动和心房颤动)，5例患者植入三腔(双房同步)心脏起搏器。方法经左镄骨下静脉穿刺，依次植入冠状静脉窦、右心室、右心房起搏电般导线，测试达到标准后，经Y型转接器将冠状窦电极和右心房电极组成新的心房双极电极，植入后分别进行DDD和双房AAT起搏。结果植入后，DDD起搏方式对2例窦性心动过缓、房性早搏较少的病例疗效显著．改为双房AAT起搏后，余3例均有疗效，其中2例疗效明显．起搏器植入及随访4～6个月中未出现合并症。结论三腔心脏起搏器能有效地防治因房间传导阻滞引起的快速性房性心律失常，该型起搏器植入技术有一定难度，但合并症少，较为安全。     

双房同步起搏技术的临床应用

双房同步起搏是恢复双房电活动同步化的一种新的起搏技术,可防治快速房性心律紊乱。笔者对１７例房内、房间传导阻滞并快速房性心律失常患者进行双房同步起搏治疗,１４例行三腔起搏（ＤＤＤ）、３例行双房起搏（ＡＡＩ）,冠状静脉窦电极均经左锁骨下静脉途径放置。起搏器及电极导线均顺利植入,未发现脱位、穿孔等并发症。冠状静脉窦电极导线顶端电极测定的Ｐ波振幅为５．６９±２．６３（２．４～９．６）ｍＶ、起搏阻抗６５５±１９４．１１（５２０～９６０）Ω、单极起搏阈值０．９２±０．６８（０．４～２．２）Ｖ。冠状静脉窦电极位置较深,则测得起搏阈值较低。随访８．６（３～１５）个月,１例猝死、１６例健在;其预防心房扑动、颤动的显效率达６２．５％、有效率达８１．２５％。结论：双房同步起搏技术是房间传导阻滞合并房性心动过速,心房扑动、颤动的有效治疗和预防方法。     

三腔起搏器的临床应用

应用三腔起搏器治疗病窦以及同时有房室传导异常合并快速房性心律失常患者６例,其中５例为阵发房颤,１例为阵发房扑,心电图示房间阻滞。植入冠状窦电极及普通右房和右室电极,用Ｙ型转换器以右房耳电极为负极,冠状窦电极为正极构成新的双极电极。将４例患者ＤＤＤ起搏器调至ＡＡＴ模式,２例患者为ＤＤＤ模式,房性快速心律失常消失。随访２～６个月,疗效满意。三腔心脏起搏器适用于治疗病窦并有房室传导异常合并房内阻滞的阵发房扑和房颤的患者。     

Biatrial pacing for paroxysmal atrial fibrillation: a randomized prospective study into the suppression of paroxysmal atrial fibrillation using biatrial pacing

OBJECTIVES: The purpose of this study was twofold: to assess whether biatrial pacing is superior to single-site pacing and capable of reducing the frequency of episodes of paroxysmal atrial fibrillation (PAF); and to compare pacing of the proximal coronary sinus (PCS) with the distal coronary sinus (DCS) and the effects of sequential or simultaneous biatrial pacing. BACKGROUND: Interatrial conduction abnormalities have a role in the initiation of PAF. Biatrial pacing alters the site and timing of atrial depolarization and may benefit those with drug-resistant PAF. METHODS: Nineteen patients with PAF who were intolerant of or refractory to medication were studied. All received right atrial (RA) and coronary sinus (CS) leads (either PCS or DCS). For three months the pacemaker was set in sensing mode only. Subsequently each patient completed three-month periods in random order in the following modes: RA pacing, CS pacing, biatrial pacing using inter-atrial delays of 15 and 70 ms. RESULTS: Sixteen patients received a benefit from one or more pacing modes. The greatest reduction in PAF episodes was seen during biatrial pacing, especially with leads sited at the high right atrium (HRA) and distal CS (p = 0.0048). There was no difference for sequential or simultaneous pacing. Three patients derived no benefit. CONCLUSIONS: In selected patients, biatrial pacing causes a significant decrease in atrial fibrillation episodes. Optimal lead sites were at the HRA and DCS. Simultaneous pacing conferred no benefit over sequential pacing.     

High-density mapping of left atrial endocardial activation during sinus rhythm and coronary sinus pacing in patients with paroxysmal atrial fibrillation

INTRODUCTION: This study was designed to record global high-density maps of left atrial endocardial activation during sinus rhythm and coronary sinus pacing. METHOD AND RESULTS: Noncontact mapping of the left atrium was performed in nine patients with paroxysmal atrial fibrillation undergoing pulmonary vein ablation procedures. High-density isopotential and isochronal activation maps were superimposed on three-dimensional reconstructions of left atrial geometry. Mapping was repeated during pacing from sites within the coronary sinus. Earliest left atrial endocardial activation occurred anterior to the right pulmonary veins in seven patients and on the anterosuperior septum in two patients. A line of conduction block was seen in the posterior wall and inferior septum in all patients. The direction of activation in the left atrial myocardium overlying the coronary sinus was different from the electrogram sequence in the coronary sinus catheter in 6 of 9 patients. During coronary sinus pacing, activation entered the left atrium a mean (SD) of 41 (13) ms after the pacing stimulus at a site 12 (10) mm from the endocardium overlying the pacing electrode. Lines of conduction block were present in the posterior wall and inferior septum. CONCLUSION: In patients with paroxysmal atrial fibrillation, lines of conduction block are present in the left atrium during sinus rhythm and coronary sinus pacing. Electrograms recorded in the coronary sinus infrequently correspond to the direction of activation in the overlying left atrial myocardium.     

Deterioration of interatrial conduction in patients with paroxysmal atrial fibrillation: Electroanatomic mapping of the right atrium and coronary sinus

OBJECTIVES: The purpose of this study was to analyze the velocities across the coronary sinus ostium (cross-CSo) and within the coronary sinus (intra-CS) in patients with and without paroxysmal atrial (AF) fibrillation and to estimate the interatrial conduction deterioration area in AF patients. BACKGROUND: Interatrial conduction delay in AF patients has been reported. However, localization of the interatrial conduction delay still is not clear. METHODS: Thirteen patients with paroxysmal AF and 10 control patients with AV nodal reentrant tachycardia or ectopic atrial tachycardia were enrolled in the study. Right atrial and CS mapping were performed using the CARTO electroanatomic mapping system during sinus rhythm and during distal CS pacing. The activation times and spatial distances of cross-CSo and intra-CS were measured between paired sites, from which the activation velocities of cross-CSo and intra-CS were obtained. RESULTS: During sinus rhythm, the activation velocities of cross-CSo in the AF group (1.2 +/- 0.2 m/s) were significantly slower than those in the control group (2.9 +/- 1.6 m/s, P < .05). During distal CS pacing, the cross-CSo velocities of the AF group (1.0 +/- 0.5 m/s) also appeared slower than those in the control group (1.4 +/- 0.2 m/s, P = .07). However, no difference was found in intra-CS activation velocities between the two groups (2.8 +/- 1.9 vs 3.2 +/- 2.2 m/s and 1.5 +/- 0.3 vs 1.4 +/- 0.3 m/s, P > .05 during sinus rhythm and distal CS pacing, respectively). CONCLUSIONS: Interatrial conduction at the posteroparaseptal region across the CS ostium was significantly slower in patients with paroxysmal AF than in control patients, further supporting the link between interatrial conduction deterioration and paroxysmal AF.     

Electrical conduits within the inferior atrial region exhibit preferential roles in interatrial activation

Differences between conduction properties of interatrial conduits and their roles in initiation and maintenance of supraventricular arrhythmias remain unclear. Our objective was to determine details of interatrial activation in inferior atrial region and to correlate intra-atrial and interatrial activation patterns with the site of origin of atrial ectopic activation. In 9 dogs, basket-catheters carrying 64 electrodes were deployed into both the right atrium (RA) and left atrium (LA). A 10-electrode catheter was inserted into the coronary sinus (CS). Activation patterns of the RA, LA, and CS were compared during pacing in the CS, in RA inferoparaseptum posterior to Eustachian ridge-tendon of Todaro (TT), and in inferior RA near the CS ostium (anterior to TT). We found that pacing in proximal and middle CS resulted in a RA breakthrough invariably at the CS ostium, consistent with conduction through a CS-RA connection. Meanwhile, LA breakthrough emerged in inferoposterior region (inferior to mitral annulus), suggesting conduction through a CS-LA connection. While pacing in distal CS, LA breakthrough shifted to middle posterolateral wall. Whereas, the RA was activated by the LA directly through the septum. During pacing in RA inferoparaseptum posterior to TT, the LA was activated directly through the septum at 22 +/- 4 ms. Whereas, during pacing anterior to TT, the LA was activated through both the CS and the septum while earliest activation was delayed by 38 +/- 5 ms. In conclusion, both the interatrial septum and CS musculature form electrical conduits in inferior atrial region in canine. Differences in activation properties between the conduits in inferior interatrial region result in selective interatrial activation patterns during ectopic activation.     

Atrial electrophysiological properties evaluated by right and left atrial pacing in patients with or without atrial fibrillation

Coronary sinus (CS) pacing has been shown to prevent induction of atrial fibrillation (AF) by suppression of the propensity of atrial premature beats at high right atrium (HRA) to induce local conduction delay at the posterior triangle of Koch. However, other mechanisms of CS pacing in preventing induction of AF have not been explored. This study investigated whether a differential conduction delay exists between the HRA and distal CS pacing in patients with paroxysmal AF but not in patients without AF. Nine patients with atrioventricular reentrant tachycardia utilizing a left accessory pathway undergoing catheter ablation were included in this study. Group 1 consisted of 5 patients with clinically documented paroxysmal AF and group 2 4 patients without a history of AF. The effective refractory periods (ERPs) of HRA, distal CS, and four different left atrial sites were determined. The interatrial conduction time and conduction delay between the HRA and distal CS during HRA or distal CS pacing were measured. The interatrial conduction delay (ICD) from the HRA to the distal CS during HRA pacing was significantly longer than that from the distal CS to the HRA during distal CS pacing in patients of group 1. However, the ICD from the HRA to the distal CS during HRA pacing was not significantly longer than that from the distal CS to the HRA during distal CS pacing in group 2 patients. A differential conduction delay between the HRA and the distal CS pacing is present in this specific population of patients with paroxysmal AF but not in patients without AF. The shorter conduction delay during DCS pacing may contribute to the prevention of induction of AF.     

Interatrial transseptal electrical conduction: comparison of patients with atrial fibrillation and normal controls

INTRODUCTION: This study analyzed the electrophysiologic properties of interatrial transseptal electrical conduction at Bachmann's bundle and the ostium of the coronary sinus (CS os) in response to pulmonary vein (PV) stimuli, which mimicked spontaneous ectopy. METHODS AND RESULTS: Forty patients with atrial fibrillation (AF) referred for ablation (15 persistent AF and 25 paroxysmal AF) and 15 control patients were enrolled in the study. During decremental extra-stimulus pacing from the PVs, right atrial activation was analyzed using noncontact mapping and multipolar catheters. The refractory periods and conduction times were calculated for Bachmann's bundle, CS os, and left atrium. The dispersion of refractoriness was calculated as the difference between the refractory periods of Bachmann's bundle and the CS os. The refractory period at Bachmann's bundle was 244 msec in the persistent AF group, 213 msec in the paroxysmal AF group, and 199 msec for controls. The refractory period at the CS os was 220 msec in the persistent AF group, 201 msec in the paroxysmal AF group, and 193 msec for controls. The dispersion of refractoriness was 54 msec in the persistent AF group; this was significantly greater than in paroxysmal AF at 32 msec (P < 0.05) and controls at 13 msec (P < 0.01). During decremental pacing, lengthening of conduction times at both Bachmann's bundle and the CS os were significantly greater in the persistent AF group compared with paroxysmal AF or control groups. A higher dispersion of refractoriness was associated with a higher incidence of inducible AF and a lower rate of ablation success. CONCLUSION: There are differences between the left to right interatrial electrical connections between patients with persistent AF, paroxysmal AF and controls.     

Attenuation of interatrial conduction using right atrial septal catheter ablation

OBJECTIVES: We sought to characterize a method of attenuating interatrial conduction using radiofrequency ablated lesions applied to the right atrial septum. BACKGROUND: Interatrial conduction occurs in specific zones. Recent data suggest that interatrial conduction can be important in triggering and sustaining atrial fibrillation. Therefore, a method for attenuating interatrial conduction may have therapeutic value. METHODS: In 13 healthy pigs, interatrial conduction was evaluated before and after sequential ablation of the right atrial septum, targeting interatrial conduction zones. In six animals, zone 1 (crista terminalis and limbus) was ablated first, followed by ablation of zone 2 (fossa ovalis and coronary sinus ostium). In the other seven animals, the order of ablation was reversed. Electrophysiologic and pathologic findings were correlated. RESULTS: After ablation of zone 1, interatrial conduction was slowed, but there was no block. After ablation of zone 2, conduction was unchanged. After ablation of both zones, complete block was observed in four animals, and there was left atrial quiescence. In the remaining nine animals, incomplete block was observed, with marked conduction slowing or block during sinus rhythm and pacing. Ablation did not adversely affect atrioventricular node conduction, nor did it facilitate sustenance of an atrial arrhythmia. Pathologic analysis revealed that complete interatrial conduction block was associated with confluent ablation of both targeted zones. CONCLUSIONS: Catheter ablation of the right atrial septum attenuated interatrial conduction without disturbing atrioventricular conduction.