不同起搏方式对人心房压力的影响

目的:32例接受导管射频消融治疗后的阵发性室上性心动过速患者,均无器质性心脏病.分别进行高位右心房(HRA)部位快速右心房起搏(AP)、右心室心尖部(RVA)快速心室起搏(RVP)、HRA+RVA部位房室同时起搏(SAVPHRA+RVA)以及冠状窦远端(CSd)+RVA部位房室同步起搏(SAVPCSd+RVA),起搏周长均为400 ms,持续时间各5 min.分别测量不同起搏方式起搏前后右心房压力.结果:与窦性节律(SR)时比较,AP对心房压力无明显影响[(9.1±4.4):(7.3±3.3)cmH2O,P>0.05];与SR及AP比较,RVP、SAVPHRA+RVA、SAVPCSd+RVA使心房压力升高[(13.5±4.2)、(12.7±4.5)、(14.7±3.8) cmH2O,P<0.01];RVP和SAVPHRA+RVA、SAVPCSd+RVA等不同起搏方式升高心房压力作用基本相当(P>0.05).结论:单纯RVP及SAVP均升高心房压力,作用相当,但单纯RVP使观察心房机械电反馈时结果更加客观,方法更简便,是替代SAVP研究心房机械电反馈的理想方法.     

心房肌急性电重构的临床研究

目的探讨快速心房激动对心房电生理特性的影响.方法以150～200ms起搏周长(PCL)对21例射频消融术后患者右心房进行S1S1刺激诱发心房颤动,心房快速刺激前、后均以400ms周长分别对高位右心房(HRA)、低位右心房(LRA)、希氏束周围(HB)、右心耳(RAA)等多部位进行S1S2扫描,测定心房有效不应期(ERP)、有效不应期空间离散度(ERPd)、右心房内及心房间传导时间(CT)的变化;以350ms、400ms和450ms3个不同周长随机对RAA进行S1S2扫描,观察有效不应期频率自适应性(ERPA)的变化.结果快速心房激动后ERP较刺激前有明显缩短,HRA的ERP[(193.2±25.5)msvs(179.7±23.3)ms,P=0.001、LRA的ERP [(198.0±30.8)msvs(182.0±22.5)ms,P=0.026]、HB的ERP[(195.0±26.6)ms vs(182.0±16.8)ms,P=0.018]、RAA的ERP(194.0±20.1)msvs(180.0±29.0)ms,P=0.014].而ERPd则无明显变化[(25.0±17.8)ms vs(28.0±16.9)ms,P=0.576];3个不同周长下RAA的ERP均较心房快速激动前有显著缩短,S1S1为350ms、400ms和450ms.心房快速激动前后ERP分别为[(186.2±24.4)ms vs(168.7±30.9)ms,P=0.006]、[(194.0±20.1)ms vs(180.0±29.0)ms,P=0.014]和[(191.2±33.1)ms vs(170.0±28.3)ms,P=0.0001];心房快速激动前、后ERP与PCL相关系数分别为(rb=0.998,P=0.041;ra=0.397,P=0.74),心房激动前斜率接近正常0.058,激动后斜率为0.015.房内房间CT无明显变化,HRA-HB[(46.5±12.5)msvs(48.4±12.0)ms,P=0.125]、HB-CSD[(47.0±14.2)ms vs(49.6±14.8)ms,P=0.153].结论快速心房激动使右心房同一周长不同部位、同一部位不同起搏周长下ERP缩短,ERPA下降;ERPd及右心房内房间传导速度无明显改变.快速心房刺激使人心房肌发生电重构,ERP缩短、ERPA下降可能是心房颤动发生、维持和发展的重要原因.     

快速起搏心房对犬心房电生理特性改变的研究

目的:研究心房颤动时心房肌的电生理改变。方法:快速持续起搏犬右心房24h制作房颤模型。比较起搏前(P0)、起搏后6h(P6)、12h(P12)和24h(P24)各时段的血压、心房传导速度和房颤波周长(atrial fibrillation cycle length,AFCL)的变化来分析心房肌的电生理改变。结果:起搏后平均动脉血压在P12[(126.06±7.01)mmHg]和P24时[(118.56±8.26)mmHg]较P0[(138.23±5.42)mmHg]明显下降。起搏24h后,P波时间是(78.91±6.21)ms,PA间期是(94±7.89)ms,与起搏前比较有显著延长(P<0.05)。连续快速起搏右心房在P6、P12和P24时的房颤自发维持的时间分别是5~10s、3~5min和15~20min。在起搏前和起搏后不同时间段,左房AFCL明显短于右房AFCL。右房房颤自发持续时间5~10s和15~20min的AFCL分别是(131.86±5.32)ms和(112.45±5.27)ms,P<0.05;左房房颤自发持续时间5~10s和15~20min的AFCL分别是(99.53±4.96)ms和(84.31±2.84)ms,P<0.05。结论:快速心房起搏建立的房颤模型可引起血压进行性下降、心房传导速度减慢和AFCL缩短。     

卡托普利对慢性实验犬心房电重构的影响

目的　研究卡托普利对长期快速起搏实验犬心房有效不应期 (AERP)和心房电重构的影响。方法　 2 4只犬随机分为 3组 ,起搏组 :实验犬右颈部皮下植入永久起搏器 ,经颈外静脉途径将起搏电极导线置入右心耳 (起搏频率 4 0 0次 /min)。起搏器植入前及起搏 8周后分别行电生理检查 ,将两条4极电极导管经股静脉途径分别送至右心房高侧壁及右心房前壁 ,作为刺激电极和记录电极 ,以 2个基本周长 (S1=30 0、2 0 0ms)分别标测AERP ;起搏加药物组 :起搏器植入及电生理检查同起搏组 ,起搏器植入前 3d至起搏 8周后 ,每日给予卡托普利 5 0mg 2次 /d口服 ;对照组 :实验犬未植入起搏器 ,仅于相应的时间行电生理检查。结果　起搏组 :起搏 8周后较起搏前 ,AERP明显缩短 [S1=30 0ms,(132 5 0±15 81)msvs(115 0 0± 16 0 3)ms,P <0 0 0 1;S1=2 0 0ms,(12 6 2 5± 10 6 1)msvs(110 0 0± 15 11)ms,P <0 0 0 1];起搏加药物组 :起搏 8周后与起搏前比较 ,AERP无明显变化 [S1=30 0ms,(133 75±15 98)msvs(131 2 5± 13 6 7)ms,P >0 0 5 ;S1=2 0 0ms ,(12 8 75± 12 4 6 )msvs(12 7 5 0± 12 82 )ms ,P>0 0 5 ];对照组 :实验 8周前后所测AERP差异无统计学意义 [S1=30 0ms,(131 2 5± 12 4 6 )msvs(135 0 0± 9 2 6     

氯沙坦对心房急性电重构的影响

目的　以地尔硫为对照 ,探讨氯沙坦对心房快速起搏诱发急性电重构的干预作用。方法　 2 1只兔随机分为盐水组、地尔硫组和氯沙坦组。 2F电极导管分别置于高位右心房 (HRA)、低位右心房 (LRA)和希氏束区 (HIS) ,以最快 1∶1起搏频率心房起搏 3h。阻断自主神经后 ,观察各组心房快速起搏前后 ,不同部位心房有效不应期 (AERP)、AERP频率适应性、AERP离散度 (AERPd)及右心房内传导时间变化。结果　 (1)心房快速起搏后 ,盐水组AERP2 0 0 和AERP150 立即缩短 ;起搏 1h达最小值(P <0 0 5 ) ,起搏 0 5h内AERP2 0 0 和AERP150 缩短速率最快 [(30 2± 10 5 )ms/h ,(2 4 1± 9 1)ms/h];地尔硫组和氯沙坦组心房快速起搏后AERP无显著缩短。 (2 )心房快速起搏前 ,盐水组HRA处(AERP2 0 0 -AERP150 ) / 5 0ms为 0 17± 0 0 8,起搏 0 5、1、2、3h后分别为 0 0 8± 0 0 6、0 0 9± 0 0 6、0 0 8± 0 0 4、0 0 9± 0 0 5 ,P <0 0 5 ,提示AERP频率适应性降低 ;地尔硫组和氯沙坦组心房快速起搏前后 ,该值差异无显著性。 (3)盐水组心房快速起搏 2、3h ,AERPd明显增大 (P <0 0 5 )。地尔硫组心房快速起搏 3h ,与起搏前比较 ,AERPd显著增大 (P <0 0 5 )。氯沙坦组心房快速起搏后 ,AERPd无显著增加。     

短联律间期房性期前收缩诱发心房颤动的电生理机制

目的:分析不同部位起源,不同联律间期房性期前收缩对心房有效不应期(ERP)、房内传导时间(CT)及波长(WL)的影响,探讨短联律间期房性期前收缩诱发心房颤动的电生理机制。方法:选自2006-04-2008-02期间25例无器质性心脏病室上性心动过速患者,程控刺激高右房(HRA),冠状窦远端(CSd),测出上述2个部位基础刺激时(500ms)心房ERP及HRA←CSd的CT。保持基础刺激不变,分别给予不同联律间期的S2期前收缩刺激(S1S1不应期+20ms,+70ms,+120ms,+170ms),测出不同期前收缩刺激后心房ERP及HRA←CSd的CT。分别对基础及不同期前收缩刺激后心房ERP,CT及WL的变化以及HRA,CSd上述刺激时各项指标的变化进行分析。结果:联律间期短的期前收缩刺激较之联律间期长者使心房ERP明显缩短(P<0·05),CT明显延长(P<0·05),WL明显缩短(P<0·05),联律间期相同而起源部位不同的房性期前收缩对心房ERP、CT及WL的影响无差别(P>0·05)。结论:短联律间期房性期前收缩可使心房ERP缩短,房内传导时间延长,WL缩短,为心房颤动形成提供了电生理基础。     

冠状静脉窦口起搏对心房激动时间影响及方法学探讨

目的观察冠状静脉窦口起搏对心房激动时间的影响，并探讨该部位起搏的方法学。方法包括两部分，首先对20例射频消融的患者行心内电生理检查，术中分别给予高位右心房（HRA）、冠状静脉窦口（CS9-10）、左心房游离壁（CS1-2）起搏，记录刺激信号至腔内电图最远A波为心房激动时间；HRA至CS1-2的AA间期作为左、右心房间激动时间差，同时测量体表心电图最长P波时限。第二部分研究在可控弯导丝系统的辅助下将心房主动电极导线固定在冠状静脉窦口，比较冠状静脉窦口起搏与HRA起搏的起搏参数及起搏后体表心电图P波时限。结果冠状静脉窦口起搏时P波时限、心房激动时间及左、右心房激动时间差较窦性心律下、高位右心房及左心房游离壁起搏时均明显缩短。两组患者术中及术后起搏参数差异无统计学意义，冠状静脉窦口起搏患者体表心电图P波宽度明显缩短。结论冠状静脉窦口起搏时心房激动时间明显缩短，左、右心房间激动时间差最短。采用可控弯导丝系统的辅助可实现冠状静脉窦口起搏。     

冠状静脉窦不同部位起搏拖带心动过速对房性心动过速的诊断价值

目的:探讨心动过速时分别在冠状静脉窦近端(CSp)和远端(CSd)快速起搏拖带心动过速的操作方法鉴别房性心动过速(AT)的价值。方法:入选67例室上性心动过速患者,在心动过速时分别以短于心动过速周长10~40 ms的间期起搏CSp和CSd,确认夺获心房后停止起搏。如果心动过速不终止,测量每次起搏停止后的第一个QRS波群起始至第一个自身A波的间期(VA间期),计算两个VA间期差值(DVA)。结果:67例患者平均年龄(41±17)岁,其中15例为AT患者,25例为房室结内折返性心动过速患者,27例为房室折返性心动过速患者(后两类患者为非AT患者)。AT患者的DVA[(79±29)ms]大于非AT患者[(4±2)ms],差异有统计学意义(P<0.01)。所有AT患者的DVA均>10 ms,而非AT患者中无一例DVA>10 ms。结论:在冠状静脉窦不同部位起搏拖带心动过速,计算停止起搏后第一个DVA是一种快速、简单、有效的诊断或除外AT的方法,在使用较少标测电极时更为实用。     

房室结慢径消融对心房电生理性质的影响

目的 慢径消融降低了心房颤动(房颤)的易感性,但具体机制不明.本文旨在探讨消融后心房电生理性质的改变及其具体机制.方法 32例房室结折返性心动过速患者,测量射频消融前后窦性心率及高位右心房、低位右心房、冠状静脉窦近端和远端各部位的有效不应期和易感窗口,以及房室结快径前传不应期的变化.结果 (1)慢径消融前后下列部位的有效不应期的变化分别为:冠状静脉窦近端(21 8.1±21.8)ms,(235.3±23.6)ms,P＜0.0001;冠状静脉窦远端(230.9±21.0)ms,(244.7±25.1)ms,P＜0.01;低位右心房(198.8±26.7)ms,(219.7±28.7)ms,P＜0.005;高位右心房(214.4±35.1)ms,(213.4±37.3)ms,P=0.6.(2)在消融术后,房颤的诱发比例下降,冠状静脉窦近端的易感窗口显著降低(P=0.03),冠状静脉窦远端和低位右心房的易感窗口有所降低,高位右心房的易感窗口不变,但差异无统计学意义.(3)消融后窦性心率有一定程度的上升(72.1±5.6)次/min对(74±6.8)次/min,但差异无统计学意义(P=0.17).(4)慢径消融使快径前传不应期缩短,消融前后分别为(391±55)ms,(369±78)ms,P＜0.01.结论 慢径消融使心房多部位的电生理性质发生了改变,导致冠状静脉窦近端和远端,以及低位右心房的有效不应期延长,房颤诱发几率降低.该现象的原因可能与消融造成的迷走神经功能改变有关.     

迷走神经活动对心房电重构的影响

目的 研究迷走神经干预对心房电重构的影响.方法 24只杂种犬随机分为3组,为排除交感神经对心房电重构的影响,3组犬均应用美托洛尔阻断交感神经效应.A组10只犬快速心房起搏过程中无迷走神经干预,B组8只犬应用阿托品阻断迷走神经效应,C组6只犬在快速心房起搏过程中同时进行迷走神经刺激.在右心房(RA)、冠状静脉窦(CS)和右心室(RV)放置多极导管.通过RA电极导管进行600次/min心房起搏30 min构建急性心房电重构模型.在右心房快速起搏前后测量基础状态(无迷走神经刺激)和迷走神经刺激下的心房有效不应期(AERP)和心房颤动(房颤)易感窗口(VW).结果 A组犬右心房快速起搏后基础状态下及迷走神经刺激时的AERP较起搏前明显缩短(P＜0.05).B组犬右心房快速起搏后基础状态下及迷走神经刺激时的AERP较起搏前无明显变化(P＞0.05).C组犬右心房快速起搏后基础状态下及迷走神经刺激时的AERP较起搏前明显缩短(P＜0.05).A组及C组右心房快速起搏后AERP缩短值明显大于B组(P＜0.05),但A组及C组AERP缩短值差异无统计学意义(P＞0.05).迷走神经刺激下,B组犬在右心房快速起搏前后均较难诱发房颤(VW接近0),A组及C组犬右心房快速起搏后较起搏前容易诱发房颤(P＜0.05).结论 短期右心房快速起搏导致的心房电重构过程中伴随着迷走神经兴奋性增强.迷走神经兴奋性增强及迷走神经刺激加重心房电重构,导致房颤易感性增加.迷走神经阻滞能减轻心房电重构,降低房颤易感性.     

Global P wave duration on the 65-lead ECG: single-site and dual-site pacing in the structurally normal human atrium

INTRODUCTION: Pacing is believed to prevent atrial fibrillation by reducing atrial activation time. Exact correlation between P wave duration (PWD) on surface ECG and endocardial atrial activation time is still unexplored. METHODS AND RESULTS: In 15 patients without structural heart disease (9 women, age 45 +/- 14 years), single site [high right atrium (HRA), coronary sinus ostium (CSos), distal CS (CSd), high RA septum (Bachmann's bundle, BB)] and dual-site pacing (various combinations) was performed after ablation of supraventricular tachycardia. A 65-lead surface ECG was recorded simultaneously. Endocardial atrial activation time was measured off-line (stimulus - last bipolar recording), and the respective PWD was assessed using the root mean square and 65-channel summary plots. PWD during pacing from BB was significantly shorter (96 +/- 12 msec) than during HRA (121 +/- 15 msec), CSos (108 +/- 9 msec), and CSd pacing (126 +/- 14 msec; P < 0,01, respectively). PWD during dual-site pacing (HRA+BB, 91 +/- 14 msec; HRA+CSos, 96 +/- 7 msec; HRA+CSd, 90 +/- 7 msec; BB+CSd, 96 +/- 12 msec) was not significantly shorter than during pacing from BB. Correlation between endocardial atrial activation time and PWD was 0.83. CONCLUSION: PWD during single-site and dual-site atrial pacing represents endocardial atrial activation time and can be measured precisely using the 65-lead surface ECG. The fact that high septal pacing results in the shortest PWD may have implications for preventive pacing in patients with atrial fibrillation.     

Author index: Volume 42

The various patterns resulting from stimulation through the catheter electrodes recording His bundle activity were evaluated in 30 patients using intracardiac electrograms from the right ventricular apex (RVA), posterosuperior wall of the left ventricle (LV), high right atrium (HRA) and left atrium (LA) in the vicinity of the coronary sinus. His bundle pacing was characterized by a QRS complex and stimulus (St)-V, St-RVA and St-LV intervals that equaled the QRS configuration, H-V, H-RVA and H-LV intervals of sinus beats. Right septal pacing produced a pattern of “complete” left bundle branch block (with normal electrical axis) associated with St-V intervals of 0 msec, and St-RVA and St-LV intervals of different duration from that of the H-RVA and H-LV intervals recorded during sinus rhythm. Fusion beats resulting from simultaneous activation of His bundle and right septal muscle were characterized by St-V Intervals of 0 msec and St-RVA or St-LV Intervals of similar duration to that of the H-RVA or H-LV intervals of sinus beats. Fusion QRS configuration depended on the type of ventricular complex present during sinus rhythm. Analysis of the retrograde atrial activation intervals permitted differentiation among impulse initiation at the low right atrium, His bundle or right septal muscle.Simultaneous recording of multiple atrial and ventricular electrograms has enhanced understanding of the complex patterns observed during attempted His bundle pacing in man.     

Atrial septal pacing to resynchronize atrial contraction and improve atrial transport function

OBJECTIVES: Atrial septal pacing via a trans-septal breakthrough site within the right atrial septum can shorten global atrial activation time, resulting in significant reduction of recurrence of atrial fibrillation events. This study examined whether this pacing method will lead to resynchronization of atrial contraction and its benefit on hemodynamic function can be maintained for 24 months. METHODS: Thirty patients with atrial fibrillation and delayed atrial conduction were enrolled (17 males, 13 females, mean age 73 +/- 7 years). Trans-septal breakthrough site within the right atrial septum was identified through pacing from the dorsal left atrium. Continuous atrial septal pacing at the trans-septal breakthrough site was performed for 24 months. Time difference (TD) between right and left atrial contractions was measured during atrial septal pacing and sinus rhythm by pulse Doppler echocardiography of the trans-tricuspid (P-At) and mitral (P-Am) blood flows (TD = P-Am - P-At). RESULTS: The atrial lead was screwed near the fossa ovalis in 29 of 30 patients. Atrial septal pacing yielded significantly shorter P wave duration (101.9 +/- 10.4 vs 139.6 +/- 14.7 msec, p < 0.001), leading to significant reduction of TD in atrial contraction (-8.8 +/- 10.0 vs 29.8 +/- 13.6 msec, p < 0.001)as compared to sinus rhythm. Both shorter P wave duration and reduced TD during atrial septal pacing remained statistically significant during the follow-up period as compared to sinus rhythm. Both left atrial diameter and A to E ratio of filling waves at mitral valve were significantly decreased at 12 months and remained decreased at 24 months. CONCLUSIONS: Atrial septal pacing at the trans-septal breakthrough site can resynchronize atrial contraction and results in improved hemodynamic effects during 24 months of follow-up.     

Effect of gender on atrial electrophysiologic changes induced by rapid atrial pacing and elevation of atrial pressure

INTRODUCTION: The incidence of atrial fibrillation is greater in men than in women, but the reasons for this gender difference are unclear. The purpose of this study was to evaluate the effects of gender on the atrial electrophysiologic effects of rapid atrial pacing and an increase in atrial pressure. METHODS AND RESULTS: Right atrial pressure and effective refractory period (ERP) were measured during sinus rhythm and during atrial and simultaneous AV pacing at a cycle length of 300 msec in 10 premenopausal women, 11 postmenopausal women, and 24 men. The postmenopausal women were significantly older than the premenopausal women (61 +/- 8 years vs 34 +/- 10 years; P < 0.01). During sinus rhythm, mean atrial ERP in premenopausal women was shorter (211 +/- 19 msec) than in postmenopausal women and age-matched men (242 +/- 18 msec and 246 +/- 34 msec, respectively; P < 0.05). Atrial ERPs in all patients shortened significantly during atrial and simultaneous AV pacing. However, the degree of shortening during atrial pacing (43 +/- 8 msec vs 70 +/- 20 msec and 74 +/- 21 msec; P < 0.05) and during simultaneous AV pacing (48 +/- 16 msec vs 91 +/- 27 msec and 84 +/- 26 msec; P < 0.05) was significantly less in premenopausal women than in postmenopausal women or age-matched men. CONCLUSION: The results of this study demonstrate a significant gender difference in atrial electrophysiologic changes in response to rapid atrial pacing and an increase in atrial pressure. The effect of menopause on the observed changes suggests that the gender differences may be mediated by the effects of estrogen on atrial electrophysiologic properties.     

Dependence of electrogram duration in right posteroseptal atrium and atrium-pulmonary vein junction on pacing site: mechanism and implications regarding atrioventricular nodal reentrant tachycardia and paroxysmal atrial fibrillation

INTRODUCTION: The fractionated atrial electrogram, a signal helpful in identifying the target site for radiofrequency catheter ablation of the slow AV nodal pathway, is considered to arise from nonuniform anisotropic electrical activity. However, the effects of pacing sites and radiofrequency ablation on these electrograms are not clear. Similarly, the nature of the fractionated atrial electrogram in the atrium-pulmonary vein junction has yet to be determined. METHODS AND RESULTS: Two experiments were performed in this study. Experiment 1 evaluated the fractionated atrial electrogram at target sites before and after slow AV nodal pathway ablation during sinus rhythm or during pacing from different sites. Group 1A consisted of 16 patients with dual AV nodal pathway physiology and AV nodal reentrant tachycardia who underwent successful ablation without residual slow AV nodal pathway. Group 1B consisted of 7 patients who underwent successful elimination of AV nodal reentry but with residual dual AV nodal pathway physiology. Group 1C consisted of 6 patients who still had AV nodal reentrant tachycardia after two applications of radiofrequency energy. In group 1D, there were 16 patients with dual AV nodal pathway physiology, but without inducible AV nodal reentrant tachycardia. In group 1E, there were 15 patients without dual AV nodal pathway physiology. Experiment 2 investigated the fractionated atrial electrogram in the ostium of the left and right superior pulmonary veins in 18 patients with paroxysmal atrial fibrillation (2A) and in 8 patients without paroxysmal atrial fibrillation (2B). Before radiofrequency ablation, electrogram duration in the right posteroseptal atrium during pacing from the middle coronary sinus or the right posterolateral atrium was shorter than that during pacing from the high right atrium (HRA) in all group 1 patients. After the successful elimination of the slow AV nodal pathway conduction in group 1A, atrial electrogram duration during HRA pacing was shorter than that before ablation. In experiment 2 patients, electrogram duration during pacing from the proximal or distal coronary sinus was shorter than that during pacing from HRA or sinus rhythm. CONCLUSION: These findings suggest that the fractionated atrial electrograms in the right posteroseptal atrium and ostium of left or right superior pulmonary veins are potentially consistent with nonuniform anisotropic propagation. Alternations of electrogram characteristics after successful radiofrequency ablation of the slow AV nodal pathway may arise from the changes of nonuniform anisotropic activity in the right posteroseptal atrium.     

房室结慢径区域消融对迷走神经功能及心房颤动易感性的影响

目的心房颤动（房颤）与房室结折返性心动过速有着某种程度的关联性,慢径区域消融可能影响了心房自主神经功能而导致窦性心动过速。但慢径区消融对心房自主神经功能的具体影响目前尚不清楚。本文旨在探讨慢径区消融对心房迷走神经调节功能及房颤易感性的影响。方法11条成年杂种犬,全身麻醉下行颈交感一迷走神经干剥离术。经右颈内静脉穿刺放置冠状静脉窦导管,经左股静脉穿刺放置右心室导管及右心房标测电极导管（Halo导管）,经右股静脉穿刺放置消融导管和希氏束导管。静脉应用美托洛尔阻断交感神经活性。测量慢径区域消融前后基础状态及迷走神经刺激下的窦性周长（SCL）及高位右心房（HRA）、低位右心房（IRA）、冠状静脉窦近端（CSp）和冠状静脉窦远端（CSd）的有效不应期（ERP）及心房易感窗口（VW）。结果（1）SCL的变化：消融前后迷走神经刺激导致的SCL缩短值无明显改变[（107±19）次／min对（108±8）次／min,P〉0．05],提示慢径区域消融没有明显改变迷走神经对窦房结的调节作用。（2）ERP的变化：消融前后迷走神经刺激导致的ERP缩短值在HRA分别为[（69±37）ms对（55±34）ms,P〉0．05],CSd分别为[（55±30）ms对（42±32）ms,P=0．08],IRA分别为[（66±24）ms对（19±21）ms,P〈0．001],CSp分别为[（46±24）ms对（7±18）ms,P〈0．001]。提示慢径区域消融对HRA及窦房结区域的迷走神经调节功能无明显影响,对CSd区域的迷走神经调节功能有一定的影响,而导致了IRA及CSp区域去迷走神经效应。（3）心房VW的变化：消融前后基础状态下各个部位刺激均较难诱发房颤（VW接近0）。消融后,HRA迷走神经刺激诱发房颤的能力较消融前没有明显变化[（63±31）ms对（63±25）ms,P〉0．05],CSd的VW有一定程度的降低[（35±37）ms对（57±28）ms,P     

Right atrial versus left atrial echo zones: A proposed new criterion for determining the atrial site of retrograde preexcitation

In a patient whose electrocardiogram (ECG) initially (1966) showed a Type A Wolff-Parkinson-White pattern, recurrent supraventricular tachycardia (SVT) developed but never subsequently showed antegrade bypass conduction. Intracardiac pacing studies (1975) revealed that premature high right atrial (induced 250–450 msec after atrial depolarization) or coronary sinus depolarization (250–550 msec) resulted in SVT. Late coronary sinus depolarization resulted in SVT without A-H prolongation. During SVT, P wave morphology changed and the coronary sinus atrial electrogram preceded that from the low right atrium; retrograde ventriculoatrial conduction time was 240 msec. Neither pacing the high right atrium or coronary sinus up to rates of 200 beats/min nor progressive atrial premature depolarizations from the high right atrium or coronary sinus resulted in antegrade bypass conduction. Failure of antegrade bypass conduction does not preclude SVT due to retrograde pre-excitation and must be distinguished from atrioventricular (A-V) nodal reentry. Atrial effective refractory period (200 msec) was shorter than the minimal time required for an atrial impulse to return to the atrium (380 msec), suggesting concealed antegrade bypass conduction. Stimulation of the atrium linked to the A-V bypass results in earlier bypass activation and recovery and explains the differing high right atrial vs coronary sinus echo zones.     

Importance of retrograde atrial activation in atrial fibrillation genesis in the initiation of atrial fibrillation in Wolff-Parkinson-White syndrome. Comparison of atrial electrophysiologic parameters between patients with different atrial fibrillation genesis (initiation sites) in atria.

The changes in the duration of atrial electrograms during different atrial activation sequences from a sinus rhythm were evaluated to test the hypothesis that the prolongation of atrial electrogram duration caused by the different atrial activation sequence is more prominent at the site of atrial fibrillation (Afib) genesis (initiation site) than other areas. In 39 patients with single retrograde left-sided accessory connection who had inducible transient atrial fibrillation during an electrophysiologic study, the site of Afib genesis was determined and classified into three groups, i.e., 1) high right atrial genesis (HRA), 2) low right atrial genesis (LRA), and 3) left atrial genesis (LA). Single premature extrastimuli after 8 basic drive trains (600 ms) were delivered at the HRA and the right ventricular apex. Three atrial electrophysiologic parameters were evaluated at three atrial sites, i.e., 1) HRA, 2) LRA, and 3) coronary sinus. The atrial vulnerability parameters were as follows; 1) %A2/A1: % prolongation of atrial electrogram duration during premature beat (A2) in comparison with basic drive (A1), 2) wavelength index (WLI): calculated as [effective refractory period]/[A2], and 3) retrograde activation index (RAI): calculated as [A1 during retrograde activation; i.e., RVA pacing/[A1 during antegrade activation, i.e., HRA pacing], shown as a percentage. The Afib genesis was HRA in 20, LRA in 12 and LA in 7 patients. At the HRA recording site, %A2/A1 and RAI were the largest and WLI the shortest in the HRA genesis group in comparison with the other two groups. Similarly, at the LRA and LA recording sites, %A2/A1 and RAI were the largest and WLI the shortest in the groups with Afib genesis at these recording sites. In patients with inducible Afib, %A2/A1 and RAI were the highest and WLI the shortest at the atrial recording site close to the site of Afib genesis. Atrial wave prolongation during retrograde atrial activation, possibly the anisotropic conduction, was considered to play a role in initiating Afib as well as a conduction delay during the atrial premature beat.     

Suppression of atrial fibrillation by multisite and septal pacing in a novel experimental model

OBJECTIVES: To evaluate the preventive efficacy of multisite and septal atrial pacing in an experimental model. METHODS: Sterile right atrial pericarditis was induced in 12 foxhounds to provide an anatomical substrate for atrial fibrillation (AF). As a trigger mechanism, atrial extrasystoles were simulated by constant asynchronous pacing at a cycle length of 1000 ms from randomly selected right or left atrial electrodes, using a biatrial epicardial multielectrode with 128 bipoles. Additionally, a transvenous pacing lead was screwed into the interatrial septum. Four electrodes located in the high and low right (HRA/LRA) and left atrium (HLA/LLA) were selected for preventive multisite stimulation. Constant pacing at a cycle length 30 ms below sinus rate was applied from the following site(s): HRA, septal, HRA+LRA, HRA+LLA, HRA+LRA+LLA and HRA+LRA+HLA+LLA (order randomized). Number and duration of AF episodes were studied during 10 min intervals, separated by 5 min pauses, respectively. To validate the model, the protocol was repeated 10 min after i.v. bolus administration of D,L-sotalol (1 mg/kg body weight). RESULTS: The number of AF episodes decreased with increasing number of pacing sites, reaching statistical significance compared to HRA stimulation for quadruple-site and single-site septal pacing only (P<0.05). Single-site septal was as efficient as quadruple-site pacing in suppressing AF. The duration of AF episodes was not significantly affected by the pacing configuration. D,L-sotalol almost completely suppressed AF irrespective of the pacing configuration used. CONCLUSIONS: In this novel experimental model, quadruple-site and septal pacing effectively suppress paroxysmal AF.