肺静脉起搏时犬房间隔激动时序特征的研究

目的 :研究肺静脉起搏时犬房间隔激动的时序特征 ,进一步了解起源于肺静脉的异位搏动引发心房颤动的电生理机制。方法 :选用 5只犬 ,放置电生理标测导管于 Bachm ann氏束 （BB）右房间隔侧、卵园窝 （FO ）及冠状窦（CS）。同步记录 BB、FO及 CS近端 （CSp）处心内电图。作左上肺静脉 （L SPV）、右下肺静脉 （L IPV）、右上肺静脉（RSPV）及右下肺静脉 （RIPV）开口处起搏 ,观察房间隔激动的时序特征。结果 :L SPV起搏时 BB及 FO为最早激动点 ,刺激波至 CSp的传导时间与 FO及 BB处相比 ,虽未达到统计学差异 ,但呈延长的倾向 （4 0± 12 ms vs 2 9± 7ms及 2 9± 15 m s）。L IPV起搏时 CSp,FO及 BB处几乎同时激动 ,刺激波至该三处的激动时间无明显差别 （2 9± 12 ,2 8± 8及 33± 10 ms）。 RSPV起搏时 BB及 FO为最早激动点 ,刺激波至 FO及 BB的时间短于至 CSp的时间 （2 6± 6ms及 2 4± 11ms vs 40± 10 m s,均 P<0 .0 5 ）。 RIPV起搏时 BB,FO及 CSp均可为最早激动点 ,刺激波至该三处的激动时间无明显差异 （2 8± 15 ,2 6± 15及 2 9± 14ms） ,L IPV起搏较窦性心律时房间隔激动时间缩短 （9± 10 ms vs2 9± 9ms,P<0 .0 5 ） ,下肺静脉与上肺静脉起搏相比 ,房间隔激动时间虽未达统计学差异 ,但呈缩短的倾向 (11± 9ms及 2 1     

射频导管消融术阻滞经冠状静脉窦传导通路的实验研究

目的　探讨利用射频导管消融术阻滞经冠状静脉窦的电传导通路的方法及可行性。方法　冠状静脉窦口内 5～ 10mm处射频导管消融 ,低位右心房起搏下 ,观察最早激动部位、冠状静脉窦激动顺序和时间、房间隔激动时间、心房激动时间。结果　 (1)冠状静脉窦口或近端射频导管消融可造成经冠状静脉窦电传导通路的完全或部分阻滞。表现在消融前 ,低位右心房起搏时 ,窦口处的电激动明显早于Bachmann束。消融后 ,窦口处的电激动迟于Bachmann束或两者基本一致 ;(2 )消融前后 ,心房激动时间由 (6 1 14± 8 36 )ms延长至 (88 4 3± 19 2 2 )ms,说明低位心房起搏时冠状静脉窦是优势传导通路 ;(3)消融前后的房间隔激动时间及冠状静脉窦激动时间分别为 (2 6 4 3± 8 87)ms对(15 2 8± 10 13)ms和 (39 4 3± 9 78)ms对 (38 0 0± 5 86 )ms。结论　冠状静脉窦近端射频导管消融术阻断经冠状静脉窦的电传导通路的方法是可行的     

3830电极在房间隔起搏中的临床观察

目的探讨Medtronic3830主动固定电极在右房间隔部起搏的可行性和安全性。方法44例需行DDD起搏的患者分为两组,房间隔组22例采用Medtronie3830主动固定电极,右心耳组22例采用Medtronic4574或stJude1642被动电极。通过比较植入时间、X线曝光时间、术中术后起搏参数、术后并发症来评价房间隔起搏的可行性。结果与右心耳组相比,房间隔组的植入时间和曝光时间稍有延长,两组的起搏参数及术后并发症无差异。房间隔组心房激动时间明显短于右心耳组[（94．6±30．8）msV8（135．5±20．3）ms,P〈0．05]。结论房间隔起搏安全可行,但操作难度稍大。     

上腔静脉隔离对迷走神经功能及心房颤动易感性的影响

目的 通过分析迷走神经调节的心房电生理指标(心房有效不应期及心房颤动易感窗口)的变化,间接揭示上腔静脉(SVC)隔离对犬的心房迷走神经功能及心房颤动(房颤)易感性的影响.方法 9条成年杂种犬,全身麻醉下行颈交感-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,经股静脉穿刺放置右心室导管(行临时右心室起搏)、环状标测导管(Lasso导管)及消融导管.静脉应用美托洛尔阻断交感神经活性.分别于SVC隔离前后在基础状态及迷走神经刺激时测量右心耳(RAA)、冠状静脉窦近端(CSp)和冠状静脉窦远端(CSd)的不应期(ERP)、心房易感窗口(VW)及窦性周长(SCL).结果 (1)窦性周长的变化SVC隔离前迷走神经刺激明显缩短SCL[(65.78±28.49)次/min vs(142.67±15.42)次/min,P《0.001],SVC隔离后基础状态及迷走神经刺激下SCL差异无统计学意义[(134.89±19.19)次/min vs(114.33±31.41)次/min,P》0.05].(2)有效不应期的变化SVC隔离前,迷走神经刺激下测得的心房ERP较基础状态下明显缩短[右心耳(RAA)分别为(51.11±18.33)ms vs(101.11±27.59)ms;CSd分别为(56.67±22.36)ms VS(98.89±14.53)ms;CSp分别为(48.89±25.22)ms vs(101.11±12.69)ms,P《0.001].SVC隔离后,迷走神经刺激所致的心房ERP缩短的能力明显下降(RAA分别为(94.40±16.70)ms vs(94.44±16.67)ms;CSd分别为(89±15)ms vs(96.7±18.0)ms;CSp分别为(93.3±18.7)ms vs(98.9±20.3)ms,P》0.05].(3)心房易感窗口的变化 SVC隔离前后基础状态下测得的VW无变化.SVC隔离后迷走神经刺激时测得的VW较隔离前明显降低[RAA分别为(6.67±11.18)ms vs(21.11±20.88)ms,CSd分别为(8.89±14.52)ms vs(16.66±23.97)ms,CSp分别为(2.22±6.67)ms vs(22.22±18.55)ms,P《0.05].结论 SVC隔离能导致迷走神经介导的窦房结抑制、心房不应期缩短能力及房颤易感窗口增加能力明显下降.提示SVC隔离可导致心房局部去神经反应,抑制迷走神经介导的房颤发生.     

房间隔起搏在心脏再同步治疗中的应用

目的通过简单的超声多普勒方法评价房间隔起搏在心脏再同步治疗（CRT）中的效果。方法在23例行CRT治疗的患者中进行了超声多普勒测量，9例患者存在房间阻滞，心房起搏导线固定在房间隔，其余14例常规固定在右心耳。结果右心耳起搏组中心房间传导延迟时间（IAD）延长[（46±20）ms vs（53±23）ms，P〈0．05]，IAD和心室间传导延迟时间（IVD）的差异增大[（53±23）ms VS（40±17）ms，P〈0．05]，左机械房室延迟时间（LMAVD）和右机械房室延迟时间（RMAVD）的差异明显增加[（172±25）ms vs（210±32）ms，P〈0．001]。房间隔起搏后IAD明显减小[（34±12）ms VS（12±11）ms，P〈0．001]，IAD和IVD的差别减少[（12±11）ms VS（18±16）ms，P〉0．05]，LMAVD和RMAVD差异无统计学意义[（187±43）ms vs（182±50）ms，P〉0．05]。二尖瓣A峰速度时间积分在房间隔起搏后明显增加[（8．9±4．9）cm vs（13．0±4．0）cm，P〈0．001]。结论房间阻滞可以导致左心和右心房室收缩顺序的差异，房间隔起搏能纠正这种差异，增加二尖瓣舒张期充盈进一步改善心脏再同步治疗。     

低位房间隔起搏的初步临床应用

目的探索主动固定电极导线在低位右心房间隔部起搏的可行性、安全性；比较低位房间隔起搏与高位右心房游离壁起搏对，心房激动时间和起搏参数的影响。方法共入选了50例，患者平均年龄（64．8±11．2）岁，随机分配到低位房间隔起搏组（n=25）和高位右心房游离壁起搏组（n=25），通过比较植入术时间、X线曝光时间、导线固定成功率、起搏参数、植入术并发症等评价低位右心房间隔起搏的可行性；测定不同部位起搏时P波宽度，以评价起搏部位对心房激动时间的影响。结果与高位右心房游离壁起搏组结果比较，低位房间隔起搏组的植入时间、X线曝光时间略有延长；低位房间隔起搏组的导线固定成功率低于右心房游离壁起搏组（84％ VS 100％），两组间的起搏参数、植入术并发症相比差异无统计学意义。低位房间隔起搏时心房激动时问明显短于高位右心房游离壁起搏[（140．5±23．0）ms VS（89．0±14．0）ms]，差异具有统计学意义。结论采用主动固定电极导线在低位房间隔起搏是安全、可行的，它明显缩短左、有心房激动时间，使心房的除极趋于同步化。但低位房间隔起搏的主动固定电极导线植入技术具有一定的难度，需要熟练掌握主动固定导线植入技术的人员方可实施。     

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     

应用MEA技术研究组织工程再造心肌对心梗大鼠心室肌电传导功能的影响

目的：应用微电极阵标测技术（MEA）研究组织工程再造心肌移植心梗大鼠的心肌电传导功能。方法：将成年SD大鼠30只随机分为假手术组、心梗组、移植组。应用MEA技术记录心室肌场电位的形态和激动传导时间。结果：正常大鼠心室除极波形多为三向波,呈RS、rSR’型。心梗组心梗面以QR或qR为主,R波圆钝;心室对立面及梗死周围面以R波为主。移植组心室心梗面主要以QR或qR为主,对立面及梗死周围区以Rs或R波为主。测量大鼠心室前壁、后壁及游离壁激动传导时间。假手术组为（6．5±2．12）ms、（11．25±1．77）nls和（7．05±0．78）ms;心梗组为（17．5±3．54）ms、（12．5±2．12）ms和（10．5±2．12）ms;移植组为（9．13±1．31）ms、（10．25±0．35）ms和（8．25±0．35）ms。与心梗组相比,移植组激动传导时间明显缩短（P〈0．05）。移植组和假手术组心梗面和周围面激动传导时间明显低于心梗组（P〈0．05）。结论：心肌细胞／胶原复合体可改善心梗组织的电传导功能。     

房间隔起搏临床应用的体会

目的　探讨有适应症的阵发性房颤患者行永久房间隔起搏的可行性及有效性。方法　先行心内电生理标测 ,寻找使双心房同步激动的房间隔最佳起搏点 ,采用主动固定起搏导线固定于该部位。结果　 4例患者窦性心律时房间传导为 10 6 0± 4 3ms ,标测后房间隔起搏房间传导时间为 11 0± 1 1ms,(P <0 0 0 1)。达到了双心房同步起搏。 3例患者成功地植入房间隔主动固定导线 ,一例患者失败。结论　永久房间隔起搏方法在伴有房间传导阻滞的阵发性房颤患者中的应用是安全可行的。     

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。     

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.     

The Impact of the Distance between the Atrial Electrode and the Atrial Wall on Atrial Undersensing in Patients with VDD Pacemakers: Long‐Term Follow‐Up

Aim: Atrial undersensing (AUS) in single‐lead VDD pacemakers may be due to diminished P‐wave amplitude secondary to local inflammation beneath the electrodes closer to atrial wall. The aim of this study was to assess the potential effect of distance between atrial electrode and atrial wall on immediate and long‐term atrial sensing stability in VDD systems. Methods: A total of 275 patients with normal sinus node function who received VDD pacemakers were enrolled into the study and were followed up for a median duration of 33 months. During each control visit, a standard 12‐lead electrocardiogram (ECG) was obtained and standard pacemaker function assessment was performed including testing for pacing threshold and atrioventricular synchrony. The distance between atrial electrode and atrial wall was measured from chest X‐ray. Results: Of the 275 patients, AUS was detected in 59 patients. Univariate predictors of AUS were use of closely spaced bipolar ring atrial electrode (CSBR) (P = 0.01), wider atrial ring‐spacing (P = 0.03), and atrial sensitivity programmed to a higher level (P = 0.001). Use of CSBR (P = 0.04) and atrial sensitivity ≥0.3 mV (P = 0.02) were observed to be the independent predictors for AUS. When the distance between atrial electrode and atrial wall was <7 mm, AUS was less with diagonally arranged bipolar ring electrodes (DABR) than it was with CSBRs (P = 0.02). Conclusions: The distance between atrial electrode and atrial wall does not appear to affect AUS incidence in VDD pacemakers. For VDD electrodes closer to atrial wall, AUS was significantly less likely in DABR‐type electrodes.     

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.     

Comparison of the acute effects of pacing the atrial septum, right atrial appendage, coronary sinus os, and the latter two sites simultaneously on the duration of atrial activation

OBJECTIVE—To compare the acute effects of right atrial appendage, atrial septal, coronary sinus os, and dual site pacing on the duration of atrial activation.
METHODS—20 patients with a variety of cardiac conditions underwent an intracardiac electrophysiological study. Electrograms were recorded from the right atrial appendage and at multiple sites within the coronary sinus. The duration of atrial activation was measured during pacing at the right atrial appendage, atrial septum, and coronary sinus os, and also during dual site stimulation.
RESULTS—The duration of atrial activation with atrial appendage pacing was notably longer (p < 0.001) than with dual site, septal, or coronary sinus os pacing, but there were no significant differences in atrial activation times between these latter three pacing modes. When stimulating the atria at a cycle length of 500 ms, the mean (SD) duration of atrial activation was 145 (37) ms for right atrial appendage pacing, 93 (26) ms for dual site pacing, 96 (28) ms for septal pacing, and 98 (28) ms for coronary sinus os pacing.
CONCLUSIONS—Assuming that the duration of atrial activation is an important determinant of predisposition to paroxysmal atrial fibrillation, atrial septal pacing or coronary sinus os pacing would appear to offer the same advantage as dual site pacing without the additional complexities associated with the latter pacing mode.


Keywords: atrial septal pacing; dual site pacing; atrial activation; atrial fibrillation     

Reduced Peak Atrial Systolic Mitral Annular Velocity Predicts the Development of Nonvalvular Atrial Fibrillation

We investigated whether the echocardiographic parameters of the left atrium (LA) can predict the development of nonvalvular atrial fibrillation (AF). Among 14,062 patients ( > 20 years old) who underwent an echocardiographic examination were evaluated, 2,606 patients who underwent follow-up ECG with an interval of > 6 months were investigated. Newly developed AF was noted in 42 (1.6%) patients with follow-up duration of 31.8 ± 8.9 months. Cox regression analysis revealed that a higher left atrial volume index (hazard ratio [HR ]= 1.06; 95% confidence interval [CI] 1.03–1.09, P < 0.001), relative wall thickness (RWT) of ≥ 0.407 (HR = 2.74, 95% CI 1.39–5.41, P = 0.004), a reduced peak atrial systolic mitral annular velocity (HR = 0.845, 95% CI 0.72–0.99, P = 0.037), and an advanced age (HR = 1.04, 95% CI 1.01–1.07, P = 0.009) were independently related to the development of nonvalvular AF. Therefore, reduced A ' , which is parameter of LA contractile function, might be an important predictor for the development of nonvalvular AF.     

Atrial Tachycardia Confined Within the Left Atrial Appendage

AT Confined Within the LAA. Left atrial tachycardias are often seen following catheter ablation of persistent atrial fibrillation (AF). We report here an unusual case where AF was converted to sinus rhythm following catheter ablation, but ongoing atrial tachycardia confined within the left atrial appendage (LAA) was observed. Although the LAA tachycardia was dissociated from the atrium in sinus rhythm, bidirectional conduction between the left atrium and the LAA was, however, demonstrated after tachycardia termination. (J Cardiovasc Electrophysiol, Vol. 21, pp. 933‐935, August 2010)     

Atrial tachycardia originating from the upper left atrial septum: demonstration of transseptal interatrial conduction using the infolded atrial walls

We report a rare case of atrial tachycardia (AT) originating from the upper left atrial septum. Electroanatomic mapping of both atria demonstrated that the earliest atrial activation during AT occurred at the upper left atrial septum 26 msec before the onset of the P wave, followed by the mid-right atrial septum (10 msec before the onset of the P wave) and then the upper right atrial septum just adjacent to the left septal AT site (1 msec before the onset of the P wave), indicating detour pathway conduction from the upper left to the upper right atrium. Embryologically, it was suggested that the superior components of the secondary atrial septum are made by the infolded atrial walls and could develop a transseptal detour pathway involving the left-side atrial septal musculature, the superior rim of the oval fossa and the right-side atrial septal musculature. A single radiofrequency application targeting the upper left atrial septum successfully abolished the AT.     

持续性心房颤动患者无症状心房颤动的发生情况及影响因素

Objective To investigate the incidence of asymptomatic atrial fibrillation( AF) and the influence factors in patients with persistent AF. Methods A total of 82 consecutive patients with 24 h Holter monitoring identified persistent AF were observed to analyze the incidence of asymptomatic AF. 24 h Holter monitoring was performed again after three months' treatment with antiarrythmic drugs in order to identify the incidence of asymptomatic AF. Multivariate logistic regression was applied for analyzing the correlation between symptoms and clinical features. Results Thirty-four patients(42% )were asymptomatic ,24 patients were symptomatic. After antiarrythmic drugs therapy for three months, 31 patients among 48 symptomatic patients, were completely asymptomatic, 4 were converted to sinus rhythm, 27 were asymptomatic atrial fibrillation. In 34 asymptomatic patients, 5 were converted to sinus rhythm, 24 remain asymptomatic atrial fibrillation. Significant differences were found between symptomatic and asymptomatic patients with persistent AF between age and valvular heart disease( P ＜ 0. 05 ). Symptoms were positively with valvular heart disease (b = 1. 959, P = 0. 001 ),and negatively with age( b = -0. 837,P = 0. 032). Conclusion The incidence of asymptomatic persistent AF was high. Antiarrythmic drugs could not only relieve the episodes of AF, but also the symptoms of AF. Elderly and nonvalvular atrial fibrillation(NVAF) patients were often asymptomatic.