选择性消融窦房与房室结周神经治疗缓慢性心律失常的心率波动频谱分析研究

目的探讨动态心电图心率波动频谱分析对选择性消融窦房结与房室结周围神经治疗缓慢性心律失常患者的作用。方法选择症状严重、拟行起搏器治疗的阵发性心动过缓患者35例,术前行动态心电图检查并进行心率波动频谱分析。对于症状及频谱分析支持心动过缓为迷走神经张力增高所致的患者,在X线与64排螺旋CT心脏解剖影像指导下,标测窦性心律下的心房激动顺序,围绕并避开心房最早激动点和His束区域,记录心内电图神经组织电位,温控射频消融,观察消融反应,随访治疗效果。结果成功的30例患者中,28例高频成分（HF）明显,低频成分（LF）存在;2例为LF缺失,HF明显。复发的5例患者中4例为LF缺失,HF明显;1例为HF明显,LF存在。术后动态心电图检查,成功的30例患者中17例HF明显降低,余无明显变化。复发的5例患者中1例HF明显降低,余无明显变化。电生理检查显示,消融后患者基础心率、SNRT、WP、AH间期都得到了明显改善（P〈0.01）。结论对于心率波动频谱分析支持心动过缓系由迷走神经张力增高所致的患者,选择性消融窦房结或房室结周围神经有较好治疗效果。     

右冠状动脉阻塞时交感神经对房室传导调节功能的实验研究

目的 研究右冠状动脉阻塞时交感神经对房室传导调节功能的影响. 方法 在去自主传出神经的动物上,结扎右冠状动脉造成急性下壁心肌梗死(AIMI)的动物模型,通过模板匹配的方法检测His束的A、H、V波,自动检测两心房波(AA)间期,心房波与His渡(AH)间期,并刺激双侧交感神经. 结果 正常动物刺激交感神经使得AH问期在未起搏与起搏时减少(14±5)%和(23±7)%;而心肌梗死时,刺激交感神经使AH间期在未起搏与起搏时减少(7±5)%和(12±2)%.后者只有前者减少幅度的50%和48%(P<0.05). 结论 在AIMI时,交感神经对心脏传导调节功能减弱,这种减弱可能参与AIMI伴房室传导阻滞发生的机制.     

双腔起搏器房室间期自动搜索功能对右心室起搏比例影响的临床研究

目的比较植入双腔起搏器患者房室（AV）间期自动搜索功能（Search AV）打开与固定长AV间期起搏,对右心室起搏比例的影响。方法入选60例病态窦房结综合征或间歇性Ⅱ度或Ⅲ度AV传导阻滞患者,均安装双腔起搏器。程控首先关闭Search AV功能,固定长AV间期（起搏房室间期220ms,感知房室间期200ms）起搏3个月,后程控打开Search AV 3个月,自身对照,比较其心房起搏比例、心室起搏比例及高频心房事件次数。再根据患者是否1：1房室传导分为2个亚组,自身对照分别比较其心房起搏比例、心室起搏比例及高频心房时间次数。结果58倒患者完成随访,固定长AV间期起搏时比Search AV（＋）自动搜索功能打开时的心室起搏比例、高频心房事件次数都高,分别为（70．5±12．4）％vs（22．4±8．3）％,（86±16）次VS（31±11）次（P=0．007,P=0．006）;而心房起搏比例二者差异无统计学意义。在1：1房室传导组（33例）及非1：1房室传导组（25例）两亚组比较中,均得出相同结果。结论Search AV功能可以减少不必要的右心室起搏,减少高频心房事件。     

心肌缺血对心电频谱的影响

目的研究缺血对心电频谱的直接影响。方法在去自主传出神经的动物上,通过结扎右冠状动脉造成心肌缺血的动物模型,测量两心房间期(AA)和心房波与心室波间期(AV),采用快速傅立叶转换(FFT)的方法将期转换为频域函数进行分析。结果缺血后,AA间期频谱低频由(8.2±3.2)nu升高为(23.6±18.9)nu(P<0.01),高频由(80.0±7.1)降低为(59.4±23.9)nu(P<0.01);AV频谱低频由(16.4±10.5)nu升高为(31.4±11.3)nu(P<0.01),高频由(72.1±11.6)nu降低为(54.4±13.4)nu(P<0.01)。结论在去自主神经状态下,结扎右冠状动脉后AA、AV频谱均出现低频升高,高频显著下降。因此缺血是心电频谱改变的一个独立的直接因素。     

心腔内超声引导下希氏束起搏和房室结消融

目的　建立心腔内超声和组织多普勒显像技术引导监控下的希氏束起搏和房室结消融方法。方法　 6只犬急性闭胸模型。经颈静脉插入超声导管确定希氏束和房室结准确空间位置、超声解剖结构标志及其内心肌激动顺序。引导心脏起搏或消融导管到达靶组织 ,监控刺激电极植入过程和确认消融电极与心内膜面接触。分别释放电脉冲进行靶点起搏和射频消融 ,同步体表心电图QRS波形态确认实现希氏束起搏和Ⅲ度房室传导阻滞。结果　实现了直接希氏束起搏 (1例 )和希氏束加室间隔起搏 (5例 )。希氏束起搏阈值为 :电压 (3 .0± 1 .0 )V ,脉宽 0 .5ms。希氏束起搏时导致了较早的室间隔电兴奋。窦性心律和希氏束起搏时QRS波宽度分别为 (59.7± 5 .3)ms和 (82 .8± 1 6 .6)ms (P =0 .0 2 )。完成希氏束起搏和房室结消融的平均操作时间分别为 40min(3～ 81min)和 3min(2～ 5min) ;平均X线曝光时间为 1 3min(1～ 55min)。病理解剖和组织切片表明希氏束起搏和房室结消融定位准确、效果肯定。结论　心腔内超声技术能够准确引导心脏介入导管实现希氏束起搏和房室结消融 ,减少导管操作和X线曝光时间     

慢快型房室结折返性心动过速伴2：1房室传导阻滞1例

患者,男,19岁。因心悸于2008年3月4日入院。既往有心悸病史、突发突止。入院心内电生理检查：患者存在房室结双径路,可经跳跃诱发心动过速,冠状窦电极A波呈向心性传导,希氏束逆传A波最早;心动过速时冠状窦电极AA间期为1／2RR间期,且规则出现,希氏束电极1～2显示经快径路逆传的A（箭头示）波稍早于V波,第2个A波经房室结慢径到达希氏束下传心室,     

病窦综合征患者起搏器术后房室传导方式对Tei指数的影响

目的:评估固定的长AV间期下的DDD起搏模式对病态窦房结综合征(SSS)患者在减少心室起搏方面的效果;比较应用固定的长AV间期保留自身房室传导与最适AV间期下房室顺序起搏两种模式的优劣性,为此类患者选择具有最佳血流动力学效应的起搏参数设置提供临床依据。方法:连续选取2009年5月至2011年4月在我院因SSS而安置双腔心脏永久起搏器进行治疗的55位患者作为研究对象,分3次随访进行,每次随访时间间隔为2个月,将起搏器程控与超声测量相结合,进行两种不同AV间期下房室顺序起搏模式的血流动力学效应评估与对比。结果:与临床经验性AV间期相比,固定的长AV间期下的房室顺序起搏使心室起搏百分比由在31.8%降低至1.18%(P=0.00017);由最适AV间期下转为固定的长AV间期(350ms)下的房室顺序起搏模式后,心脏总体舒张和收缩功能指标(Tei指数)存在差异,且以左室Tei指数下降更为显著(0.67±0.17比0.45±0.09,P<0.0001)。结论:固定的长AV间期(350ms)下的房室顺序起搏能够有效减少心室起搏,且在血流动力学方面优于最适AV间期下的房室顺序起搏。     

希氏束电图临床应用的研究——附80例分析

导管法希氏束电图(简称HBE)在描记的同时,如有必要还可进行其他电生理检查,包括了解窦房结的空能,测定房室传导系统各部位的反拗期,以及通过心房起搏发现隐匿性房室传导阻滞和推测预激综合征中旁路的位置等,从而提供更多有价值的资料,有助于心脏传导系统疾病的及时诊断、正确处理和判断预后,故在心血管临床上有较广泛的应用。     

射频消融术后迟发房室传导阻滞伴阿-斯综合症1例护理体会

1病历资料患者男,36岁,因反复室上性心动过速入院,病史10余年,以往可自行或刺激迷走神经终止发作,近年来发作频繁,静脉滴注胺碘酮尚可终止发作。心内电生理检查诊断为希氏束旁隐匿性旁路。在希氏束电极旁可记录到VA融和、其前无H波的靶点电图,输出功率25～30w,放电12次,累计放电400s。心动过速终止后出现一度房室传导阻滞(Ⅰ。AVB),P-R间期0.28s,给予地塞米松10mg静脉推注,心房连续刺激频率为160次/min,房室呈1:1传导,手术持续2.5h。术后心电图示窦性心律,心率60次/min,P-R间期0.20s.第2d凌晨突发神志不清、抽搐,心电图为三度房室传导阻…     

间隔部房室交界区解剖

正间隔部房室交界区主要包括Koch三角(内含房室结)、膜部室间隔、希氏束、左右束支等重要解剖结构。希氏束-浦肯野纤维传导系统的最重要解剖结构是:被分割成两部分的希氏束(包括希氏束的穿越部分和希氏束的分支部分)。房室交界区是心房与心室之间唯一的电通路,从组织学的角度上讲,它是指连接心房工作肌与希氏束之间的3种不同的特化组织:(1)心房肌和致密结之间的过渡细胞区;     

An Optimized AV Delay Algorithm for Patients with Intermittent Atrioventricular Conduction

Detection and promotion of an intermittent atrioventricular (A V) conduction is the objective of an AV delay hysteresis algorithm in dual chamber pacemaker (DDDj pacing. The AV delay following an atrial event is automatically extended by a programmable interval (AV hysteresis interval) if the previous cycle showed spontaneous AV conduction, i.e., a ventricular event was detected within the previous AV delay. An automatic search mode scans for spontaneous ventricular events during the hysteresis interval: a single AV delay extension (equal to the programmed AV delay hysteresis) will occur after a successive, programmable number of AV cycles with ventricular pacing. If a spontaneous AV conduction is present, the AV delay will remain extended by the hysteresis interval. Our first results in 17 patients with intermittent AV block disclosed a satisfactorily working algorithm with effective reduction of ventricular stimuli. In relation to the underlying conduction disturbance and pacemaker settings, the majority of our patients showed a reduction of ventricular pacing events up to 90% without any adverse hemodynamic or electrophysiological changes. Based on clinical (promotion of a physiological activation and contraction sequence) and technical (reduction of power consumption) advantages, the AV hysteresis principle could be of incremental value for future dual chamber pacing in patients with intermittent complete heart block.     

Full Ventricular Capture Indicated by the QT Interval Function

The atrioventricular (AV) interval is critical in dual chamber (DDD) pacing in patients with hypertrophic obstructive cardiomyopathy (HOCM) to obtain full ventricular capture (FVC) with maximal reduction of the left ventricular (LV) outflow gradient and optimal LV diastolic filling. We studied the relationship of FVC, fusion, spontaneous AV conduction, and the QT interval. Methods: 11 patients with various cardiac diseases and stable AV conduction received a QT sensing Diamond (tm) Vitatron, DDD pacemaker. Software was downloaded into the pacemaker. In the DDD pacing mode, with the QT interval measured from the ventricular pacing stimulus to the end of the T wave, the AV interval was shortened from 400 ms, in 20-ms steps, to 90 ms. At 90 ms the stimulation rate was increased by 30 beats/mm and the AV interval was increased stepwise. FVC and fusion was examined on the surface ECG, Results: At 400 ms interval, spontaneous AV conduction inhibited the pacemaker. Shortening the AV interval resulted in pacing with a short QT interval. Further reduction of the AV interval resulted in a longer QT interval up to a point where the QT interval became stable. This point, the bending point in the plot of measured QT interval versus shortened AV intervals, coincided with the point of FVC. The relation of the QT-AV interval plot and the point of fusion was comparable when lengthening the AV interval at a 30 beats/mm faster stimulation rate. Conclusion: The bending point in the QT interval versus AV interval plots showed a good correlation with the FVC and fusion points observed on ECG. The results suggest that automatic discrimination between fusion and full capture using QT interval measurements may be feasible.     

Effect of Isoetharine on Cardiac Conduction in Man

The effects of isoetharine on the His bundle electrogram were studied in 10 patients with heart disease. Recordings were made at varied heart rates using atrial pacing. Isoetharine significantly reduced the AH interval with atrial pacing, but it had no effect on the HV interval. Second degree heart block occurred at higher pacing rates after isoetharine treatment as compared to the control state. The heart rate and blood pressure showed no significant change after isoetharine. The functional and effective refractory period were measured with the use of the extra-stimulus technique. The functional refractory period of the AV node, as well as the effective refractory period of the atrium, significantly decreased after isoetharine. Thus, isoetharine can improve conduction through the atrioventricular node. The drug does have a cardiac effect as measured by its action on the human conduction system.     

Effects of Different Pacing Modes on Left Ventricular Relaxation in Closed-Chest Dogs

Ventricular relaxation is an important determinant of ventricular filling; impaired relaxation may decrease cardiac output and stroke volume. Relaxation hos been shown to occur more quickly following beats with an increased extent of systolic fiber shortening. Since cardiac output and stroke volume are greater during atrioventricular (AV) sequential pacing than during ventricular pacing at identical heart rates, we reasoned that AV sequential pacing would improve relaxation. To assess this hypothesis we studied 11 dogs with chronic (1-3 months) complete heart block (CHB) induced by radiofrequency catheter ablation of the His bundle. Right and left heart pressures, thermodilution cardiac output, und single plane ventriculography were recorded during baseline rhythm (CHB), and VVI, and AV sequential pacing at a heart rate greater than the sinus rate. None had ventriculoatrial conduction. During AV sequential pacing, the AV interval was set at 150 msec. Cardiac output and stroke volume were significantly increased in the AV sequential compared to the VVI pacing mode. Left ventricular pressures, maximal positive and negative dP/dt, and the time constant (T) of isovolumic pressure decay were not different in the two modes. We conclude that despite increased stroke volume in the AV sequential pacing mode, relaxation is unchanged. We believe the lack of change in relaxation is due to nonuniform ventricular activation when depolarization is initiated at the right ventricular apex.     

Evaluation of Direct Respiratory Modulation of the QT Interval Variability

To investigate the direct respiration-mediated vagal modulation of the QT interval variability, spectral analyses of the RTp interval (from the R wave peak to the T wave peak) variability (RTpV) and the RR interval variability (RRV) were performed in 12 subjects with normal ventricular repolarization under three conditions while the respiration frequency was kept at 0.2 Hz: during sinus rhythm, during fixed atrial pacing, and during fixed atrial pacing with autonomic blockade. The cross-spectrum between the RRV and RTpV was quantified by the squared coherence. During sinus rhythm the RRV power spectrum showed two peaks: a broad peak in the low frequency (LF) band and a sharp peak at 0.2 Hz which corresponded to the controlled respiration frequency. The RTpV power spectrum showed corresponding peaks to the RRV peaks in both the LF and high frequency (HF) bands with high coherence (mean maximum values of the squared coherence in the LF band 0.59 ± 0.22, and in the HF band 0.74 ± 0.14). During atrial pacing mean total power of the RTpV decreased from during sinus rhythm (from 16.3 ± 5.6 ms² to 12.9 ± 5.4 ms², P < 0.05) and the RTpV spectral peaks were abolished in both the LF and HF bands concordant with disappearance of the RRV peaks. Autonomic blockade gave no additional change to the RTpV power spectrum independently of the RRV during fixed atrial pacing. The present study suggested that the direct respiration-mediated vagal modulation may not affect the short-term variability of the QT interval in subjects without repolarization abnormality.     

A Microcomputer System for On-Line Study of Atrioventricular Node Accommodation

An automated on-line programmable stimulator and interval measurement system was developed to study atrioventricular node (AVN) accommodation. This dedicated microcomputer system measures and stores the stimulus-to-His bundle (S-H) interval from His bundle electrogram (HBE) recordings. Interval measurements for each beat are accurate to within 500 microsecond. This user-controlled system has been used to stimulate at any rate up to 6.5 Hz and to measure intervals up to 125 ms in isolated perfused guinea pig hearts. A built-in timer-reset mechanism prevents failure of the system in the absence of a His potential (i.e., 2:1 AV block). It may be modified for use in clinical studies or other experimental systems and has the ability to measure other physiological intervals. The system provides the precision in pacing and accuracy in the measurement of AVN conduction time that is necessary for meaningful analysis of AVN accommodation and has the simplicity of design and use that is not available in previously described systems. Furthermore, this computer system can be used not only in studies involving AV conduction, but also in any setting where programmed stimulation and interval measurement and recording need to be performed simultaneously.     

Evidence for adenosine mediation of atrioventricular block in the ischemic canine myocardium.

Adenosine levels in oxygen-deprived myocardium can rise to 10- 100 microM concentrations known to cause atrioventricular (AV) conduction delay and block. We reported that the AV conduction delay and block caused by hypoxia is markedly attenuated by 10 microM aminophylline, and adenosine competitive antagonist. THe purpose of the present study was to investigate adenosine's role in ischemic AV conduction disturbances. Dogs were anesthetized and instrumented for His bundle and surface electrogram recordings. The total AV conduction time was subdivided in to atrial-His bundle (AH) and His bundle-ventricle intervals. The atrioventricular node artery (AVNA) was cannulated for selective injection of drugs in the AV node region. Adenosine (10 to 100 microgram), as a 2-ml bolus injection, rapidly produced a dose-dependent, transient increase in the AH interval; a 1,000-microgram dose caused second degree AV block. The duration of the increase in AH interval was also dose-dependent. Dipyridamole, and inhibitor of nucleoside transport, potentiated the negative dromotropic effects of adenosine, whereas aminophylline attenuated them. In some dogs, after cannulation of the AVNA, first and second degree AV block occurred spontaneously or were induced by rapid atrial pacing. Injection of the aminophylline (5 mg/kg, i.e.) or theophylline (100-1,000 microgram) into the AVNA rapidly reversed the AV blocks. Upon washout of the drugs the AV blocks recurred. We conclude that endogenously released adenosine may account for a major fraction of the AV conduction delay and block associated with impaired blood supply to the AV node, and the theophylline and aminophylline reverse the AV conduction defect by antagonizing the effects of adenosine.     

Anatomy of the cardiac conduction system

The specialized cardiomyocytes that constitute the conduction system in the human heart, initiate the electric impulse and result in rhythmic and synchronized contraction of the atria and ventricles. Although the atrioventricular (AV) conduction axis was described more than a century ago by Sunao Tawara, the anatomic pathway for propagation of impulse from atria to the ventricles has been a topic of debate for years. Over the past 2 decades, there has been a resurgence of conduction system pacing (CSP) by implanting pacing leads in the His bundle region in lieu of chronic right ventricular pacing that is associated with worse clinical outcomes. The inherent limitations of implanting the leads in the His bundle region has led to the emergence of left bundle branch area pacing in the past 3 years as an alternative strategy for CSP. The clinical experience from performing CSP has helped electrophysiologists gain deeper insight into the anatomy and physiology of cardiac conduction system. This review details the anatomy of the cardiac conduction system, and highlights some of the recently published articles that aid in better understanding of the AV conduction axis and its variations, the knowledge of which is critical for CSP. The remarkable evolution in technology has led to visualization of the cardiac conduction system using noninvasive, nondestructive high‐resolution contrast‐enhanced micro‐computed tomography imaging that may aid in future CSP. We also discuss from anatomical perspective, the differences seen clinically with His bundle pacing and left bundle branch area pacing.