不同起搏方式对血流动力学的急性影响

目的：探讨不同起搏方式对病窦综合征患者血流动力学的急性影响。方法：Swan-Ganz漂浮导管测量14例病窦综合征患者起搏前及VVI、AAI、DDD起搏时血流动力学参数；并根据VVI起搏时室房传导的情况分组对比。结果：起搏前及起搏时，平均动脉压(MAP)无明显差异。AAI、DDD起搏时，右房压(RAP)、平均肺动脉压(PAP)、肺毛细血管楔嵌压(PCWP)与起搏前对比无明显改变，但较VVI起搏明显下降(P＜0．01)；心输出量(CO)较起搏前及VVI起搏时显著增加(P＜0．01)。AAI、DDD起搏间对比无显著性差异。VVI起搏时，RAP、PAP、PCWP较起搏前显著增加，室房传导组更为明显；无室房传导组较起搏前CO略有增加(P＜0．05)，而室房传导组CO改变不明显；室房传导组较无室房传导组RAP、PCWP显著增加(P＜0．05)。结论：AAI、DDD起搏可以显著增加CO，对血流动力学影响较小；VVI起搏特别存有室房传导时，可导致血流动力学明显异常；AAI、DDD起搏明显优于VVI起搏。     

CDFI评价房室非同步,同步起搏对血流动力学的影响

本文应用彩色多普勒血流显像仪对17例安置永久性心脏起搏器患者进行了血流动力学研究。结果表明:房室同步起搏的SV、CO及PFVE、ETVI、PFVE/PFVA较之房室非同步起搏明显增加,房室非同步起搏后SBP、MAP降低、体重增加、心房内径增大、瓣膜返流率高,提示房室非同步起搏对瓣膜功能、血流动力学影响明显,是促发起搏器综合征(PMS)的主要动因。     

超声心动图在评价人工心脏起搏对心脏功能影响中的应用

目的：探讨超声心动图法在房室同步和心室同步对左心室收缩功能影响中的应用。方法：20例置入双腔起搏器的患者，随机将起搏方式程控为抑制型按需心房起搏(AAI)、抑制型按需心室起搏(VVI)、非同步房室起搏(DOO)，每种起搏方式稳定5min后，在超声心动图下测量左室收缩功能指标。结果：与VVI和DOO起搏相比，AAI起搏时每搏输出量(SV)、心输出量(CO)、左室射血分数(LVEF)等均显著增高(P＜0．05)，而心室收缩末期容积(ESV)显著降低(P＜0．05)；与VVI起搏相比，DOO起搏时SV、CO等均显著增高(P＜0．05)。结论：房室同步和心室同步对左心室收缩功能有重要的影响，在人工心脏起搏治疗中，对于合适的患者保持房室同步和心室同步具有重要的意义；超声心动图作为一种无创、简便、安全的检查技术，能够客观反映不同起搏方式对心脏功能的影响，值得在临床和科研工作中推广。     

多普勒超声心动图（PDE）评价不同起搏方式对右心功能的影响

对17例安装永久性起搏器者应用脉冲多普勒记录肺动脉血流频谱,对比分析不同方式起搏器植入前后其右心功能的变化。结果显示:DDD起搏较VVI起搏的右室每搏量(SV)、心输出量(CO)增加(P<0.05、P<0.02),肺动脉峰值流速(PPFV)显著增加(P<0.01)。两组舒张早、晚期右室充盈指标均增加,DDD组舒张早期峰值流速(PFVE)显著增加(P<0.01)。表明:房室同步起搏较单纯心室起搏有更好的血液动力学效应,肺动脉血流参数可用于估价右室功能。     

CD检测评价尿毒症合并心力衰竭时血液动力学改变分析

目的 探讨尿毒症合并心力衰竭时的血液动力学改变并分析其发生原因。方法 使用血液循环动力学信息检测仪(CD)检测23例尿毒症合并心力衰竭及31例尿毒症无心力衰竭。结果 充血性心力衰竭组左室舒张末期压力、左室舒张末期容量、心输出量、射血阻抗、心肌耗氧量、左室有效功率均明显增高，射血分数明显降低。结论 CD检测简单方便，重复性好。心力衰竭根本原因左室收缩乏力、顺应性降低、β受体兴奋而不是有效循环血量增加。     

永久性心脏起搏器植入对左心室重构影响研究

目的:分析心脏起搏器植入后不同起搏方式对左心室重构的影响。方法:共入选34例患者,其中VVI起搏器20例,DDD起搏器14例,分别在术前及术后5~12个月,用超声心动图观测左室舒张末期内径、左室收缩末期内径、左室射血分数。结果:34例起搏器植入患者均出现左心室重构,VVI组观测指标植入前后比较差异有统计学意义,DDD组观测指标差异无统计学意义。结论:起搏器植入后均可出现左心室重构,提示右室心尖部起搏对左心室的收缩、舒张功能产生不利影响;起搏器植入应选用生理性或接近生理性起搏方式。     

房室结双径路伴房室结折返性心动过速的室房传导探讨

根据电生理检查结果,将接受射频消融术患者62例分为房室旁道伴房室折返性心动过速(AVRT)32例,房室结双径路(DAVNP)伴房室结折返性心动过速(AVNRT)30例。以房室旁道伴AVRT室房(VA)传导特征为对照,探讨DAVNP伴AVNRT VA传导特征。结果表明DAVNP伴AVNRT其VA传导发生率为100％;室房逆传多经房室结快径;快径逆传具有房室旁道逆传特征。     

超声心动图对心内膜弹力纤维增生症患儿血流动力学变？…

目的　应用二维多普勒超声心动图技术对心内膜弹力纤维增生症 (EFE)患儿的血流动力学变化进行分析研究。方法　超声心动图检查EFE患者 3 2例 ,平均年龄 ( 1.5± 0 .6)岁 ,正常对照 (NC)组 3 0例。结果　EFE组与NC组比较 ,各指标均有显著性差异 (P <0 .0 0 1) ,超声参数的特点为舒张期左房内径 (LADd)、左室内径 (LVDd)、室间隔厚度 (IVSTd)、左房射血力 (LAF)、室壁应力指数 (WSⅠ～Ⅲ )、峰值速度A(A峰 )及等容舒张时间 (IRTs)增大 ;但射血分数 (EF)、心脏指数 (CI)、心室短轴缩短率 (FS)、峰值速度E(E峰 )、峰值速度比 (E/A)、舒张早期快速充盈加速度 (AC)、1/3及 1/2充盈分数 ( 1/3FF、1/2FF)及标准化充盈分数 (NPFR)降低 ;将EFE组治疗前后比较除IVSd、A峰及IRTs无显著性差异 ( P >0 .0 5 )外 ,其余各指标均有显著性差异 (P <0 .0 1～ 0 .0 0 1)。结论　EFE患儿可出现房室腔扩大、心脏收缩和舒张功能降低、室壁应力增大及左房射血力代偿性增加 ;而二维多普勒超声心动图对于EFE患儿的早期诊断、疗效评价及预后估测都有极为重要的临床价值。     

多普勒超声心动图探讨心肌梗塞后左室重构对左室功能的影响

目的 :运用多普勒超声心动图分析心肌梗塞后左室重构对左室功能的影响。方法 :将 5 2例心肌梗塞患者分为左室不扩大组与左室扩大组 ,并选取 4 6例正常对照者 ,分别检测左室舒张末内径、容积、左室心肌重量指数、左室射血分数指标以及二尖瓣、肺静脉血流指标 ,对检测结果作统计分析。结果 :左室扩大组的左室舒张末内径和左室心肌重量指数大于左室不扩大组 (P<0 .0 1 ) ,左室射血分数低于左室不扩大组 (P<0 .0 1 )。左室扩大组中左室舒张末容积与左室射血分数呈中度负相关 (r=- 0 .6 4 4 ,P<0 .0 5 )。 5 2例心肌梗塞患者均有不同程度的舒张功能损害 ,但左室扩大组严重受损者有 6例而左室不扩大组则没有。结论 :心肌梗塞后左室重构影响左室收缩功能及舒张功能 ,且左室重构越明显 ,左室收缩功能及舒张功能受损越严重     

永久性植入不同类型心脏起搏器对心功能的影响

目的探讨永久性植入不同类型心脏起搏器对心脏功能的影响。方法选取接受永久性植入心脏起搏器治疗的患者60例,按心脏起搏器类型分为单腔起搏器组34例与双腔起搏器组26例。计算2组患者的起搏成功率,采用超声心电图于心脏起搏器植入前与植入6个月后检测2组患者左室收缩末期容积(LVESV)、左室舒张末期容积(LVEDV)与左室射血分数(LVEF),采用SF-36问卷评价2组患者的生活质量。结果 2组患者起搏成功率差异无统计学意义(P 0. 05);与植入前比较,单腔起搏器组植入6个月后LVESV显著升高(P 0. 05),LVEF显著降低(P 0. 05),LVEDV差异无统计学意义(P 0. 05);双腔起搏器组植入6个月后的LVESV、LVEDV、LVEF与植入前比较,差异无统计学意义(P 0. 05);植入6个月后,与双腔起搏器组比较,单腔起搏器组LVESV显著更高(P 0. 05),LVEF显著更低(P 0. 05),LVEDV差异无统计学意义(P 0. 05); 2组SF-36问卷各维度评分差异无统计学意义(P 0. 05)。结论单腔起搏器长期植入可降低患者心脏收缩功能,而双腔起搏器无此种影响。     

Hemodynamic Findings During Sinus Rhythm, Atrial and AV Sequential Pacing Compared to Ventricular Pacing In a Dog Model

The hemodynamic responses of atrial lAF], atrioventricu-lar sequential (AVP) and ventricuJar pacing (VP) were compared to sinus rhythm (SfiJ in seventeen anesthetized dogs with intact AV conduction. The atrium and/or ventricle were paced at fixed rates above the control sinus rate. An AV interval shorter than normal conduction was selected to capture the ventricle. The changes of pulmonary capillary wedge pressure (PCWP, mmHg). mean aortic pressure (MAP, mmHg), cardiac output (CO, L/min), systemic vascular resistance (SVR, dynes/s/cm⁻⁵), left ventricular stroke work index (SWI) and mean systolic ejection rate (MSER, ml/s) during sinus rhythm, atrial pacing and atrio-ventricular sequential pacing (expressed in percentages of the individual values during ventricular pacing) were:
The importance of atrial systole for cardiac performance was clearly demonstrated in dogs with normally compliant hearts. In both atrial and atrioventricular sequential pacing compared to ventricular pacing there was a reduction of pulmonary capillary wedge pressure (PCWP) (p < 0.01) and systemic vascular resistance (SVR) (p < 0.01) despite an increase in cardiac output (CO). The lesser mean systolic ejection rate (MSER) found during atrioventricular sequential pacing compared to sinus rhythm and atrial pacing may be explained by the abnormal ventricular depolarization in this pacing mode; nevertheless, the mean systolic ejection rate was still greater than that found during ventricular pacing (p < 0.05).     

Noninvasive Assessment by Doppler and M-Mode Echocardiography of Hemodynamic Responses to Temporary Pacing and to Ventriculoatrial Conduction

A new, dual-chamber temporary pacing lead was introduced via the subclavian vein in 20 patients who needed a temporary pacemaker. Stroke volume (SV) was measured continuously by combining M-mode and noninvasive Doppier echocardiography during spontaneous rhythm (SR), AV sequential pacing at a positive AV interval (DP), ventricular pacing (VP) and AV sequential pacing at a negative AV interval (VA pacing). The valvular functions were determined by Doppler echocardiography. Left ventricular dimensions and function, and left atrial size were measured by M-mode echocardiography. In the nine patients with no valvular heart disease and with no ventriculoatrial (VA) conduction (group I) the CO increased 83 ±11% during DP and 42 ± 9% during VP as compared to during SR when the heart rate (HE) was increased from 34 ± 3 to 72 ± 1 beats/min. The CO was 29 ± 3% higher during DP than that during VP. In the seven patients with valvulox heart disease and with no VA conduction (group II), the increment in CO compared to that during Sfi was SZ ± 12% during DP and 31 ±17% during VP: the CO was 17 ± 4% higher during DP than that during VP. In the four patients with spontaneous VA conduction (group III), the CO during DP was 35 ± 10% greater than that during VP, which did not result in an increase in the CO compared to that during SR in spile of an increase in HR from 52 ± 8 to 74 ± 2 beats/min. The study demonstrated that DP is the preferred temporary pacing mode and also that VA conduction during VP resulted in a mean decrease of 20% in CO compared to that during VP without VA conduction. The hemodynamic benefit from DP compared to SR seems to decrease when the left ventricular end-diastolic dimension increases. Furthermore, patients with large left ventricular end-systolic dimensions seem to have a lower increase in stroke index during DP as compared to that during VP than patients with smaller end-systolic dimensions.     

速度向量成像评价右室不同部位起搏对左心房收缩功能及同步性的影响

目的利用速度向量成像(VVI)评价右心室心尖部起搏(RVAP)和流出道起搏(RVOP)对左心房收缩功能及同步性的影响。方法分析57例起搏器植入术后2年的患者及35例正常人的心尖四腔心二维图像,得到左房峰值应变(Ss)、舒张晚期峰值应变(Sa)、收缩期应变率(s-SR)、舒张晚期应变率(a-SR),以及收缩期、舒张晚期应变达峰时间标准差(SDs、SDa)。结果与对照组比较,起搏器组的Ss、s-SR、a-SR减低,SDs、SDa增大(P<0.05),Sa两组间差异无统计学意义;流出道起搏组的Ss、s-SR、a-SR均大于心尖部起搏组(P<0.05);RVOP组术后2年SDs、SDa小于RVAP组(P<0.05)。结论持续RVOP和RVAP均可导致缓慢性心律失常患者左房储器功能及泵功能减低,收缩运动失同步化,但RVOP的不良影响较小,VVI可以灵敏地发现起搏器患者的左房功能变化。     

Left Atrial Size and Wall Motion in Patients with Permanent Ventricular and Atrial Pacing

KUBICA, J., ET AL.: Left Atrial Size and Wall Motion in Patients with Permanent Ventricular and Atrial Pacing. It is well known that during permanent ventricular pacing atrial arrhythmias and embolic complications occur much more frequently in comparison to permanent atrial or sequential pacing. He-modynamic disturbances caused by ventriculoatrial conduction (VAC) are thought to be responsible for those complications. The aim of this study was to compare the left atrial size and its wall motion in three groups of patients with sick sinus syndrome. Group 1: 58 patients with VVI pacing and VAC observed (22 males, 36 females, aged 31–86, mean 62.3). Group 2: 43 patients with primary AAI pacing (13 males, 30 females, aged 27–74, mean 57.8). Group 3: 13 patients with AAI or DDD replacing the primary VVI mode due to pacemaker syndrome and/or heart failure, all with VAC present during VVI pacing (7 males, 6 females, aged 26–80, mean 59.8). Two-dimensional/M-mode echocardiography was performed in all these patients. In group 1 mean diastolic as well as mean systolic atrial diameters were significantly greater (p < 0.005) and wall motion significantly smaller (p < 0.005) in comparison to the other groups. Left atrial wall motion amounted to only 7.4% of the mean diastolic diameter in this group. Mean left atrial diastolic and systolic diameters and wall motion in patients with pacemakers preserving atrioventricular synchrony (group 2 and group 3) were almost identical and wall motion amounted to about 22% of the diastolic diameter in both these groups. We conclude that ventriculoatrial conduction leads to significant enlargement of left atrium and to the atrial wall-motion decrease. This predisposes to arrhythmias and embolic complications. Changes in atrial size and performance seem to be reversible with restoration of the physiological atrioventricular synchrony.     

右室不同部位起搏对左室重构及脑钠肽的影响

目的 比较右室流出道间隔部(RVS)与右室心尖部(RVA)起搏对左室重构及脑钠肽的影响.方法 60例具备起搏器植入指征的患者,随机分为RVA组与RVS组,分别于治疗前及治疗后6、12、24个月采血应用夹心酶联免疫吸附法检测血浆脑钠肽(BNP)水平,超声测量左心室舒张末期内径(LVEDD)、左室舒张末期容积(INEDV)和左室射血分数(LVEF),观察2组患者起搏前后心室重构指标及BNP的变化.结果 RVA组起搏术后各个时间点BNP水平显著升高[术后6、12、24个月分别为(108.2±29.8)、(190.3±46.7)、(308.2±56.5)ng/L],与术前[(60.2±15.7)ng/L]比较差异均有统计学意义(P均<0.05);RVS组起搏术后仅24个月时BNP水平较术前升高[(75.2±15.8)ng/L与(63.9±15.1)ng/L],差异有统计学意义(P<0.05).RVA起搏组随着起搏时间的延长,与术前相比,12个月时LVEDD、LVEDV增加,LVEF下降,差异均有统计学意义(P均<0.05).而RVS组LVEDD无明显增大,LVEDV轻度增加,LVEF呈下降趋势,差异均无统计学意义(P均>0.05).结论 RVS起搏较RVA起搏能改善心肌重构,改善左室功能.减轻神经内分泌激活.     

Hemodynamic and symptomatic consequences of ventricular pacing

After implantation of a ventricular demand pacemaker (VVI), occasional patients continue to have dizziness, syncope, or near syncope ("pacemaker syndrome"). To identify patients in whom VVI pacing may have deleterious effects, we compared cuff blood pressure responses to VVI pacing with blood pressure responses to atrioventricular sequential pacing (DVI) or sinus rhythm in 50 consecutive patients. Patients with intact ventriculoatrial conduction had a much greater decrease in systolic blood pressure with VVI pacing (24 +/- 11 mm Hg) than those with ventriculoatrial dissociation (-4 +/- 15 mm Hg) (P less than 0.005). Patients who were in heart failure had a lesser decrease in blood pressure with VVI pacing than did those without failure (P less than 0.05); 13 of the 14 heart failure patients lacked ventriculoatrial conduction. Ten patients had symptomatic dizziness after VVI pacing; the incidence of symptoms was higher in patients with ventriculoatrial conduction (9 of 23) than in those without ventriculoatrial conduction (1 of 27) (P less than 0.003). We conclude that the presence of intact ventriculoatrial conduction appears to be a crucial determinant of the hemodynamic response to VVI pacing, and its presence may identify patients who are at risk for "pacemaker syndrome."     

Cardiac resynchronization therapy

About 30% of patients with left ventricular systolic dysfunction also have ventricular conduction delays (prolonged QRS duration greater than 0.12 second) most frequently seen as left bundle branch block. This intraventricular conduction delay causes nonsynchronous ventricular activation between the right ventricle and the left ventricle (or dyssychrony), compromising cardiac function. Cardiac resynchronization therapy, or biventricular pacing, is a recent intervention for ventricular dyssychrony that incorporates 3 leads for pacing the right atrium and simultaneous pacing of the right ventricle and left ventricle. Left ventricular lead placement can be difficult to implant because of coronary venous anatomy and can require longer procedure time for the patient. Restoring ventricular synchrony has been shown to decrease septal wall dyskinesis, decrease mitral regurgitation, increase left ventricular filling time, decrease pulmonary capillary wedge pressure, and reverse ventricular modeling.     

组织多普勒成像评价右心室心尖部与右心室流出道间隔部起搏对心功能的影响

目的运用组织多普勒成像技术（TDI）比较右心室流出道（RVOT）间隔部起搏和右心室心尖部（RVA）起搏对心功能的影响。方法将缓慢心律失常患者65例随机分为RVA起搏组（n=30）、RVOT起搏组（n=35）。于起搏器置入术前、术后1个月、3个月、6个月及12个月分别采用组织多普勒速度-时间曲线测量二尖瓣环舒张早期运动速度（Ea）、收缩期运动速度（Sa）、Tei指数;采用SIMPSON法测量左心室射血分数（LVEF）;采用脉冲多普勒测定二尖瓣口舒张早期最大血流速度（E）,并计算E与Ea比值（E/Ea）。结果 RVA与RVOT两组术前与术后1、3个月的各项指标差异均无统计学意义;术后1、3个月LVEF（61.89±3.37）%vs（61.51±3.11）%,（60.22±4.85）%vs（60.32±4.25）%,Sa（11.38±1.14）cm/s vs（11.44±2.14）,（10.88±1.91）cm/s vs（11.02±1.31）cm/s,E/A 0.96±0.19 vs 0.97±0.23,0.95±0.15 vs 0.96±0.13,E/Ea 8.8±3.6 vs 8.4±4.3,9.1±4.3 vs 8.8±3.2,Tei指数0.48±0.05 vs 0.47±0.08,0.50±0.20 vs 0.47±0.11（均P〉0.05）;术后6个月时RVA起搏组与RVOT起搏组比较,Tei指数及E/Ea增高（0.76±0.26 vs 0.67±0.32,10.9±3.96 vs 9.0±2.8,均P〈0.05）,术后12个月Sa降低,（8.22±1.72）cm/s vs（9.52±2.56）cm/s（P〈0.05）。结论 RVA起搏引起心脏收缩不同步,从而损害左心室收缩和舒张功能。RVOT间隔部可获得较RVA起搏更为优化的心功能参数,是较好的右心室起搏部位。     

Pacemaker Syndrome Evaluated by Cardiopulmonary Exercise Testing

Two patients who presented with dyspnea on effort, persisting after insertion of a fixed rate ventricular demand pacemaker (VVI) for sick sinus syndrome, were evaluated by cardiopulmonary exercise testing. During VVI pacing a heightened ventilatory response to exercise and a fluctuation of ventilation occurred. The high ventilatory equivalent for CO2 throughout exercise with VVI pacing suggests that the patients had ventilation-perfusion mismatching due to an increase in the pulmonary capillary wedge pressure caused by 1:1 ventriculoatrial conduction. Rate responsive ventricular (VVIR) pacing associated with intact 1:1 ventriculoatrial conduction exaggerated the exertional dyspnea, while rate responsive atrial (AAIR) pacing improved the ventilatory response to exercise. We suggest that a heightened ventilatory response to exercise due to ventilation-perfusion mismatching may be an important factor causing the pacemaker syndrome, and that cardiopulmonary exercise testing is useful in identifying the exercise-induced symptoms with ventricular pacing.