不同起搏方式房室延迟优化的对比研究

目的观察双腔起搏(DDD)患者不同起搏方式时最佳房室延迟(AVD)的差异。方法对20例置入DDD起搏器的患者经左侧锁骨下静脉插入Swan-Ganz导管,分别测量DDD方式及心房感知心室起搏(VDD)方式下的不同AVD起搏的急性血流动力学效应。结果DDD右心耳起搏优化AVD(149±15ms)比VDD起搏AVD(114±12ms)延长了38±12ms,差异有非常显著性意义(P<0.01)。结论双腔起搏时DDD右心耳起搏可使AVD达到最优。     

双腔起搏器不同房室间期起搏对心功能影响的研究

探讨双腔起搏器不同房室间期 (AVD)起搏对即时心功能的影响 ,并观察根据即时心功能调定的最佳房室间期对CHF患者长期疗效的影响。用M型和B型超声心动图比较了 6例无心力衰竭DDD起搏者和 14例CHFDDD起搏患者 (其中 13例存在缓慢型心律失常 )不同AVD起搏时心功能参数的变化。 14例CHFDDD起搏患者常规起搏 3个月后随机分为常规起搏组 (7组 )和最佳房室间期起搏组 (7例 ) ,起搏 3个月后随访心功能 (NYHA分级 )和心室腔径的改变。结果 :CHF组和无心力衰竭组不同AVD起搏时各项心功能指标变化均无差异 (P >0 .0 5 ) ;常规起搏组和最佳AVD起搏组起搏 3个月后NYHA分级和心室腔径无显著变化 (P >0 .0 5 )。结论 :经调定的短AVDDDD起搏不能改善CHF患者的心功能和心室重构。不宜将双腔起搏器最佳AVD起搏作为CHF患者的常规非药物疗法 ,对因纠治心脏电学异常而安装DDD起搏器的CHF患者 ,在无其他证据之前仍宜采用常规AVD起搏     

不同房室间期对双腔起搏左室收缩功能的影响

为探讨双腔起搏不同房室间期对左室收缩功能的影响及最佳房室间期 ,选择 18例置入DDD起搏器的病窦综合征患者 ,在DOO起搏方式下随机将房室 (AV)间期程控为 10 0 ,130 ,15 0 ,170 ,2 0 0ms,在超声心动图下观察左室收缩功能指标 ,每次测量间隔 5min以上。结果 :AV间期为 15 0ms时左室收缩功能最好 ,与AV间期为 10 0ms时相比 ,左室收缩功能明显改善。以心输出量 (CO)为标准 ,18例中有 9例AV间期在 15 0ms时CO最佳 ,5例在 2 0 0ms时CO最佳 ,3例在 170ms时CO最佳 ,1例在 130ms时CO最佳 ;以CO为标准 ,DOO起搏方式最佳AV间期为 16 6±2 4ms。结论 :双腔起搏的AV间期对左室收缩功能有重要的影响 ,以CO为标准 ,个体化地选择双腔起搏的最佳AV间期对改善患者的心脏功能有重要的意义。     

双腔起搏房室延迟时间对心功能的影响

目的观察不同房室延迟(AVD)的双腔起搏对心脏收缩、舒张功能的影响及不同心功能状态下的优化AVD。方法测量20例心力衰竭患者及10例心功能正常者(对照组)不同房室延迟起搏的急性血流动力学效应,同时以脉冲多普勒超声心动描记术测量心脏收缩、舒张功能指标。结果心力衰竭组房室延迟在134±13、131±12、136±10ms起搏时,血流动力学指标及左心室收缩功能、右心室舒张功能指标较AVD基线穴100ms雪及250ms显著改善;140±17ms起搏时,左心室舒张功能指标较AVD基线及250ms显著改善。对照组AVD在162±14ms起搏时,血流动力学参数较AVD基线及250ms显著改善。结论优化AVD可即刻改善心力衰竭患者心脏收缩及舒张功能,优化AVD随心功能状态不同而改变。     

快速心房起搏时SV间期与SS间期的比值在房室结折返性心动过速慢径消融中的应用

评价快速心房起搏时最快 1∶1房室传导的SV间期 (SV间期 )与 1∶1房室传导的最短S1S1间期 (SS间期 )的比值 (SV/SS)在房室结折返性心动过速 (AVNRT)慢径消融中的应用 ,将AVNRT分为房室结功能曲线连续组 (Ⅰ组 ,10例 )及房室结功能曲线不连续组 (Ⅱ组 ,17例 )测量心房分级递增刺激时的SS间期与SV间期及SV/SS ,并进行消融前、后和组间比较。结果显示 ,两组消融后SV间期较消融前明显缩短 (Ⅰ组 :2 2 1.0± 2 2 .3vs 35 7.0± 43.7ms;Ⅱ组 :2 0 2 .1± 30 .6vs 379.4± 44 .2ms,P均 <0 .0 5 ) ;消融前后SS间期无明显变化 (Ⅰ组 :310 .0± 40 .6vs 30 8.0± 36 .8ms;Ⅱ组 :332 .9± 48.1vs 336 .5± 6 2 .3ms) ;两组中所有患者消融前SV/SS比值均 >1,而消融后SV/SS比值均 <1。结论 :SV/SS可作为慢径消融成功终点的辅助观察指标之一 ,尤其对于房室结传导曲线呈连续性者 ,使用此方法可简便地观察消融终点 ,增加消融的目的性。     

房室间期优化对三度房室传导阻滞患者房室顺序起搏心功能的影响

目的:探讨不同房室间期(AVD)对三度房室传导阻滞(Ⅲ°AVB)患者房室顺序起搏(DDD)后心功能的影响。方法:接受DDD起搏治疗的Ⅲ°AVB患者16例,其中男女比例3∶1,平均年龄(64.50±15.96)岁。起搏器术后调整不同的AVD,应用左心导管检查测量左心室内压力上升/下降的速率(±dP/dT),评价不同AVD对Ⅲ°AVB患者DDD起搏后心功能的影响。结果:个体间最佳AVD的离散度较大(120～260 ms);不同AVD时,±dP/dT组内差异有统计学意义(P0.05),最佳AVD在160～220 ms区间的分布较集中;在160～220 ms区间的+dP/dT水平与其他区间的+dP/dT水平比较差异有统计学意义(P0.05);+dP/dT组最佳AVD与-dP/dT组最佳AVD比较差异无统计学意义(P0.05)。结论:不同的AVD对Ⅲ°AVB患者DDD起搏后心脏的收缩及舒张功能均有影响,最佳AVD能使其心脏的收缩及舒张功能达到最佳状态。     

多普勒超声心动图在双腔心脏起搏最佳房室间期设置中的应用价值

目的 :探讨多普勒超声心动图在双腔心脏起搏最佳房室间期设置中的应用价值。方法 :19例患有完全性房室传导阻滞并植入永久性双腔心脏起搏器的患者 ,程控房室间期从 90ms逐渐递增至 2 5 0ms ,每次递增量 2 0ms ,脉冲多普勒测量不同房室间期时每搏量和二尖瓣血流频谱的变化。结果 :每搏量最大时的最佳房室间期为 (16 8.9± 15 .6 )ms ,二尖瓣血流频谱的A波终末与二尖瓣叶完全关闭信号同步时的房室间期为 (178.4±2 3.4 )ms ,两者之间存在良好的线性回归关系 (Y =86 .2± 0 .5X ,r =0 .70 ,SEE =11.5 ,P <0 .0 1)。结论 :多普勒超声可以对双腔心脏起搏时的最佳房室间期作出准确地选择 ,并且具有无创、可重复和简便易行的特点。     

DDD起搏最佳房室延迟的设置及血流动力学评价

目的 对不同房室延迟DDD起搏患者进行血流动力学评价,探讨DDD起搏最佳房室延迟的设置方法。方法 应用超声心动图研究17例植入DDD起搏器患者不同AV间期时心排出量（CO）、舒张期二尖瓣返流（DMRD）、A波结束至二尖瓣完全关闭时间间期及同步心电图QT间期等的变化。结果（1）当 AV延迟调至（16.9±19.9）ms时,A波结束与二尖瓣关闭同时出现,此时将AV延迟分别延长20ms、40ms、60ms、80ms,A波结束至二尖瓣完全关闭的间期分别延长（13.9±3.7）ms、（31.5±5.1）ms、（52.8±4.1）ms、（72.4±4.0）ms,而且在此间期可发现舒张期二尖瓣返流;（2）CO最大时的AV延迟（即最佳房室延迟）与预测的最佳 AV延迟呈明显正相关（r=0.893,P<0.05）;（3）临界AV间期与最佳AV间期有显著正相关（r=0.884,P<0.05）,临界AV间期较最佳AV间期长;（4）临界AV间期及其后不同AV间期预测的最佳AV间期之间差异均无显著性（P>0.05）。结论 （1）临界AV间期可代表最佳AV间期的上限,可用临界AV间期减去A波结束至二尖瓣完全关闭的时间间期来预测最佳AV间期;（2）最佳AV延迟可按以下公式预测:先设置一个较长的AV间期,然后于超声心动图下测量A波结束至二尖瓣完全关闭的时间间期,则最佳AV间期等于此较长的AV间期减去A波结束至二尖瓣完全关闭的     

Ⅲ度房室传导阻滞患者行不同房室间期起搏对血流动力学及功能的影响

目的探讨Ⅲ度房室传导阻滞(AVB)患者不同房室间期(AVD)起搏对血流动力学及功能的影响。方法选择植入双腔起搏器的Ⅲ度AVB患者51例,按不同AVD分为前后4期:A期AVD为心房感知(SAV)90 ms、心室起搏(PAV)120 ms;B期为SAV 120 ms、PAV 150 ms;C期为SAV 150 ms、PAV 180 ms;D期为SAV 180 ms、PAV 210 ms。每期观察2个月,分别比较Ⅲ度AVB患者4期心电图QRS波时限和形态,血清氨基末端脑钠肽前体(NT-proBNP)水平及心脏超声左房内径(LAD)、左室收缩末期内径(LVDs)、左室舒张末期内径(LVDd)、室间隔厚度(IVST)、左室后壁厚度(LVPWT)、左室射血分数(LVEF)及二、三尖瓣返流等参数。结果Ⅲ度AVB患者行不同AVD起搏时LAD、LVDd、LVDs、IVST、LVPWT及LVEF无变化;而二尖瓣及三尖瓣返流随AVD的延长而依次减少;起搏QRS波时限A期较D期长(149.21±8.10 ms vs 145.27±6.94 ms,P<0.05);NT-proBNP随AVD的延长而减少(中位值分别为365.51,327.54,279.13和270.10 pg/ml)。结论Ⅲ度AVD患者不同AVD起搏对心脏血流动力学会产生影响,短期内对心脏的结构及功能影响不明显,选择起搏间期为SAV180 ms、PAV 210 ms时患者的获益最大。     

DDD起搏器不同房室延迟对血流动力学的影响

笔者对 15例Ⅲ度房室阻滞置入DDD起搏器的患者 ,观察不同的AV间期时超声心动图左室射血分数 (EF)与心输出量 (CO)、血浆心钠素水平及平板运动试验参数的变化 ,以评价不同AV间期对血流动力学的影响。结果显示不同的AV间期将产生不同的左室EF与CO及血浆心钠素水平 ,当AV间期最佳时 (15 3 .67± 18.75ms)将产生最佳左室EF与CO ,血浆心钠素水平最低。结论 :对置入DDD起搏器的病人应加强随访 ,调整AV间期可使起搏器发挥最大效能。     

短QT间期的心电图诊断标准探讨

目的用2种已报道的诊断标准研究一组心电图短QT间期者所占比例,并比较2种方法的异同。方法随机选取547例健康人,做常规12导联心电图,准确测量QT间期,根据RR间期(RR)和心率(HR)计算QT间期校正值(QTc)和QT间期预计值(QTp),以QT相似文献   

双腔起搏房室延迟优化对心功能及神经内分泌因子的影响

观察双腔起搏不同房室延迟(AVD)对即刻心功能的影响,并探讨以优化的AVD起搏对心功能及神经内分泌因子的影响。用SwanGanz导管和彩色多谱勒心脏超声仪分别测定20例心功能ⅡⅢ级患者不同AVD起搏时心功能参数的变化,将心排血量(CO)最大的和/或平均肺毛细血管楔嵌压(MPCWP)下降最明显的AVD定为优化AVD。其后,所有患者分别进行8周常规AVD及8周优化AVD起搏,分别在8周结束时对患者进行心脏B超测试及测定血浆内皮素(ET)、心钠素(ANP)、肾素活性(PRA)、血管紧张素Ⅱ(AngⅡ)、醛固酮(ALD)。结果:根据心导管及心脏B超测量的优化AVD分别为134±13ms及131±12ms。优化AVD组较常规AVD组对左室收缩功能指标有改善,但未达有统计学显著性差异。左室舒张功能指标在优化AVD组较常规AVD组明显改善。神经内分泌因子在优化AVD组较常规AVD组明显减低。结论:优化AVD起搏对心力衰竭患者远期心功能有改善作用,能明显降低有关神经内分泌因子。     

对QT离散度实质的探讨

为探讨ＱＴ离散度（ＱＴｄ）的真实意义，观察１３９例急性心肌梗死（ＡＭＩ，ＡＭＩ组）及１０９例正常人（对照组）的最长ＱＴ间期（ＱＴｍａｘ）、校正ＱＴｍａｘ（ＱＴｃｍａｘ）及ＱＴｄ的变化。结果：①ＡＭＩ组的ＱＴｍａｘ、ＱＴｃｍａｘ和ＱＴｄ均显著高于对照组（分别为４２２．６０±３０．５１ｍｓｖｓ３８２．４６±２３．４０ｍｓ、４６０．２１±２８．９６ｍｓｖｓ３８８．５１±２０．１５ｍｓ、５９．８０±２８．４０ｍｓｖｓ３９．４３±１２．２１ｍｓ，Ｐ均＜０．００１）。②ＡＭＩ组中发生严重室性心律失常（ＶＡ）患者（１１４例）的ＱＴｍａｘ、ＱＴｃｍａｘ、ＱＴｄ与无ＶＡ的患者（２５例）相比，均有显著差异（分别为４４８．５８±３３．４０ｍｓｖｓ４１６．１０±３５．３０ｍｓ、４８１．４３±３５．１７ｍｓｖｓ４３９．６０±２７．１０ｍｓ、６６．９０±２０．７２ｍｓｖｓ４８．３２±２３．６１ｍｓ，Ｐ均＜０．００１）。认为ＡＭＩ时ＱＴｄ系Ｔ向量环在不同导联上的“投影”差异所引起的，其异常的本质是ＱＴ间期延长     

经心内膜右房线形消融治疗心房颤动的安全性评价

为探讨经心内膜右房线形消融治疗心房颤动（简称房颤）的安全性，１２只犬以乙酰胆碱静脉滴注和（或）电刺激建立房颤模型，观察射频导管消融前、后实验犬的病理生理变化。结果显示：①与消融前相比，消融后窦性心率（１５０．８２±３６．７１ｂｐｍｖｓ１６３．６７±３０．９９ｂｐｍ）、窦性Ｐ波时限（７３．６４±１６．８０ｍｓｖｓ６９．５８±１２．１４ｍｓ）、ＰＲ间期（１２０．７３±２６．２９ｍｓｖｓ１１４．０２±１９．２１ｍｓ）、校正窦房结恢复时间（７６．２５±１８．８７ｍｓｖｓ７２．５０±１１．９０ｍｓ）、右房压力（０．４９±０．０６ｋＰａｖｓ０．４６±０．０８ｋＰａ）以及血浆心钠素（０．４８±０．１１ｎｇ／ｍｌｖｓ０．５０±０．０７ｎｇ／ｍｌ）变化均无显著性差异（Ｐ均＞０．０５）。血清磷酸肌酸激酶于消融后即刻明显升高（５２５．９５±４２６．４９Ｕ／Ｌｖｓ１１５．２７±２８．７０Ｕ／Ｌ，Ｐ＜０．０１），但术后１４日与消融前相比已无显著性差异（１１４．０２±２３．３５Ｕ／Ｌｖｓ１１５．２７±２８．７０Ｕ／Ｌ，Ｐ＞０．０５）。②４只犬发生并发症，其中１只损伤窦房结，２只发现心脏巨大附壁血栓，另１只术后出现一过性房性早搏、短阵房?     

Beneficial hemodynamic response to chronic prazosin therapy in congestive heart failure

Thirteen patients with advanced congestive heart failure (CHF) were treated with prazosin. Following the first dose, cardiac output (CO) (mean ± SD) rose from 3.2 ± 1.2 to 4.3 ± 1.1 L/min, pulmonary artery diastolic pressure (PAD) decreased from 23 ± 12 to 18 ± 11 mm Hg, mean arterial pressure (MAP) decreased from 85 ± 10 to 76 ± 10 mm Hg, and heart rate did not change (92 ± 15 vs 92 ± 14 bpm). At the end of a 48 to 72 hour titration to an optimal regimen, significant effects on CO (3.2 ± 1.1 vs 4.5 ± 1.3 L/min), PAD (24 ± 12 vs 18 ± 8 mm Hg), and MAP (84 ± 10 vs 76 ± 10 mm Hg) were still seen. The patients were restudied after 3 months of treatment. In contrast to reports of rapid development of tolerance to prazosin, we found continued beneficial effects on CO (3.0 ± 1.3 vs 3.8 ± 1.0 L/min) and PAD (23 ± 12 vs 18 ± 10 mm Hg), without significant change in MAP (81 ± 11 vs 78 ± 8 mm Hg). We found wide variability in the CO rise in response to prazosin, which was not accounted for by differences in plasma prazosin concentration. Systemic vascular resistance in the untreated state did correlate with the percentage change in CO. In addition, excessive lowering of the PAD appeared to blunt the CO response in some cases.     

双腔起搏器置入患者最佳房室延迟不同设置方法的临床研究

对不同最佳房室延迟(OAVD)设置方法进行比较,探讨OAVD设置的简单、实用的方法。选择36例置入双腔起搏器的患者,设置不同的AVD,于超声心动图下记录左室射血分数(EF)、舒张期二尖瓣返流、A波结束至二尖瓣完全关闭的时间间期(Time1)、最早出现舒张期二尖瓣返流的AVD(临界AVD),并通过同步心电图测定QT间期(QTI)、QT离散度(QTD)及QRS波群时间(QRSI)。将各指标预测的OAVD与OAVD(EF最大时的AVD)进行比较。结果:①心功能正常者心房起搏或心房感知时在AVD为170ms或140~160ms时EF达到最大,且与OAVD时EF相比差异均无显著性;心功能不全者在AVD为130~140ms时EF达到最大,但与OAVD时EF相比差异有显著性。②三种心电图指标预测的OAVD与OAVD比较差异均无显著性,其预测的OAVD在心功能不全患者与OAVD显著相关。③预测OAVD、AVD=200或180ms时预测的OAVD与OAVD比较差异均无显著性。结论:在实际工作中,可通过下述简单方法设置OAVD:OAVD=200ms(或180ms)减去200ms(或180ms)时Time1,以提高随访效率。     

Is QT Dispersion Associated with Sudden Cardiac Death in Patients with Hypertrophic Cardiomyopathy?

QT dispersion is significantly greater in patients with hypertrophic cardiomyopathy (HCM) than that in healthy subjects. Few data exist regarding the prognostic value of QT dispersion in HCM. In this study, we retrospectively investigated the association between QT dispersion and sudden cardiac death in 46 patients with HCM (mean 33.1 ±; 15.5 years, 32 men). The case group consisted of 23 HCM patients who died suddenly, and the control group consisted of 23 HCM patients who survived uneventfully during follow‐up. Study patients were pair‐matched for age, gender, and maximum left ventricular wall thickness. QT dispersion (maximum minus minimum QT interval) was manually measured on early 12‐lead ECGs using a digitizing; board. An in‐house program was used for calculating QT interval, QT dispersion, JT interval, and JT dispersion (maximum minus minimum J point to T end interval). Patients in the case group tended to have shorter RR intervals than those in the control group (777 ±; 171 vs 856 ±; 192 ms, P = 0.08). Maximum corrected QT and JT intervals did not discriminate the case group from controls (489 ±; 29 vs 479 ±; 27 ms, P = NS; 375 ±; 36 vs 366 ±; 22 ms, P = NS, respectively). Greater QT dispersion and JT dispersion were found in the case group compared with controls (74 ±; 28 vs 59 ±; 21 ms, P = 0.02 and 76 ±; 32 vs 59 ±; 26 ms, P = 0.03, respectively). The measurements of maximum QT, JT, and T peak to T end intervals, precordial QT and JT dispersion, and T peak and T end dispersion were all comparable between the two groups (P = NS for all). No systematic changes in ECG measurements were found from late ECGs of the case group compared to those from early ECGs (P = NS). No correlation between maximum left ventricular wall thickness and QT dispersion, JT dispersion, maximum QTc or JTc intervals was observed (r < 0.29, P > 0.05 for all). Our results; show that increased QT dispersion and JT dispersion is weakly associated with sudden cardiac death in the selected patients with HCM. A.N.E. 2001; 6(3):209–215     

Relationship between atrioventricular delay, QT interval and cardiac function in patients with implanted DDD pacemakers.

QT interval may change when cardiac function is improved by optimizing the atrioventricular the (AV) delay. The relationship between AV delay, QT interval and cardiac function in patients with implanted DDD pacemakers was studied in 12 patients (aged 71+/-12 SD years) with complete or high degree AV block. Cardiac output (CO) was measured using a Swan-Ganz catheter or by continuous Doppler echocardiography. The pacing rate was fixed at 70-80/min to eliminate the influence of heart rate. The AV delay was prolonged stepwise by 30 ms starting from 90 ms. All measurements were performed after 5 min of pacing. When the AV delay was prolonged, the CO and QT interval gradually increased and reached a peak, and then decreased. When the CO was increased from the minimum to the maximum value by optimizing the AV delay, the QT interval was significantly prolonged from 440+/-40 to 456+/-39 ms (P<0.002). The CO increased from 5.5+/-2.5 to 6.0+/-2.5 l x min(-1) (P<0.002) when the AV delay was changed, during which the QT interval was prolonged from the minimum to the maximum value. There was a significant positive correlation between the optimal AV delay at which CO was maximal (161+/-33 ms) and the optimal AV delay predicted from the maximum QT interval (167+/-29 ms, r=0.85, P<0.001). In conclusion, the optimal AV delay can be predicted from the QT interval.     

Sildenafil Citrate Does Not Alter Ventricular Repolarization Properties: Novel Evidence from Dynamic QT Analysis

Background: Sildenafil citrate may have direct cardiac electrophysiological effects, and is possibly responsible for some cardiac events. The aim of our study was to investigate the effects of sildenafil citrate on QT dynamicity properties with a new QT analysis program showing even small changes in ventricular repolarization. Methods: Twenty‐four‐hour Holter electrocardiographic recordings were used to obtain the data in the predrug phase (1‐hour rest position before drug administration), and in the postdrug phase (1‐hour rest position, which began 60 minutes after 50 mg oral sildenafil citrate administration). With the special QT analysis program (Verda, Reynolds Medical Ltd., UK); mean values of RR, QT, QT_o (corrected QT), J (the exponent of correction formula) and S (QT/RR plots slope) parameters together with QT variability indexes (QTVI) were calculated for study phases. Results: Mean ± SEM values for RR and QT were higher in postdrug phase than in predrug phase (RR: 845 ± 42 ms vs 816 ± 46 ms, P < 0.05; QT: 371 ± 8 ms vs 361 ± 9 ms, P < 0.05). However, sildenafil did not induce any significant change in mean ± SEM values for QT_o, J, and S in postdrug phase compared with predrug phase (408 ± 10 ms vs 406 ± 8 ms, 0.474 ± 0.030 vs 0.433 ± 0.025, 0221 ± 0.020 vs 0.198 ± 0.017, respectively; P > 0.05). QTVIs were also not different in each phase (predrug: ?0.874 ± 0.071 vs postdrug: ?0.997 ± 0.067, P = 0.109). Conclusions: Fifty milligrams sildenafil does not affect QT dynamicity properties. The cardiac events associated with sildenafil could not be explained with ventricular arrhythmias.