VDD起搏对缓慢性心律失常心力衰竭的血液动力学影响

为了评估ＶＤＤ起搏对缓慢性心律失常心力衰竭的血液动力学影响，对２１例心功能Ⅲ～Ⅳ级的缓慢性心律失常病人安置ＶＤＤ起搏器，并用Ｓｗａｎ－Ｇａｎｚ导管监测起搏前和起搏后３０ｍｉｎ、２４ｈ、４８ｈ、７２ｈ的心输出量（ＣＯ）、心脏指数（ＣＩ）、右房压（ＲＡＰ）、平均肺动脉压（ＭＰＡＰ）和肺毛细血管楔嵌压（ＰＣＷＰ），并记录各时期的心房率（ＡＲ）和心室率（ＶＲ）。结果：ＶＲ在术后即时及各时期显著升高（Ｐ均＜０．０５），ＣＯ、ＣＩ在起搏后３０ｍｉｎ即显著升高〔分别为４．１８±０．８１Ｌ／ｍｉｎｖｓ２．８１±０．９３Ｌ／ｍｉｎ、２．３６±０．６６Ｌ／（ｍｉｎｍ２）ｖｓ１．１８±０．６３Ｌ／（ｍｉｎｍ２），Ｐ均＜０．０５〕，起搏４８ｈ达高峰；ＲＡＰ、ＭＰＡＰ、ＰＣＷＰ在起搏后３０ｍｉｎ无显著改变（Ｐ＞０．０５），但２４ｈ开始显著性下降（分别为１．２８±０．４１ｋＰａｖｓ１．４１±０．３４ｋＰａ、２．６０±０．５１ｋＰａｖｓ３．４０±０．５６ｋＰａ、３．１０±０．５６ｋＰａｖｓ３．５４±０．６８ｋＰａ，Ｐ均＜０．０５），７２ｈ后进一步降低。结果提示ＶＤＤ起搏治疗能显著改善缓慢性心律失常心力衰竭的血液动力学，可作为治疗缓慢性心?     

腹主动脉结扎大鼠心房纤维化的实验研究

高血压患者有较高心律失常的发生率，房性心律失常可能与左房扩大或心房纤维化有关。为观察压力负荷增高大鼠中心房纤维化的发生情况，将Ｗｉｓｔａｒ大鼠随机分成假手术组和手术组，手术组大鼠行肾上腹主动脉部分结扎。术后４，８，１２周分别测定大鼠颈动脉压及心房胶原容积分数（ＣＶＦ），结果发现：①手术组左室舒张压明显高于假手术组（４，８，１２周分别为１８．５±２．５ｋＰａｖｓ１５．７±１．９ｋＰａ，１８．６±２．７ｋＰａｖｓ１５．３±１．３ｋＰａ，１９．６±３．１ｋＰａｖｓ１５．２±１．９ｋＰａ，Ｐ＜０．０５或０．０１）。②手术组心房ＣＶＦ明显高于假手术组（４，８，１２周左、右房分别比较：４．２３±０．７６％ｖｓ２．９３±０．８７％，４．６５±１．４５％ｖｓ３．１１±１．０７％，５．６２±１．６２％ｖｓ３．２３±１．２８％；３．８８±１．１５％ｖｓ２．５１±０．８４％，４．２４±１．６５％ｖｓ２．５１±０．８４％，５．３４±１．３２％ｖｓ２．３３±１．１４％；Ｐ＜０．０５或０．０１），手术组心房ＣＶＦ有逐渐上升趋势。③左房ＣＶＦ与左室舒张压之间无直线相关关系（ｒ＝０．１６９１，Ｐ＞０．０５）。提示在高血压大鼠模型中存在心房?     

不同起搏方式对病窦综合征患者远期效果的影响

为了解不同起搏方式对病窦综合征特别是慢－快综合征患者心功能及房性心律失常的影响，利用超声心动图、体表心电图及Ｈｏｌｔｅｒ检查，对２１１例病窦综合征患者采用自身对照方法进行回顾性分析。结果发现：生理性起搏（ＡＡＩ／ＤＤＤ）组术后左室射血分数（ＬＶＥＦ）、心输出量（ＣＯ）明显增加（ＡＡＩ：５３．５±６．１％ｖｓ４７．２±７．８％，４．９５±０．５７Ｌ／ｍｉｎｖｓ４．２０±０．６２Ｌ／ｍｉｎ；ＤＤＤ：５２．５±６．８％ｖｓ４４．３±０．１％，５．１２±０．７１Ｌ／ｍｉｎｖｓ４．４１±０．３８Ｌ／ｍｉｎ；Ｐ均＜０．０１），左房内径（ＬＡＤ）无明显变化；ＤＤＤ组Ｅ／Ａ比值明显增加（０．９８±０．０９ｖｓ０．８７±０．１５，Ｐ＜０．０１），ＡＡＩ组Ｅ／Ａ比值呈增加趋势（Ｐ＝０．０５７）。房性心律失常发生率明显减少（１５．９％ｖｓ５０％，Ｐ＜０．０１）。非生理性起搏（ＶＶＩ）组术后ＬＶＥＦ、ＣＯ明显下降（４４．１±４．７％ｖｓ４８．３±４．３％，３．７７±０．４２Ｌ／ｍｉｎｖｓ４．１７±０．８５Ｌ／ｍｉｎ，Ｐ均＜０．０１），ＬＡＤ明显增大（３９．２６±２．３７ｍｍｖｓ３６．８１±２．３５ｍｍ，Ｐ＜０．０１），Ｅ／Ａ比值呈?     

经皮冠状动脉腔内成形术对不稳定型心绞痛患者心率变异的影响

应用长程心电图分析系统对１６例不稳定型心绞痛患者（ＵＡＰ组）入院后第２日、经皮冠状动脉腔内成形术（ＲＴＣＡ）后第１，３，３０日以及１４８例健康中、老年人（对照组）２４ｈ心电图进行心率变异（ＨＲＶ）分析。结果：ＵＡＰ组２４ｈ连续正常ＲＲ间期的标准差（ＳＤＮＮ）、２４ｈ内连续５ｍｉｎ节段平均正常ＲＲ间期的标准差（ＳＤＡＮＮｉ）、相邻ＲＲ间期差的均方根（ｒＭＳＳＤ），相邻两个正常心动周期差值大于５０ｍｓ个数占总搏数的百分比（ＰＮＮ５０）、低频功率（ＬＦ）及高频功率（ＨＦ）均明显低于对照组（分别为９２．７±１４．３ｍｓｖｓ１２８．９±１７．８ｍｓ、７８．８±１０．６ｍｓｖｓ１１８．６±１９．１ｍｓ、１９．３±７．７ｍｓｖｓ２９．８±１２．７ｍｓ、３．６±１．７％ｖｓ６．５±５．５％、３１７．２±１４８．３ｍｓ２ｖｓ４７６．５±２８７．３ｍｓ２，Ｐ均＜０．０５），而ＬＦ／ＨＦ高于对照组（３．５±１．３ｖｓ２．４±１．１，Ｐ＜０．０５）。ＰＴＣＡ术后３０天ＵＡＰ患者ＨＲＶ逐渐恢复正常。结果提示ＵＡＰ患者交感神经和迷走神经张力下降，而以后者更明显；ＰＴＣＡ后ＨＲＶ逐渐恢复，说明ＰＴＣＡ能改善ＵＡＰ患者的ＨＲＶ。     

心肌缺血大鼠的心率功率谱变化及其与心脏性猝死关系的研究

采用心率变异（ＨＲＶ）频域指标定量评价心肌缺血大鼠的心脏自主神经功能变化及其与心脏性猝死（ＳＣＤ）的关系。Ｈｏｌｔｅｒ监测仪记录假手术组（２０只）及心肌缺血后存活组（５４只）与ＳＣＤ组（３６只）大鼠的心电信号。结果显示存活组或ＳＣＤ组大鼠于心肌缺血初始１５ｍｉｎ内的低频（ＬＦ）及低频／高频比值（ＬＦ／ＨＦ）较假手术组明显升高〔ＬＦ（ｍｓ２／Ｈｚ）：１９８．８±４１．３或２２６．７±５６．４ｖｓ６５．４±１９．６，Ｐ均＜０．０１；ＬＦ／ＨＦ：４．０８±１．１或５．１２±１．４ｖｓ１．８７±０．７，Ｐ均＜０．０１〕，而且ＳＣＤ组大鼠的ＬＦ与ＬＦ／ＨＦ较存活组增高〔ＬＦ（ｍｓ２／Ｈｚ）：２２６．７±５６．４ｖｓ１９８．８±４１．３，Ｐ均＜０．０５；ＬＦ／ＨＦ：５．１２±１．４ｖｓ４．０８±１．１，Ｐ＜０．０５〕，各组间ＨＦ无明显变化；ＳＣＤ组大鼠于ＳＣＤ发生前１５ｍｉｎ内，心率功率谱动态变化表现为ＬＦ及ＬＦ／ＨＦ随死亡时间的濒临而呈进行性升高（Ｐ＜０．０１及０．０５）。表明大鼠心肌缺血后其交感神经活性明显亢进，ＨＲＶ降低与ＳＣＤ的发生密切相关。     

实验性心肌缺血大鼠心脏自主神经活性的动态变化及意义

采用心率变异（ＨＲＶ）时域及频域指标分析急性心肌缺血２４ｈ大鼠心脏自主神经功能的变化以探讨其意义。将实验动物分成三组，即正常对照组（２０只）、假手术组（２０只）与心肌缺血组（４８只），并运用动态心电图记录２４ｈ心电信号变化。结果显示：与假手术组及正常对照组分别比较，心肌缺血组正常窦性心律ＲＲ间期标准差（ＳＤＮＮ）下降（２８．９±９．４ｍｓｖｓ３４．４±１３．７ｍｓ或３５．１±１４．３ｍｓ，Ｐ均＜０．０５），低频（ＬＦ）及低频与高频的比值（ＬＦ／ＨＦ）明显增加（１８９．４±３６．５ｍｓ２／Ｈｚｖｓ５７．３±１７．８ｍｓ２／Ｈｚ或５１．８±１８．６ｍｓ２／Ｈｚ；３．８５±０．９１ｖｓ１．７６±０．６３或１．６８±０．５７，Ｐ均＜０．０１）；２４ｈ心率功率谱示心肌缺血组ＬＦ及ＬＦ／ＨＦ波动幅度较假手术组及正常对照组增高，缺血大鼠ＬＦ与ＬＦ／ＨＦ在缺血后０～３ｈ（２６７．５±１２．４ｍｓ２／Ｈｚ、４．３３±１．０８）及９～１２ｈ（２４４．７±１３．９ｍｓ２／Ｈｚ、３．９６±０．９８）期间增高显著，而在缺血后５～７ｈ（１４９．２±８．７ｍｓ２／Ｈｚ、２．０５±０．４２）内则相对较低。结果表明大鼠心肌缺血后ＨＲＶ降低主?     

心率变异对甲状腺机能亢进患者自主神经功能的评价

采用短时采样的时域、频域法对１８例初诊甲状腺机能亢进（简称甲亢）患者（甲亢组）进行心率变异分析，并以１８例正常人作为对照（对照组），了解甲亢患者自主神经功能的改变。与对照组相比，甲亢组平均ＲＲ间期、ＲＲ平均值标准差、相邻ＲＲ间期差值的均方根、相邻ＲＲ间期相差＞５０ｍｓ占总心动周期数的百分比均明显降低（分别为５５４．５３±６７．７９ｍｓｖｓ８５８．３６±９０．４３ｍｓ、１６．４１±５．５０ｍｓｖｓ４３．０８±１１．０４ｍｓ、１１．３２±３．１６ｍｓｖｓ３７．４３±１０．１２ｍｓ、０．３３±０．５１％ｖｓ１５．２２±１２．８４％，Ｐ均＜０．００１）。极低频段成分明显升高、高频段（ＨＦ）成分明显降低（分别为３８．３２±８．６０ｍｓ２／Ｈｚｖｓ２５．１１±１０．７８ｍｓ２／Ｈｚ、１２．７７±７．０４ｍｓ２／Ｈｚｖｓ３５．６５±１５．０８ｍｓ２／Ｈｚ，Ｐ均＜０．００１）、低频段（ＬＦ）成分无明显改变（２７．１２±１１．３４ｍｓ２／Ｈｚｖｓ２９．６０±１０．３１ｍｓ２／Ｈｚ，Ｐ＞０．０５），ＬＦ／ＨＦ明显增高（２．７６±１．７１ｖｓ１．１７±１．０８，Ｐ＜０．００２），心率总功率谱密度无明显变化。提示甲亢患者不仅交感神?     

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?     

用实验性心力衰竭制作持续性心房颤动模型

为探讨实验性心力衰竭（简称心衰）形成持续性心房颤动（简称房颤）的可行性，用２００～２５０ｐｐｍ的频率以ＶＯＯ方式起搏犬心室３～７周形成实验性心衰，在犬清醒状态下观察心衰前、后刺激诱发的房性快速心律失常。快速起搏右室３～７周，８条犬均发生充血性心衰，３周时体重由心衰前的２８±６ｋｇ降至２４±４ｋｇ（Ｐ＜０．０５）；左室射血分数由０．６４±０．０６降至０．２３±０．０９（Ｐ＜０．０１），右房直径由２５±３ｍｍ增至３６±６ｍｍ（Ｐ＜０．０１），心房不应期由１１６±５ｍｓ增至１３７±１２ｍｓ（Ｐ＝０．０１），不应期离散度无显著性改变（１６±１２ｍｓｖｓ２０±９ｍｓ，Ｐ＝０．２０），心房平均传导时间亦无显著性变化（６１±１９ｍｓｖｓ６６±２４ｍｓ，Ｐ＝０．２０）。１条犬于起搏后第６周夜间突然死亡。心衰前，８条犬均未诱发心房扑动，４条犬诱发短暂房颤；心衰后，８条犬均可反复诱发心房扑动和持续性房颤（持续时间超过１５ｍｉｎ，平均周长９５±５ｍｓ），最长者持续２４ｈ以上。结果表明起搏心室导致犬心衰可形成非瓣膜病性慢性房颤的实验模型。     

心房起搏阈值的随访分析

对３３例植入心房电极者进行起搏阈值的随访，结果表明：起搏阈值峰值为１．４４±０．７４Ｖ／０．５ｍｓ，出现在植入后两周内；慢性期起搏阈值为１．２２±０．４０Ｖ／０．５ｍｓ；伴器质性心脏病患者慢性期起搏阈值（１．７０士０．３７Ｖ／０．５ｍｓ）明显高于不伴器质性心脏病者（１．１６±０．３７Ｖ／０．５ｍｓ），Ｐ＜０．０１；激素电极的起搏阈值峰值（１．１２±０．２９Ｖ／０．５ｍｓ）和慢性期起搏阈值（０．７７±０．１７Ｖ／０．５ｍｓ）均显著低于非激素电极（１．８０±０．６８Ｖ／０．５ｍｓ和１．４０±０．３３Ｖ／０．５ｍｓ），Ｐ＜０．０５及０．００１。提出在非特殊情况下，将出厂时的电能由５．０Ｖ／０．５ｍｓ降至２．５Ｖ／０．５ｍｓ既可保证有效起搏，又可节省电能，从而延长起搏器的使用寿命。     

DDD起搏器选择心室起搏部位对血流动力学的影响

目的比较右室间隔部(RVS)和右室心尖部(RVA)起搏对血流动力学的影响。方法42例置入DDD起搏器的患者,分为RVS组和RVA组;比较2组术前和术后3个月随访的左室射血分数(LVEF)、心脏指数(CI)、每搏量(SV)、左室最大压力上升速率(dp/dtmax)、左室最大压力下降速率(-dp/dtmax)、二尖瓣血流E峰和A峰最大充盈速度比值(E/A)、等容舒张时间(IVRT)差异。结果与术前相比,RVA组3个月随访的LVEF、CI、SV、dp/dtmax、-dp/dtmax、E/A、IVRT均显著降低(0.51±0.04vs0.54±0.03;2.33±0.09L/min.m-2vs2.68±0.11L/min.m-2;71.11±14.2mlvs80.17±16.12ml;1614±133mmHg/svs1702±155mmHg/s;2230±234mm-Hg/svs2404±242mmHg/s;1.38±0.47vs1.86±0.28;73.2±3.86msvs77.6±4.15ms,均P<0.05),RVS组无明显变化。3个月随访RVS组LVEF、CISV、SV、dp/dtmax均显著高于RVA组(P<0.05)。结论RVS起搏对血流动力学无不良影响。     

III度房室阻滞患者VVI起搏时运动耐力和心力储备的研究

采用心肺运动试验的方法，对１６例ＶＶＩ起搏的ＩＩ度房室阻滞患者行最大症状限制性运动试验，以测定病人的心力储备和耐力储备。结果表明病人运动时心脏指数较运动前增加１倍。最大作功８８．６±１６．３６Ｗ／ｍｉｎ，最大氧耗量１７．３８±４．４８ｍｌ／ｍｉｎ。１６例中有９例未测出无氧阈。极量运动时每个病人都出现运动性心律失常。认为ＶＶＩ起搏的患者极量运动时病理生理特点是低无氧阈、低最大氧耗量、低心输出量、低全身耐力。     

右房左室起搏治疗慢性心力衰竭伴室内传导阻滞患者的初步临床观察

观察右房 左室起搏治疗慢性心力衰竭 (简称心衰 )的临床效果。选择 1 6例充血性心衰患者 (NYHA分级Ⅲ Ⅳ级 ) ,男 1 0例、女 6例 ,年龄 6 8.4± 6岁 ;均为窦性心律 ,合并有Ⅰ度房室阻滞 ,完全性左束支阻滞。按安置起搏器的模式分为右房 左室起搏治疗组 (LV组 ,n =6 ) ,右房双室起搏治疗组 (BiV组 ,n =1 0 )。左室起搏电极分别放置于心大静脉左室侧后分支 9例 ,心大静脉左室后分支 7例。观察起搏治疗前后左室心功能参数、6min步行距离、左室壁运动的同步性及体表心电图的变化。结果 :BiV组左室射血分数 (LVEF)由术前的 0 .2 3提高至 0 .31 (P <0 .0 0 1 ) ;在LV组LVEF由术前的 0 .2 4提高至 0 .33(P <0 .0 0 1 ) ;左室舒张末期容积指数在二组分别由术前的 1 4 9± 5 1ml/m2 和 1 5 3±5 3ml/m2 下降至 1 1 6± 38ml/m2 和 1 2 1± 4 1ml/m2 (P均 <0 .0 0 1 ) ;室间隔与左室后壁运动的延迟时间在二组分别由术前的 1 95± 94ms和 1 97± 89ms下降至 1 7± 6 0ms及 1 6± 5 6ms(P均 <0 .0 0 1 )。 6min步行距离则分别由术前的4 0 3± 5 3m和 4 0 1± 5 9m提高至 4 4 1± 6 2m和 4 4 2± 6 7m(P均 <0 .0 5 )。结论 :初步临床观察提示右房 左室起搏治疗与右房双室起搏治疗相比 ,同样可有效地改善慢性心衰?     

Acute hemodynamic deterioration during rapid atrial pacing in patients with hypertrophic cardiomyopathy

Background and hypothesis: Supraventricular tachycardia and ventricular tachycardia are often observed in patients with hypertrophic cardiomyopathy (HCM) and they often alter the clinical features of HCM. We examine the influence of supra-ventricular tachycardia on cardiac function and assess the clinical characteristics of patients with HCM. Methods: We studied 32 patients with HCM and 8 normal volunteers using echocardiography under transesophageal rapid atrial pacing. Results: Presyncope-associated hypotension was observed during rapid atrial pacing in 8 HCM patients, but in none of the normal controls. During rapid atrial pacing (144 ± 8 beats/min in HCM, 146 ± 5 beats/min in controls), systolic blood pressure (SBP), the product of left ventricular filling volume (FV) and heart rate, and fractional shortening (%FS) in the HCM patients decreased significantly compared with the basal values (138 ± 19 mmHg vs. 99 ± 24 mmHg, 5.0 ± 1.21/min vs. 2.9 ± 0.91/min, 41.7 ± 6.2 % vs. 35.2 ± 6.0%, respectively), but these decreases were not observed in normal controls. The decrement of SBP during rapid atrial pacing in HCM patients with a history of syncope was more marked than that in those without such history. The decrement correlated positively with the indices of left ventricular hypertrophy (maximal wall thickness and wall thickness index) and with %FS, and correlated negatively with the endsystolic left ventricular diameter at rest. Conclusions: In some patients with HCM, supraventricular tachycardia causes marked hemodynamic deterioration that may be related to a history of syncope, marked hypertrophy, hyperkinesis, small cavity size, and small filling volume of the left ventricle.     

双室同步起搏的临床应用及置入左室电极的初步体会

观察双室同步起搏治疗充血性心力衰竭 (CHF)的疗效 ,探讨左室电极置入的方法及注意事项。 10例患者均为原发性扩张型心肌病 (DCM)并CHF ,符合双室同步起搏治疗的指征。其中 8例置入Medtronic 2 187电极 ,1例置入Medtronic 2 188电极 ,1例置入右室主动固定电极。 9例左室电极置入成功 ,1例失败改行右室双部位起搏 ,术后患者左室舒张未径、左室射血分数及 6min步行距离均有改善 (术后 3个月与术前分别比较 :70 .8± 9.5vs 79.5± 12 .5mm ,0 .4 2± 0 .13vs 0 .2 5± 0 .10 ,384 .8± 4 5 .4vs 2 78.6± 34.5m ;P <0 .0 5或 0 .0 1)。借助电生理冠状静脉窦 (CS)标测电极、CS造影 (包括直接逆行CS造影和冠状动脉造影使CS间接显像 )对指导左室电极的置入有较大的价值。结论 :双室同步起搏治疗CHF疗效肯定 ,借助CS标测电极及CS造影可提高左室电极置入的成功率     

Reversibility of hypotension and shock by atrial or atrioventricular sequential pacing in patients with right ventricular infarction

Hypotension and shock associated with heart block and other forms of atrioventricular (AV) dissociation frequently accompany right ventricular infarction (RVI). Such patients do not invariably improve with ventricular pacing. We evaluated the relative effects of AV dissociated rhythms (ventricular pacing or nodal rhythm) and AV synchronous rhythms (atrial pacing, AV sequential pacing, or return to normal sinus rhythm) in seven patients with RVI complicated by AV dissociation, who had hypotension or shock. Hemodynamic monitoring demonstrated the characteristic features of RVI in all patients. Restoration of AV synchrony resulted in a highly significant (p ≤ 0.001) increase in systolic blood pressure (88.0 ± 16.5 mm Hg to 133.0 ± 21.8 mm Hg), cardiac output (3.8 ± 0.9 L/min to 5.7 ± 0.9 L/min), and stroke volume (40.5 ± 6.9 cc to 61.0 ± 10.0 cc). We conclude that restoration of normal AV synchrony has a marked effect on stroke volume in this setting and that atrial or AV pacing can reverse hypotension and shock in RVI complicated by AV dissociation.     

Effects of nitric oxide synthesis inhibitor in long-term treatment onhyperdynamic circulatory state in cirrhotic rats

AIM To investigate the effects of low dosage of nitric oxide synthesis (NOS) inhibitor NG-nitro-L-argininemethyl ester (L-NAME) in long-term treatment on hyperdynamic circulatory state in rats with cirrhosis.METHODS Cirrhosis model was induced in male SD rats by injection of 60% CC14 oily solutionsubcutaneously. Cirrhotic rats were treated with L-NAME (0.5 mg·kg-1·d-1) by gavage for two weeks. Meanarterial pressure (MAP), cardiac output (CO), cardiac index (CI), splanchnic vascular resistance (SVR),splanchnic blood flow (SBF) and serum NO levels were determinded in L-NAME-treated, L-NAME-untreated cirrhotic rats and controls by using 57Co-Labled microsphere technique and a fluorometric assay,respectively.RESULTS Untreated cirrhotic rats had significantly lower MAP, SVR and higher PP, CO, CI, SBF andNO concentration than controls ( 14.42±0,47 kPa vs 17.05±0.34 kPa, 2.974±0.186 kPa·mL-1·min-1 vs4.234±0.118 kPa·mL-1·min-1, 1.665±0.067 kPa vs 1.123±0.096 kPa, 189.99±9.26 mL/min vs 135.5±3.55 mL/min, 55.89±1.82 mL-1·min-1·100g-1 BW vs 39.68±1.64 mL-1·min-1·100g-1 BW, 4.60±1.25μmol/L vs 0.53±0.26 μmol/L, P<0.01, respectively). In treated cirrhotic rats, L-NAME significantlyattenuated the increase of CO, CI, SBF, NO concentration and the decrease of MAP and SVR. In treatedcirrhotic rats, L-NAME induced a marked decrement of NO concentration than untreated cirrhotic rats(1.471 ±0.907 μmol/L vs 4.204±1.253 μmol/L, P<0.01).CONCLUSION The endogenous NO may play an important role in the changes of hemodynamics pattern incirrhosis,and hyperdynamic circulatory state in rats with cirrhosis can be ameliorated by long-term low doseL-NAME treatment.     

Prevention of Spontaneous Sustained Ventricular Tachycardia in the Postinfarction Dog by Left Stellate Ganglionectomy

Suppression of Sustained VT by Left Stellectomy. Holter monitoring and ventricular pacing were used to examine control, right stellate ganglionectomy, and left stellate ganglionectomy treatment groups, 6-24 hours after left anterior descending coronary artery ligation in dogs. In nine of 27 controls (33%), spontaneous ventricular triplets (358 ± 8 beats/min) initiated sustained monomorphic ventricular tachycardia (386 ± 16 beats/min), followed by ventricular fibrillation at 12.6 ± 1.4 hours. Ventricular pacing produced sustained monomorphic ventricular tachycardia in 13 of 18 survivors (73%) at 24 hours. Left but not right stellectomy performed 15 minutes before coronary artery ligation reduced the incidence of spontaneous sustained monomorphic ventricular tachycardia (2 of 27, 7%, P = 0.06; 7 of 27, 26%, P = 0.50, respectively) and reduced the maximal ventricular triplet rate (332 ± 12, P <0.05 and 358 ± 10 beats/min, respectively, P = NS vs control). Neither left nor right stellectomy altered the incidence of ventricular triplets during the 6-24 hour period (153 ± 58 and 222 ± 55/hour, respectively, vs control, 177 ± 59/hour, P = NS) nor prevented pacing-induced sustained monomorphic ventricular tachycardia in the survivors at 24 hours (20 of 24, 75%; and 16 of 20, 80%, P = NS). The data demonstrate that left but not right stellectomy reduces spontaneous sustained ventricular tachycardia and ventricular fibrillation during the 6-24 hour period following coronary artery ligation in the dog. Left stellectomy reduces the triggers for sustained monomorphic ventricular tachycardia (rapid ventricular triplets) without altering the underlying reentrant substrate for sustained ventricular tachycardia.     

Effects of nonsystemic ventricular pacing in patients with transposition of the great arteries and atrial redirection

Ventricular Pacing in Transposition of the Great Arteries. Introduction: Ventricular pacing may add additional risk for right ventricular (RV) dysfunction in patients with transposition of the great arteries (TGA) and atrial redirection. The aim of our study was to evaluate the effects of long‐term nonsystemic ventricular pacing on cardiac function, dyssynchrony, and clinical performance in patients with systemic RV. Methods and Results: Forty‐six adults with TGA and atrial redirection, of whom 11 were permanently paced at the nonsystemic ventricle, underwent assessment of clinical status and exercise stress testing, as well as echocardiography to assess parameters of RV function and dyssynchrony. In paced patients, median NYHA functional class was II, which was significantly higher than in nonpaced patients (median class I; P = 0.002). Maximum performance and peak oxygen consumption on exercise testing were significantly lower in paced patients when compared with nonpaced patients (100 ± 30 vs 120 ± 32 W and 22 ± 6 vs 27 ± 7 mLO₂/kg/min, respectively; P < 0.05 for both). On echocardiography, RV shortening fraction (27 ± 11 vs 33 ± 10%), RV ejection fraction (39 ± 7 vs 44 ± 10%) and RV dP/dt_max (891 ± 470 vs 1,024 ± 318 mmHg/s) were significantly lower (P < 0.05 for all) in paced versus nonpaced patients. Inter‐ and intraventricular dyssynchrony was most pronounced in the paced group (99 ± 10 vs 25 ± 9 ms and 70 ± 29 vs 21 ± 15 ms, respectively; P < 0.001 for both). Conclusions: Long‐term pacing of the nonsystemic ventricle in patients with atrial switch for TGA was associated with significantly impaired functional status, exercise capacity, and systemic ventricular function. (J Cardiovasc Electrophysiol, Vol. 23, pp. 766‐770, July 2012)