Atrial pacing lead location alters the hemodynamic effects of atrial-ventricular delay in dogs with pacing induced cardiomyopathy.
Atrial pacing lead location alters the hemodynamic effects of atrial-ventricular delay in dogs with pacing induced cardiomyopathy.
复制标题
心房起搏导线位置改变了患有起搏诱发心肌病的狗的心房-心室延迟的血流动力学效应。
DOI：
10.1046/j.1460-9592.2003.t01-1-00150.x
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发表时间：
2003
期刊：
影响因子：
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通讯作者：
Pagel,PaulS
中科院分区：
文献类型：
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作者：
Hettrick,DouglasA;Mittelstadt,JacquelineR;Kehl,Franz;Kress,TobiasT;Tessmer,JohnP;Krolikowski,JohnG;Kersten,JudyR;Warltier,DavidC;Pagel,PaulS
HETTRICK，D.A.，等：心房起搏电极导线位置改变起搏诱发心肌病犬房室延迟的血流动力学效应心房电极导线位置在受损心室功能障碍的心血管功能中的作用尚不清楚。我们检验了左心房（LA）和左心室（LV）血流动力学受AV延迟改变的影响以及受扩张型心肌病犬心房起搏部位影响的假设。犬（n = 7）以220次/min的速度长期起搏3周以产生心肌病，然后安装仪器测量LA、LV舒张末期压（LVEDP）和平均动脉压（MAP）、LA容积、LV短轴直径以及主动脉和肺静脉血流量。分别在右心耳（RAA）、冠状窦口（CSO）和左心房下侧壁（LAW）测量器械植入后和心房起搏过程中的血流动力学。然后消融房室结，并在20和350 ms之间的几个AV延迟从每个心房电极位置的双腔AV起搏（右心室心尖）期间比较血流动力学。不同部位的心房起搏没有改变血流动力学。双腔起搏时心输出量（CO）、每搏输出量（SV）、LVEDP、MAP和+dLVP/dt随AV延迟的变化有显著性差异（P < 0.05）。LAW起搏时CO高于RAA和CSO起搏（2.3 ± 0.4vs2.1 ± 0.3vs2.0 ± 0.3 l/min），LAW的MAP高于RAA和CSO（65 ± 9vs59 ± 9vs54 ± 11mmHg，）在AV延迟350 ms时，心房电极导线位置影响双腔起搏犬的LV性能指数，与AV延迟无关，心肌病(PACE 2003; 26[Pt.第一卷，第853-861页）
HETTRICK, D.A.,et al.: Atrial Pacing Lead Location Alters the Hemodynamic Effects of Atrial Ventricular Delay in Dogs with Pacing Induced Cardiomyopathy.The role of atrial lead location in cardiovascular function in the presence of impaired ventricular dysfunction is unknown. We tested the hypothesis that left atrial (LA) and left ventricular (LV) hemodynamics are affected by alterations in AV delay and are influenced by atrial pacing site in dogs with dilated cardiomyopathy. Dogs(n = 7)were chronically paced at 220 beats/min for 3 weeks to produce cardiomyopathy and then instrumented for measurement of LA, LV end diastolic pressure (LVEDP) and mean arterial pressure (MAP), LA volume, LV short‐axis diameter, and aortic and pulmonary venous blood flow. Hemodynamics were measured after instrumentation and during atrial overdrive pacing from the right atrial appendage (RAA), coronary sinus ostium (CSO) and lower LA lateral wall (LAW). The AV node was then ablated, and hemodynamics were compared during dual chamber AV pacing (right ventricular apex) from each atrial lead location at several AV delays between 20 and 350 ms. Atrial overdrive pacing from different sites did not alter hemodynamics. Cardiac output (CO), stroke volume, LVEDP, MAP and +dLVP/dt demonstrated significant (P < 0.05) variation with AV delay during dual chamber pacing. CO was higher during LAW pacing than RAA and CSO pacing (2.3 ± 0.4vs2.1 ± 0.3vs2.0 ± 0.3 l/min, respectively) at an AV delay of 120 ms. Also, MAP was higher in the LAW than RAA and CSO (65 ± 9vs59 ± 9vs54 ± 11 mmHg, respectively) at an AV delay of 350 ms. Atrial lead location affects indices of LV performance independent of AV delay during dual chamber pacing in dogs with cardiomyopathy. (PACE 2003; 26[Pt. I]:853–861)