Endresen K, Amlie J P
Medical Department B, Rikshospitalet, Oslo University Hospital, Norway.
Pacing Clin Electrophysiol. 1989 Aug;12(8):1347-54. doi: 10.1111/j.1540-8159.1989.tb05048.x.
Monophasic action potentials (MAP) were obtained from the outflow tract of the right ventricle during apical pacing in 20 patients with coronary artery disease. The electrical restitution was studied by interpolation of extrasystoles with various coupling intervals to the preceding steady-state beat at basic paced cycle lengths (CL) of 700, 600, and 500 msec. At higher frequencies the ventricular effective refractory periods (V-ERP) and duration of MAPs became shorter and the electrical restitution curves were displaced downwards (P less than 0.001). With increasing diastolic intervals preceding the extrasystole up to a maximum of 100 msec, the duration of premature MAPs increased at all frequencies. An obvious hump of the electrical restitution curve was observed at coupling intervals of 100 msec due to a later transient decrease (P less than 0.01) in duration of MAPs at the basic CL of 500 msec. No significant hump was observed at lower heart rates. Thus, a different time course of the electrical restitution was observed at various CLs. The intraventricular conduction intervals were shorter at the shorter basic CLs when compared to the 700 msec cycles (P less than 0.05). The conduction intervals were also modified by the coupling interval between the interpolated stimulus and the preceding steady-state action potential (AP). The premature beats elicited 30 msec or earlier after refractoriness were conducted more slowly at all basic cycle lengths (P less than 0.005), and those between 60 and 150 msec after the V-ERP more rapidly (P less than 0.01) than the steady-state beats. These observations have implications for the protocols used for introducing two or more frequencies during programmed stimulation in man. Furthermore, the conduction pattern in vivo cannot be interpreted from single cell studies.
在20例冠心病患者的心尖部起搏过程中，从右心室流出道记录到单相动作电位（MAP）。通过在700、600和500毫秒的基础起搏周期长度（CL）下，用不同耦合间期的期外收缩插入到前一个稳态搏动中来研究电恢复。在较高频率时，心室有效不应期（V-ERP）和MAP的持续时间变短，电恢复曲线向下移位（P<0.001）。随着期外收缩前舒张间期增加至最长100毫秒，所有频率下提前MAP的持续时间均增加。在500毫秒基础CL时，由于MAP持续时间后期短暂缩短（P<0.01），在100毫秒耦合间期观察到电恢复曲线有明显的驼峰。在较低心率时未观察到明显的驼峰。因此，在不同CL下观察到电恢复的时间进程不同。与700毫秒周期相比，在较短的基础CL时，心室内传导间期较短（P<0.05）。传导间期也受插入刺激与前一个稳态动作电位（AP）之间的耦合间期影响。在所有基础周期长度下，在不应期后30毫秒或更早诱发的早搏传导较慢（P<0.005），而在V-ERP后60至150毫秒之间诱发的早搏比稳态搏动传导更快（P<0.01）。这些观察结果对人体程控刺激中引入两种或更多频率的方案有影响。此外，体内的传导模式不能从单细胞研究中推断出来。
