TRANSMURAL ACTIVATIONS AND STIMULUS POTENTIALS IN 3-DIMENSIONAL ANISOTROPIC CANINE MYOCARDIUM
TRANSMURAL ACTIVATIONS AND STIMULUS POTENTIALS IN 3-DIMENSIONAL ANISOTROPIC CANINE MYOCARDIUM
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DOI：
10.1161/01.res.63.1.135
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发表时间：
1988-07-01
影响因子：
20.1
通讯作者：
IDEKER, RE
中科院分区：
文献类型：
--
作者：
FRAZIER, DW;KRASSOWSKA, W;IDEKER, RE
心外膜和心内膜起搏被广泛使用，但人们对起搏刺激产生的电位的三维分布或这些起搏部位的激活扩散知之甚少。在 6 只开胸狗中，在 35 次时间内通过 40 个插入电极中的 120 个透壁电极进行同步记录。 20次心外膜和心内膜起搏期间右心室流出道的 5 毫米部分，强度为舒张阈值的两倍，电流为 1 mA。比较起搏部位近端（< 10-12 mm）和远端区域的刺激产生的细胞外电位的大小和激活时间。在每个记录电极处通过组织学确定局部纤维取向。对于心内膜起搏，仅在近端区域心内膜电位大于心外膜电位（p < 0.001）；而在远端区域，心外膜电位更大（p < 0.001），并且两个区域的心内膜激活都早于心外膜激活（p < 0.001）。对于心外膜起搏，两个区域的心外膜电位均大于心内膜电位（p < 0.001），并且仅在近端区域心外膜激活较早发生（p < 0.02），而在远端区域心内膜激活发生在心外膜激活之前（p < 0.01）。在平行于心外膜和内膜的记录电极平面中，初始等时线是椭圆形的，椭圆的长轴沿着起搏部位和记录平面之间的平均纤维取向，而不是沿着记录平面中的局部纤维取向。因此，每个平面中的椭圆相对于彼此旋转，使得在三个维度中激活前沿是螺旋形的，但螺旋的扭曲小于纤维的相应透壁旋转的扭曲。对于从右心室流出道起搏，我们得出的结论是，距离心内膜和心外膜起搏部位超过 10-12 mm，两种情况下的心外膜刺激电位都大于心内膜电位，因为心壁内外的电阻率差异，并且由于心内膜传导快速，两种情况下的激活主要是心内膜到心外膜，我们得出的结论是，激活的初始传播是螺旋形的，并由跨壁纤维方向决定。
Epicardial and endocardial pacing are widely used, yet little is known about the three-dimensional distribution of potentials generated by the pacing stimulus or the spread of activation from these pacing sites. In six open-chest dogs, simultaneous recordings were made from 120 transmural electrodes in 40 plunge electrodes within a 35 .times. 20 .times. 5-mm portion of the right ventricular outflow tract during epicardial and endocardial pacing at a strength of twice diastolic threshold and at 1 mA. The magnitude of extracellular potentials generated by the stimulus and the activation times were compared in regions proximal (< 10-12 mm) and distal to the pacing site. Local fiber orientation was histologically determined at each recording electrode. For endocardial pacing, endocardial potentials were larger than epicardial potentials only in the proximal region (p < 0.001); while in the distal region, epicardial potentials were larger (p < 0.001), and endocardial activation occurred earlier than epicardial activation for both regions (p < 0.001). For epicardial pacing, epicardial potentials were larger than endocardial potentials in both regions (p < 0.001), and epicardial activation occurred earlier only in the proximal region (p < 0.02), while endocardial activation occurred before epicardial activation in the distal region (p < 0.01). In planes of recording electrodes parallel to the epicardium and endocarium, the initial isochrones were elliptical with the major axes of the ellipses along the mean fiber orientation between the pacing site and recording plane rather than along the local fiber orientation in the recording plane. Thus, the ellipses in each plane rotated with respect to each other so that in three dimensions the activation front was helicoid, yet the twist of the helix was less than that of the corresponding transmural rotation of fibers. For pacing from the right ventricular outflow tract, we conclude that beyond 10-12 mm from endocardial and epicardial pacing sites epicardial stimulus potentials in both cases are larger than endocardial potentials because of resistivity differences inside and outside the heart wall and activation in both cases is primarily endocardial to epicardial because of rapid endocardial conduction, and we conclude that the initial spread of activation is helicoid and determined by transmural fiber direction.