Boineau J P, Miller C B, Schuessler R B, Roeske W R, Autry L J, Wylds A C, Hill D A
Circ Res. 1984 Mar;54(3):332-47. doi: 10.1161/01.res.54.3.332.
We examined the onset of atrial epicardial excitation by recording unipolar potentials from 360 electrodes arranged in templates affixed to the superior vena cava and right atrium in dogs. Both activation sequence and potential distribution maps were obtained for the period of impulse origin beginning before the surface P wave and continuing through the first 15-20 msec of atrial depolarization. The activation maps demonstrated impulse origin from multiple widely separated sites, resulting in two to three individual wavefronts that merged to form a single widely disseminated wavefront spread over a 50 X 20 mm area by 10-15 msec. Atrial potential maps obtained for the same time periods revealed multiple sites of primary negativity corresponding to the points of impulse origin in the activation maps. The potential distributions and evolution of these maps also indicated the presence of multiple wavefronts originating from widely separated locations, and suggested an extensively dispersed source of impulse origin. One of these sites at the superior cavo-appendicular junction corresponded to the rostral portion of the sinus node and the site of classical unifocal origin. Additional sites of impulse origin and primary negativity distant to the sinus node were noted either concurrently in the same map or in other maps associated with different patterns of impulse initiation. Classical physiological and pharmacological interventions were used to alter adrenergic and cholinergic input to the atrium, and resulted in coincident changes of both the patterns of impulse origin and heart rate. In addition, we examined spontaneous changes in the patterns of impulse initiation which accompanied beat-to-beat changes in cycle length (sinus arrhythmia). There was close agreement between activation and potential maps over the entire steady state and dynamic range of impulse origin. The data can be explained by the concept of a widely distributed system of functionally differentiated but coordinated atrial pacemakers.
我们通过记录固定在犬上腔静脉和右心房的模板中360个电极的单极电位，研究了心房心外膜兴奋的起始情况。在表面P波之前开始并持续到心房去极化的最初15 - 20毫秒的冲动起源期，获得了激活序列图和电位分布图。激活图显示冲动起源于多个广泛分离的部位，产生两到三个单独的波前，这些波前合并形成一个单一的广泛传播的波前，在10 - 15毫秒内扩散到50×20毫米的区域。同一时期获得的心房电位图显示了多个主要负电位部位，与激活图中的冲动起源点相对应。这些图的电位分布和演变也表明存在多个起源于广泛分离位置的波前，并提示冲动起源有广泛分散的来源。上腔静脉 - 心耳交界处的其中一个部位对应于窦房结的头端部分和经典单灶起源部位。在同一图中或与不同冲动起始模式相关的其他图中，同时注意到了远离窦房结的其他冲动起源部位和主要负电位部位。使用经典的生理和药理干预来改变心房的肾上腺素能和胆碱能输入，并导致冲动起源模式和心率的同时变化。此外，我们研究了伴随逐搏周期长度变化（窦性心律失常）的冲动起始模式的自发变化。在冲动起源的整个稳态和动态范围内，激活图和电位图之间有密切的一致性。这些数据可以用功能分化但协调的心房起搏器广泛分布系统的概念来解释。
