Mor-Avi V, Akselrod S
School of Physics and Astronomy, Raymond and Beverly Sackler Faculty of the Exact Sciences, Tel Aviv University, Israel.
Circ Res. 1990 Jun;66(6):1681-91. doi: 10.1161/01.res.66.6.1681.
Power spectra of epicardial electrograms were studied in 13 anesthetized dogs subjected to occlusion of the left anterior descending coronary artery. Electrograms were obtained from a bipolar electrode placed on the epicardial surface of the left ventricle and recorded before and after coronary occlusion. After digitization, power spectra of the first and every 50th subsequent waveform were evaluated and compared with the power spectrum of the average waveform obtained from the baseline recording. In particular, we examined variations in relative power content in three frequency ranges: 150-250 Hz, previously shown to be directly affected by myocardial ischemia; 40-150 Hz, presumably corresponding to the fine notches and slurs on the body surface QRS; and 2-40 Hz, the low-frequency range. Apart from a mild initial rise during the first 50 heart beats, the power in the high-frequency range gradually decreased, reaching 5% of the control value at wave 500. The power in the mid-frequency range showed a monotonous decrease after the occlusion and reached 16% of the control. The power in the low-frequency range showed a gradual buildup to 140% of the control after 500 heart beats. Therefore, ischemia causes a shift of the high-frequency spectral components of the local electrographic waveform to lower frequencies. Our findings and the fact that body surface ECG is produced by spatial summation of local electric potentials over the different regions of the myocardial tissue may explain two previously described effects of acute myocardial ischemia on the body surface ECG complex. First, local loss of spectral components in the range 150-250 Hz may produce a zone of reduced amplitude within a QRS complex band-pass filtered in this range. Second, displacement of power in the frequency domain may suggest an explanation to the increased incidence of visible notches and slurs on the surface QRS complex, characteristic to various myocardial pathologies.
在13只接受左冠状动脉前降支闭塞的麻醉犬身上研究了心外膜电图的功率谱。通过放置在左心室心外膜表面的双极电极获取电图，并在冠状动脉闭塞前后进行记录。数字化后，评估第一个以及随后每隔50个波形的功率谱，并与从基线记录中获得的平均波形的功率谱进行比较。特别地，我们检查了三个频率范围内相对功率含量的变化：150 - 250Hz，先前已证明直接受心肌缺血影响；40 - 150Hz，大概对应体表QRS波上的细微切迹和顿挫；以及2 - 40Hz，低频范围。除了在最初50次心跳期间有轻微的初始上升外，高频范围内的功率逐渐下降，在第500个波形时降至对照值的5%。闭塞后中频范围内的功率呈单调下降，降至对照值的16%。低频范围内的功率在500次心跳后逐渐增加至对照值的140%。因此，缺血导致局部电图波形的高频频谱成分向低频转移。我们的发现以及体表心电图是由心肌组织不同区域局部电位的空间总和产生这一事实，可能解释了先前描述的急性心肌缺血对体表心电图复合波的两种影响。首先，在150 - 250Hz范围内频谱成分的局部损失可能在该范围内进行带通滤波的QRS复合波带内产生一个幅度降低的区域。其次，频域中功率的位移可能为体表QRS复合波上可见切迹和顿挫发生率增加提供一种解释，这是各种心肌病变的特征。
