Vanderark C R, Reynolds E W
Circulation. 1975 Feb;51(2):257-62. doi: 10.1161/01.cir.51.2.257.
High frequency notching of the QRS complex is associated with transmural infarction, cardiomyopathies, and ventricular hypertrophy from any cause. The mechanism producing notching is unknown; but the presence of a discrete anatomic lesion is not an essential feature. The hypothesis that notching was produced by activation across, rather than along, myocardial fibers was investigated by stimulation at 12 points around a clock electrode attached to the epicardium while mapping isoschronous lines in the area activated. All fibers at the subendocardial layer beneath the clock electrode were ligated by a pursestring suture. Propagation direction, as measured by isoschronous maps, produced more notched QRS compleses when the path was across, rather than paralled with, the myocardial fibers. Using grouped data and a 5 times 6 table, notches versus the angle formed between fiber direction and orientation of the direction of travel were shown to be related (P less than 0.001). The hypothesis that cross-fiber activation enhances notching was confirmed. retrograde activation did not increase notching nor did ligation of subendocardial fibers.
QRS波群的高频切迹与透壁性梗死、心肌病以及任何原因引起的心室肥厚有关。产生切迹的机制尚不清楚;但离散解剖病变的存在并非其基本特征。通过在附着于心外膜的钟形电极周围的12个点进行刺激,同时在激活区域绘制等时线,研究了切迹是由心肌纤维间而非沿心肌纤维的激活所产生的假说。钟形电极下方的心内膜下层的所有纤维均用荷包缝合线结扎。通过等时图测量,当传播路径与心肌纤维交叉而非平行时,产生的QRS波群切迹更多。使用分组数据和5×6表格,显示切迹与纤维方向和传播方向之间形成的角度有关(P<0.001)。交叉纤维激活增强切迹的假说得到证实。逆向激活并未增加切迹,心内膜下纤维结扎也未增加切迹。