Scherlag B J, El-Sherif N, Hope R R, Lazzara R
J Electrocardiol. 1978 Oct;11(4):343-54. doi: 10.1016/s0022-0736(78)80140-x.
Fractionated His bundle potentials were induced by ischemia or trauma in 30 anesthetized dogs, in vivo. Functional dissociation, i.e., alteration of the activation sequence of portions of these His bundle potentials was demonstrated in vivo as well as in 10 in vitro preparations of the His-Purkinje system. In vivo, plunge wire and electrode catheters were utilized to record from portions of the His bundle. During vagal-induced slowing of the heart rate, atrial pacing or His bundle pacing, His-Purkinje conduction as measured by the H-V interval was constant over a wide range of heart rates, 50-300/min. One or two hours after anterior septal artery ligation, His bundle damage manifested as split His bundle potentials (H, H'). Atrial pacing or proximal His bundle pacing induced H-H' delays with concomitant right or left bundle branch block patterns in ECG leads. However, distal His bundle pacing at comparable or even higher rates produced normal QRS complexes. In other cases, during atrial pacing or with progressive ischemia at a constant rate, H' progressively delayed during the H-V interval or even disappeared into the QRS complex with a concomitant occurrence of right or left bundle branch block. In vitro, a dissected septal preparation was studied containing the His bundle, proximal and distal right bundle and left bundle branches. Normal conduction throughout the His-Purkinje system was observed at pacing rates of 30-220/min. Punctate lesions, anatomically placed above the branching His bundle caused tachycardia-dependent, complete bundle branch blocked with concurrent temporal reversal of proximal and distal His bundle action potentials. These data suggest that ischemic or traumatic lesions in the His bundle may manifest on the electrocardiogram as bundle branch block patterns. From a clinical point of view, a critical site of lesion would markedly increase the liability for A-V blocked although the electrocardiogram alone would not indicate the actual site of lesion. Predestination of fiber tracts and alternative proposals to the pedestination theory are considered to explain QRS aberration due to exclusive His bundle lesions.
在30只麻醉犬体内,通过缺血或创伤诱发出了希氏束电位的分离现象。在体内以及10个希氏-浦肯野系统的体外标本中均证实了功能分离,即这些希氏束电位各部分激活顺序的改变。在体内,采用穿刺线和电极导管记录希氏束的各部分。在迷走神经介导的心率减慢、心房起搏或希氏束起搏过程中,通过H-V间期测量的希氏-浦肯野传导在50-300次/分钟的广泛心率范围内保持恒定。前间隔动脉结扎1或2小时后,希氏束损伤表现为希氏束电位分裂(H,H')。心房起搏或希氏束近端起搏可诱发H-H'延迟,并伴有心电图导联上的右或左束支传导阻滞图形。然而,以相当或更高的频率进行希氏束远端起搏会产生正常的QRS复合波。在其他情况下,在心房起搏期间或以恒定速率进行渐进性缺血时,H'在H-V间期逐渐延迟,甚至消失于QRS复合波中,并伴有右或左束支传导阻滞。在体外,研究了一个包含希氏束、右束支近端和远端以及左束支的分离间隔标本。在30-220次/分钟的起搏频率下观察到整个希氏-浦肯野系统的正常传导。在希氏束分支上方解剖学定位的点状病变导致心动过速依赖性完全性束支传导阻滞,并伴有希氏束近端和远端动作电位的同时时间反转。这些数据表明,希氏束的缺血或创伤性病变在心电图上可能表现为束支传导阻滞图形。从临床角度来看,一个关键的病变部位会显著增加房室传导阻滞的风险,尽管仅靠心电图无法指示病变的实际部位。考虑纤维束的预定以及对预定理论的替代方案来解释由于单纯希氏束病变导致的QRS波异常。