Puech P
Adv Cardiol. 1975;14:178-88. doi: 10.1159/000397649.
The participation of intraventricular conduction defects in the AV delays and blocks has been investigated by His bundle electrogram recording in 239 patients with different degrees of AV blocks and QRS enlargement (greater than 0.12 sec). In absence of PR prolongation, the His bundle electrogram can demonstrate intraventricular conduction delay (HV superior to 55 msec) with an increasing frequency in right bundle branch block and right bundle branch with left axis deviation, left bundle branch block and right bundle block with right axis deviation. In cases of first-degree AV block (PR greater than 0.20 sec) delay within the His bundle is present in 20% of the cases and HV prolongation, isolated or associated with an upper conduction defect is demonstrated in 66% of the cases. Second-degree AV block with QRS enlargement in the conducted beats is due to a subnodal lesions of the conducting tissue in 80% of the cases. Wenckebach phenomenon and bundle branch block is as frequent above as below the site of His bundle electrogram recording. Möbitz II block has always an infranodal localization. Third-degree AV block with wide QRS complexes is the consequence of a lesion within the His bundle in 11% and of a complete bilateral bundle branch block in 78% of the cases. Exploration of the AV conduction in acute myocardial infarction with AV block confirms the usual bilateral bundle branch lesion in anterior myocardial necrosis and the AH localization of the AV block in posterior myocardial infarction even in presence of enlarged QRS complexes. Unidirectional block occurs in 19 of the 82 cases of complete anterograde bilateral bundle branch block, with retrograde conduction to the atria in 11 and concealed retrograde conduction in 8 cases.
通过对239例不同程度房室传导阻滞及QRS波增宽(大于0.12秒)患者进行希氏束电图记录,研究了室内传导缺陷在房室延迟和阻滞中的作用。在无PR间期延长时,希氏束电图可显示室内传导延迟(HV间期大于55毫秒),在右束支传导阻滞、右束支传导阻滞伴左前分支阻滞、左束支传导阻滞及右束支传导阻滞伴右后分支阻滞中,其出现频率增加。在一度房室传导阻滞(PR间期大于0.20秒)患者中,20%的病例存在希氏束内延迟,66%的病例显示HV间期延长,可单独出现或与上传导缺陷并存。二度房室传导阻滞伴传导搏动的QRS波增宽,80%的病例是由于传导组织的结下病变所致。文氏现象和束支传导阻滞在希氏束电图记录部位上方和下方出现的频率相同。莫氏Ⅱ型阻滞总是位于结下。三度房室传导阻滞伴宽QRS波群,11%的病例是希氏束内病变的结果,78%的病例是完全性双侧束支传导阻滞的结果。对伴有房室传导阻滞的急性心肌梗死患者的房室传导进行探查,证实前壁心肌坏死时常见双侧束支病变,后壁心肌梗死时房室传导阻滞位于AH段,即使存在QRS波增宽。在82例完全性顺行性双侧束支传导阻滞患者中,19例出现单向阻滞,其中11例有逆行心房传导,8例有隐匿性逆行传导。