Akhtar M, Damato A N, Batsford W P, Ruskin J N, Ogunkelu J B
Circulation. 1975 Nov;52(5):766-78. doi: 10.1161/01.cir.52.5.766.
Patterns of antegrade and retrograde conduction and refractory periods were studied using His bundle electrogram recordings, incremental atrial and ventricular pacing and the extrastimulus technique. In 36/50 patients antegrade conduction was "better" than retrograde conduction (group I), as evidenced by a) onset of retrograde atrioventricular (A-V) nodal Wenckebach phenomenon at a slower rate compared to the antegrade counterpart (25 patients: group IA) or b) no ventriculo-atrial conduction at all ventricular paced rates (11 pts: group IB). The site of retrograde block in group IB patients was the A-V node. In eight patients (group II), antegrade and retrograde conduction appeared to be equal up to maximum paced rates of 160 beats/min. In six patients (group III) retrograde conduction was "better" than antegrade conduction, as indicated by onset of antegrade A-V nodal Wenckebach periods at slower rates than retrograde Wenckebach periods. During antegrade refractory period studies the area of maximum refractoriness was the A-V node in 19/40 patients, the His-Purkinje system (HPS) 6/40, and the atrial muscle in 15/40. During retrograde refractory period studies the A-V node was the area of maximum refractoriness in 12/36 pts (4/40 patients had A-V dissociation during ventricular pacing), the HPS in 12/36, and the ventricular muscle in 10/36. In 2/36 patients the site of maximum refractoriness retrogradely could not be determined: The area of maximum refractoriness during both antegrade and retrograde refractory period studies was the same in 11 patients (A-V node in seve and HPS in four), was different (i.e., A-V node or HPS) in 18 patients, and was the artrial or ventricular muscle in six patients. In five patients, including four patients in whom V-A conduction failed to occur, the above comparisons were not made. It is concluded that 1) antegrade conduction is better than retrograde conduction in most patients; 2) it is not always possible to predict area of maximum refractoriness during premature stimulation (both atrium and ventricle) from observations made during incremental pacing; 3) it is equally difficult to extrapolate patterns of retrograde conduction and refractory periods from results of antegrade conduction and refractory period studies.
利用希氏束电图记录、递增性心房和心室起搏以及期外刺激技术,对顺行和逆行传导模式及不应期进行了研究。在50例患者中的36例,顺行传导“优于”逆行传导(I组),这表现为:a)逆行房室结文氏现象的起始频率低于顺行时(25例患者:IA组),或b)在所有心室起搏频率下均无室房传导(11例患者:IB组)。IB组患者的逆行阻滞部位为房室结。在8例患者(II组)中,直至160次/分钟的最大起搏频率,顺行和逆行传导似乎相等。在6例患者(III组)中,逆行传导“优于”顺行传导,表现为顺行房室结文氏周期的起始频率低于逆行文氏周期。在顺行不应期研究中,40例患者中有19例最大不应期区域为房室结,6例为希氏-浦肯野系统(HPS),15例为心房肌。在逆行不应期研究中,36例患者中有12例最大不应期区域为房室结(40例患者中有4例在心室起搏时出现房室分离),12例为HPS,10例为心室肌。在36例患者中有2例无法确定逆行最大不应期部位:在11例患者中,顺行和逆行不应期研究中的最大不应期区域相同(7例为房室结,4例为HPS),18例不同(即房室结或HPS),6例为心房或心室肌。在5例患者中,包括4例未发生室房传导的患者,未进行上述比较。得出的结论为:1)大多数患者中顺行传导优于逆行传导;2)根据递增起搏期间的观察结果,并不总是能够预测过早刺激(心房和心室)时的最大不应期区域;3)从顺行传导和不应期研究结果推断逆行传导和不应期模式同样困难。