This report presents electrophysiological data in 27 patients (out of a series of 110) which suggest longitudinal dissociation in the His Bundle (BH). Twenty-five patients showed left bundle branch block (LBBB) which was rate related in three and two had isolated left axis deviation (LAD) with narrow QRS complexes. BH recordings were performed via the right heart, and in each patient the same electrode catheter was used for stimulation of the BH at different sites. The H-V time was prolonged (range 50-70 msec, mean 59) in all 22 patients with constant LBBB, in one of the three of the rate related LBBB, and in one of the two with isolated LAD; and remained unchanged throughout. In all 25 patients with LBBB proximal BH stimulation exhibited QRST complexes identical to those ON THE BASIS of their extensive histological studies, James and Sherf have recently reported that the longitudinal separation of Purkinje strands by collagen along with specialized nature of intercellular junctions within each strand form an anatomic basis for longitudinal separation of conduction within the normal His bundle.' These investigators have proposed the concept of "sinoventricular conduction" which implies that the individual components of the with normal sinus rhythm with a PI-R interval equal to the H-V time. BH stimulation at a constant cycle length, but at a slightly distal site, abolished the LBBB (constant or rate related) and resulted in narrow QRS complexes (_ 95 msec) with a PI-R interval shorter than the H-V time by 5 to 20 msec. In the two patients with isolated LAD, BH stimulation abolished LAD with a PI-R interval identical to the H-V time. These findings suggest that a bundle branch block pattern and/or axis deviation may result from a focal lesion or an area of altered refractoriness within the BH. The duration of the QRS complexes and/or a shift in QRS axis was normalized by BH stimulation distal to the lesion due to synchronous impulse conduction to both the bundle branches. activation wavefront leaving the sinus node, atrium and A-V node are predestined for specific areas of ventricular myocardium.2 It was further postulated that the propagation wavefront may be altered in the His bundle (BH) by physiological influences or by focal disease and result in any form of bundle branch block, ventricular aberration and preexcitation. They do admit that their observations provide an anatomic substrate for the concept of longitudinal dissociation of conduction within the His bundle, under both normal and pathologic circumstances, but do not prove the concept.' Others have attempted to reproduce the physiological counterpart of these anatomical findings in isolated tissue and animal experiments.3The purpose of this report is to present our data in 27 patients (left bundle branch block in 25 and isolated left axis deviation in two) which suggest longitudinal dissociation in the His bundle. Stimulation from the proximal BH showed 996 CIRCULATION by guest on May 16, 2015 http://circ.ahajournals.org/ Downloaded from

SUMMARYThe phenomenon of postpacing depression of cardiac pacemakers was utilized to evaluate the sinus-node function in 56 patients by analyzing the sinus-node recovery time (SRT), that is, the interval between the last paced P wave and the following sinus P wave. Corrected SRT (CSRT) is defined as the recovery interval in excess of the sinus cycle (SRT -sinus cycle length). The SRT was measured following sinusnode suppression by (1) isolated premature beats (PABs) and (2) atrial pacing (AP) at rates of 100 to 140/min for periods of 2 to 5 min at each level. Twentyeight patients had normal heart rates (group A), and 28 patients had sinus bradyeardia (SB; group B). Ten of the 28 patients with SB were restudied after receiving atropine (2 mg intravenously). The CSRT with PABs was similar in both group A and group B patients and remained essentially unchanged after atropine despite a decrease in sinus cycle length. The phenomenon of interpolated PABs was demonstrated in seven of the 56 patients. In 27 of the 28 patients with normal heart rates (group A), the CSRT with AP ranged from 110 to 525 msec and was essentially independent of the rate and duration of AP. In the remaining one patient of group A, despite a normal heart rate, the CSRT was prolonged (1810 msec) and directly dependent on the rate and duration of AP. In 12 of the 28 patients with SB, the CSRT was comparable to that in group A (<525 msec). In the remaining 16 patients with SB (group B), the CSRT ranged from 560 to 3740 msec and was usually directly proportional to the rate and duration of AP. After atropine in most of the patients with a prolonged CSRT, the CSRT remained abnormal whereas in others junctional escape beats appeared first, followed eventually by normal sinus rhythm. In a single patient with SB and an abnormal CSRT, restudy 7,i months later again showed a prolonged CSRT indicating the reproducibility of the measurement. The CSRT with AP provides a potentially useful clinical means of assessing the sinus-node function and thereby aids in the diagnosis of the "sick sinus syndrome." It is stressed that AP was found to be more reliable than PABs in eliciting an abnormal response. Furthermore, a normal sinus (atrial) rate does not necessarily provide assurance of a normal sinusnode response to AP, that is, normal sinus-node function.

This study describes a new method (NM) for estimation of sinoatrial conduction time (SACT), which utilizes constant atrial pacing (AP) instead of the premature atrial beats (PABs) used in the method reported in 1973 by Strauss et al. The SACTs were obtained by both methods in 20 patients. The SACT by the Strauss method (SM) was calculated as A2A3 minus A1A1. The NM consists of high right AP for a train of eight consecutive beats at rates less than or equal to 10 beats/min faster than the sinus rhythm. The interval between the last paced atrial electrogram (Ap) and the first escape atrial electrogram (A) of sinus origin (Ap-A) was measured along with several post pacing sinus cycles. The SACT by the NM was calculated as follows: SACT = Ap-A minus A1A1. The effect of AP at higher rates was also analyzed. In two patients, the SACT with the SM could not be defined, as all the A2A3 intervals were fully compensatory; with the NM the SACT was 217 and 320 msec. In the remaining 18 patients the SACT was obtainable by both methods. With SM, the SACT ranged 105--452 msec (mean 219 +/- 102 SD) and with the NM it was 85--492 msec (mean 201 +/- 112 SD), and the difference was statistically significant (P = 0.0162). The coefficient of correlation between the two methods was r = 0.97. During AP at faster rates, a rate related increment in Ap-A intervals and also post pacing sinus cycles was noted. This study describes a new and simple method for measurement of SACT in man.

SUMMARYHis bundle electrograms were recorded and A-V junction pacing was achieved in 30 patients by a pervenous electrode catheter technic. His