Faculty Bibliography

Factors that facilitate the occurrence of cholinergic atrial arrhythmias were studied on 16 rabbit biatrial preparations in spontaneous rhythm. Sinus cycle length and characteristics of the atrial action potential were measured by the microelectrode technique in the basal state, then in the presence of acetylcholine at a concentration of 1.4 x 10(-5) M. Induction of arrhythmia was attempted by programmed stimulation, using an increasing number of extrastimuli. In the presence of acetylcholine the sinus cycle length increased by 106 +/- 63 p. 100 (p less than 0.0001) and the action potential duration, measured at 90 p. 100 repolarization (APD90) decreased from 60 +/- 15 ms to 40 +/- 11 ms (p less than 0.001). Reentrant activities, which had not been found in the basal state, were induced in 5 preparations. Under acetylcholine the sinus cycle of inducible preparations was shorter than that of non inducible preparations (663 +/- 272 ms vs 1218 +/- 531 ms, p less than 0.05). The percentage of sinus cycle lengthening was significantly smaller in inducible preparations (54 +/- 31 p. 100 vs 129 +/- 60 p. 100, p less than 0.05). Although sinus cycle lengthening was different in the two types of preparations, the APD90 was shortened in the same proportions. The vulnerability of the preparations seemed to depend mainly on a frequency effect. Vagal atrial arrhythmias occurred with a relatively small reduction in sinus rhythm. It is probable that an overpotent vagal effect is less arrhythmogenic because of its more homogeneous action on tissues.

In order to determine the respective roles of catheter (Ct) physical properties and of energy levels in myocardial effects of fulguration, we delivered an electrical shock between the tip electrode of a Ct placed at the apex of the right ventricle and a large cutaneous cathodal electrode in 12 dogs. Two energy levels were used: Group A = 25 J (n = 6) and group B = 100 J (n = 6), and three Cts were studied. These Cts had different resistances (R) and active surface electrodes (S): Ct 1 (R = 0.3 omega, S = 12 mm2), Ct 2 (R = 0.3 omega, S = 2 mm2), Ct 3 (R = 2 omega, S = 13 mm2). Complex ventricular arrhythmias were observed in 5/6 cases at 100 J but only in 1/6 cases at 25 J and were independent of the Ct type. Following the shock, the effective ventricular refractory period (S1 S1 = 300 msec) increased significantly only at 100 J (11%, p = 0.03). Anatomical lesions were wider (10.6 vs. 5.2 mm, p less than 0.05) and deeper (100 vs. 55%, p less than 0.05) in the 100 J group. In contrast, there was no significant difference in the electrophysiological and anatomical changes between the three Cts. In conclusion, arrhythmogenic adverse effects of ventricular Ct fulguration are related to the delivered energy; on the contrary, they seem only slightly dependent on Ct physical properties at these energy levels; a 2 J/kg shock is not only effective but also seems to be safe.

Spatial inhomogeneity of refractory periods, as measured during clinical electrophysiological studies, is a known predisposing factor of arrhythmia. We studied effective refractory periods (ERP) and action potential duration (ADP90) on isolated human atrium. Twelve samples of right atrium obtained during cardiac surgery from patients with (n = 6) and without (n = 6) atrial fibrillation (AF) were studied by microelectrode technique. For each preparation, ERP were measured at basic cycle lengths (BCL) of 1,600, 1,200, 800, and 400 msec in five different cells located around (0.8 mm) the stimulating electrode. Dispersion of ERP was significantly greater in the AF group (96.7 +/- 9 versus 70.9 +/- 9 msec, p = 0.01). In the non-AF group, we observed a positive linear correlation between ERP and BCL (r = 0.86) ADP90 and BCL (r = 0.93). On the contrary, in the AF group this correlation was absent between ERP and BCL (r = 0.28), poor between ADP90 and BCL (r = 0.62). These results suggest that nonhomogeneous recovery of excitability (dispersion and poor adaptation) may be an important factor of arrhythmia. This inhomogeneity is present at the cellular level as well as in the entire heart.

Sinoatrial conduction times, estimated by premature atrial stimulation, were compared with direct measurement of the sinoatrial conduction time in 15 isolated rabbit sinus node preparations before and after intrasinusal pacemaker shifts induced by cooling. Transmembrane potentials and surface electrograms were recorded from the sinus node and crista terminalis. Extracellular sinus node activity was recorded in five preparations. Mapping was performed at 38 degrees C and 35 degrees C to determine the site of the dominant pacemaker. The sinus cycle was significantly longer at 35 degrees C (319.4 ms vs 258.1 ms). Intracellular measured conduction time was significantly shorter (63.8 ms vs 70.4 ms) because of caudal shift of the dominant pacemaker. Estimated sinoatrial conduction time was significantly longer (110.3 ms vs 85.4 ms) owing to the depression of automaticity by the extrastimulus. Extracellular measured conduction time did not differ significantly from intracellular measured conduction time. These results suggest that intrasinusal pacemaker shift may explain inaccuracies in indirect estimations of sinoatrial conduction time by atrial pacing techniques. Extracellular recordings appear to be a better method of evaluating sinoatrial conduction times.