Sinoatrial Conduction Time Research Articles

Bedside evaluation of postoperative sinus node function in children

Sinus node dysfunction in children frequently results from the surgical correction of congenital heart defects. We evaluated postoperative sinus node function at the bedside in 25 children by utilizing atrial epicardial electrodes which were placed near the sinus node at the time of operation. Sinoatrial conduction times (SACTs) and corrected sinus node recovery times (CSNRTs) were determined within 3 days of operation in each patient. Group 1 consisted of 20 patients (aged 1 month to 13 years) with normal postoperative sinus node function. Mean (+/- SD) SACTs and CSNRTs were 122 +/- 33 msec (range 61 to 187 msec) and 165 +/- 54 msec (range 52 to 253 msec), respectively. Preoperative evaluation of sinus node function during cardiac catheterization showed that preoperative and postoperative SACTs and CSNRTs were not significantly different (p greater than 0.05) in any of nine patients. Group 2 was composed of five children (aged 1 to 14 years) with postoperative sinus node dysfunction. Three had abnormal SACTs of 230 msec or greater and two children had first-degree sinus node entrance block. Two patients had prolonged CSNRTs. Electrocardiographic (ECG) monitoring revealed evidence of sinus node dysfunction in four of the five patients in Group 2. This report describes a simple and safe means of evaluating postoperative sinus node function at the bedside. The data are comparable to those obtained using more conventional methods during cardiac catheterization.

Electrophysiologic effects on combined autonomic blockade in patients with sinus node disease.

Thirty-two patients were studied before and after i.v. administration of 0.15-0.20 mg/kg of propranolol. Twenty-one of the 32 underwent combined autonomic blockade with the additional infusion of 0.04 mg of atropine. Twenty other patients with sinus node disease underwent electrophysiologic studies both before and after i.v. administration of 0.04 mg of atropine alone. Spontaneous cycle length, maximal corrected sinus node recovery time, sinoatrial conduction time, secondary pauses and intrinsic heart rate were measured. Secondary pauses were more common in those with abnormal intrinsic heart rates, and they did not correlate with changes in maximal corrected sinus node recovery time or sinoatrial conduction time. In patients with normal intrinsic heart rate, abnormal test measurements usually returned to normal after combined blockade (hypervagotonia); however, some patients showed a new abnormality after propranolol that was not reversible with atropine (catecholamine-dependent). Abnormal test responses in patients with abnormal intrinsic heart rate persisted or increased after combined blockade. We conclude that patients with sinus node disease may be categorized as (1) those with intrinsic sinus node disease; (2) those with normal intrinsic sinus node function but either relative hypervagotonia or catecholamine dependency; and (3) those with abnormal intrinsic sinus node function affected by vagal or catecholamine factors.

EFFECT OF VERAPAMIL ON SINOATRIAL AND ATRIOVENTRICULAR CONDUCTION TIME IN DOGS

The effect of verapamil on sinoatrial and atrioventricural conduction were studied on 11 dogs under the urethane-chloralose anesthesia.The sinoatrial conduction time determinded by using the premature atrial stimulation method and represened as antegrade plus retrograde conduction time was significantly prolonged following the intravenous administration of 0.05mg/kg of verapamil. However, the sinoatrial conduction time was almost unchanged when larger doses of verapamil were administrated. On the other hand, the sinus cycle length and A-H time were prolonged as to the verapamil dose was increased, while H-V time was unchanged. The systolic and diastolic pressures were depressed as to the verapamil dose was increased.The present rather curious observation that the sinoatrial conduction time was not affected by larger dose of verapamil was suspected to be resulted from the prolongation of sinus cycle length and/ or the increased reflex sympathetic tone.

Electrophysiologic properties of cimetidine in man.

Severe bradycardia has been reported with the use of cimetidine. This observation has been explained by histamines' known action in increasing the contraction rate of the spontaneously beating right atrium, strips of ventricular muscle, and whole heart of guinea pigs. Histamine can also produce cardiac arrhythmias in animals. There is evidence for H2 receptors in the heart. Black and his associates have shown that the characteristic effect of histamine on isolated guinea pig atrium could be selectively blocked by anti-H2 drugs. Thus cimetidine probably can produce a sinus bradycardia by blocking the H2-receptor site in the heart. Recently Engel and Luck reported that 300 mgs of intravenously administered cimetidine did not affect heart rate, sinus node recovery time, or sinoatrial conduction time. These workers concluded that there is insufficient evidence to demonstrate that cimetidine caused appreciable sinus node dysfunction in man. In view of the disparity in these reports, we investigated the effects of 300 mgs of intravenously administered cimetidine on the human conduction system.

Methods for recording electrograms of the sinoatrial node during cardiac surgery in man.

Recent reports have shown that it is possible to record extracellular electrograms from the rabbit and dog sinoatrial (SA) node. We applied similar techniques to record SA nodal activity in 23 patients who underwent cardiac surgery for various forms of heart disease. Both a bipolar technique, using pairs of electrodes at various interelectrode distances, and a unipolar technique, using an exploring and an indifferent electrode, were used. To record SA nodal electrograms, polarity was reversed from the conventional electrocardiographic recording; high amplification (100 microV/cm) and low-pass filters (0.15-20 Hz) were used. SA nodal electrograms were recorded from eight of 12 patients using the bipolar method and from nine of 11 patients using the unipolar method. There were no significant differences in the success rate or quality of the recording between the two methods. However, the unipolar method allowed a more accurate localization of the SA node. Human SA nodal electrograms resembled those of the dog and rabbit and showed two distinct slopes: a diastolic slope and an upstroke slope preceding the P wave of the ECG, SA conduction times were 32.4 +/- 2.8 msec (mean +/- SEM) at sinus (PP) cycle lengths of 587.6 +/- 35.6 msec for the bipolar method, and 38.2 +/- 3.2 msec at sinus (PP) cycle lengths of 712.2 +/- 50.7 msec for the unipolar method. These methods for recording of extracellular SA nodal electrograms in man may prove useful in 1) localization of the SA node during open heart surgery and 2) assessment of SA nodal function in health and disease.

Method for recording electrical activity of the sinoatrial node and automatic atrial foci during cardiac catheterization in human subjects

A method for recording electrical activity of the sinoatrial (S-A) node and automatic atrial foci in human subjects is described. To record S-A nodal electrograms, an electrode catheter was inserted percutaneously into the femoral vein and advanced under fluoroscopic control to the superior vena caval-right atrial junction. The distal terminal of the catheter was placed in the area of the S-A node and the proximal terminal on the free right atrial wall or in the right atrial lumen. Polarity was reversed from the conventional electrocardiographic recording; high amplification (about 100 μV/cm) and selective filters (0.1 to 20 hertz) were used. S-A nodal electrograms recorded with this method in human subjects were similar to electrograms obtained previously from the dog and rabbit and revealed negatively directed diastolic and upstroke slopes preceding the P wave of the electrocardiogram. Sinoatrial conduction time measured from the S-A nodal electrograms in 15 cases was 34.9 ± 2.1 ms (mean ± standard error of the mean) for a sinus cycle length of 736.4 ± 38.6 ms. The coronary sinus electrograms in a patient with coronary sinus rhythm were recorded by the same technique except that the distal terminal of the catheter was placed at the coronary sinus ostium. A negatively directed diastolic slope preceding the P wave was consistently recorded. This method for recording electrograms of the S-A node and ectopic automatic atrial foci should prove useful in (1) assessment of both normal and abnormal S-A nodal function, (2) direct determination of conduction time from the S-A nodal pacemaker to the atrium, and (3) localization of automatic atrial foci.

Electrophysiologic diagnosis of patients with sinus node dysfunction: with special reference to a modified method for calculating sinoatrial conduction time.

The diagnostic value of maximum corrected sinus node recovery time (CSNRT) and sinoatrial conduction time (SACT) was assessed in 15 patients with clinical evidence of sinus node (SN) dysfunction and 16 control subjects. The SACT was calculated by a modified method using only those sinus cycles with A1-A1 intervals falling within one standard deviation of the mean. We also obtained a maximum SACT and a ratio of maximum/mean SACT. We found that the maximum/mean SACT ratio being useful for identifying patients with sinus arrest or sinoatrial block. Abnormal value of the ratio (greater than or equal to 1.85) was also more frequently observed in patients with syncope or dizzy spells than those without (55.6% vs. 33.3%). By applying mean SACT and maximum/mean SACT ratio, calculated by the modified method, together with maximum CSNRT, all patients with SN dysfunction could be completely isolated from the normal subjects.

Autonomic tone of patients during an electrophysiological catheterization: The role of autonomic influences on the reproducibility of sinus node function studies

Urinary catecholamine excretion remained unchanged and total electromechanical systole, QS 2I, increased during the electrophysiological study of 16 patients (eight normals, eight with sinus node dysfunction) when compared to values obtained the day before and the day after the study. The mean values of the sinus node function studies (sinoatrial conduction and recovery times) repeated the day after the procedure were not significantly different from those obtained during the electrophysiological study in both the normal patients and patients with sinus node dysfunction. Individual patients in the sinus node dysfunction group showed slight variation in the sinus node studies; four of these patients showed normalization of SA node function the day after the electrophysiological procedure. These studies suggest that the electrophysiological procedure does not provoke a hyperadrenergic state. The sinus node function studies are reproducible in patients with normal baseline values. While the mean sinus node function results for the group with abnormal SA node function did not change significantly on repeat testing, some individual variation occurred; this variation is probably related to autonomic disturbances of SA node function.

Electrophysiologic effect of digitalis on sinoatrial nodal function in children

Despite the prevalence of digitalis usage in children, the electrophysiologic effects of digitalis on sinoatrial (S-A) nodal function is unknown in this age group. The purpose of this study was to determine the effect of digitalis on sinoatrial conduction time as well as on S-A nodal automaticity. Ten subjects (mean age 10.5 years) underwent electrophysiologic assessment of S-A nodal function before and 30 minutes after administration of ouabain (0.01 mg/kg). Total S-A conduction time increased in each subject and the mean value after ouabain (182 msec ± 13 standard errors of the mean [SEM]) was significantly higher ( P < 0.01) than before (149 msec ± 11). The sinus cycle length was variable after ouabain ( P > 0.1). The corrected sinus nodal recovery time also was variable ( P > 0.1), decreasing substantially in three subjects. Mechanisms of the effect of digitalis on the S-A node and atrium are proposed and discussed. It is concluded that digitalis prolongs the S-A conduction time in children with normal S-A nodal function. By prolonging the S-A conduction time, digitalis may artifactually shorten corrected S-A nodal recovery time in some patients.

The estimation of sinoatrial conduction time in rabbit heart by the constant atrial pacing technique.

This study compared estimates of sinoatrial conduction time (SACT) obtained by constant atrial pacing (CAP) and premature atrial stimulation (PAS) with measured SACT in isolated rabbit right atrial preparations. Transmembrane potentials and surface electrograms were recorded from the sinus node and crista terminalis, respectively. The crista terminalis was paced 5, 10 and 15 beats/min faster than the spontaneous sinus rate with a train of eight pulses. Estimate of SACT by CAP was taken as the difference between the first atrial return cycle and the mean spontaneous cycle length. SACTs at 5, 10 and 15 beats/min faster were 76 +/- 10, 86 +/- 10 and 96 +/- 10 msec (mean +/- SEM; n = 12), respectively; correlation coefficients with the true SACT were 0.7, 0.54 and 0.4. Consecutive determinations of SACT by PAS and CAP in the same preparation (n = 6) at 10 beats/min faster gave SACTs of 86 +/- 13 and 79 +/- 14 msec, respectively, compared with true SACTs of 79 +/- 10 msec. Shortening of sinus node action potential, depression of automaticity and shifts in the site of the primary pacemaker contributed to the errors in both techniques. Estimation of SACT by CAP may be further complicated by failure of sinus node capture. Principles to minimize some of these errors are also presented.

Human electropharmacology of the calcium antagonist dimeditiapramine (Ro 11-1781) in coronary patients.

The electrophysiological effect of dimeditiapramine (Ro 11-1781), a Ca2+ antagonist, was evaluated in 20 patients with coronary heart disease. Electrophysiological measurements, including sinus cycle length, sinoatrial conduction time, intra-atrial conduction time, atrial, atrioventricular, nodal and ventricular refractory periods and intraventricular conduction time were recorded before and after the intravenous administration of Ro 11-1781. At a dose which is effective against cardiac arrhythmias, Ro 11-1781 produced no statistical significant changes in the sinoatrial and intraventricular conduction time. Similarly, neither the sinoatrial nor the ventricular refractory period was affected. Ro 11-1781, however, increased the atrioventricular conduction time and decreased the systolic blood pressure to a statistically significant extent. The tolerance was very good.

Effects of digoxin on sinus nodal function before and after vagal blockade in patients with sinus nodal dysfunction: A clue to the mechanisms of the action of digitalis on the sinus node

To increase the limited knowledge of the effects of digitalis on sinus nodal function in patients with sinus nodal dysfunction and to initiate an investigation into the mechanisms underlying its effects, 34 patients with sinus nodal dysfunction were studied. Twenty patients underwent determination of sinus cycle length, estimated sinoatrial conduction time and maximal corrected sinus recovery time before and after the administration of 0.75 mg of intravenous digoxin. For the group, sinus cycle length did not change, sinoatrial conduction time increased insignificantly and maximal corrected sinus recovery time shortened; however, individual variation occurred. The effects of acute digitalization appeared to predict the effects of chronic digitalis administration on sinus nodal function in the eight patients who subsequently continued to take digoxin. Fourteen patients received digoxin after vagal blockade with atropine. After vagal blockade, digoxin lengthened sinus cycle length, sinoatrial conduction time and maximal corrected sinus recovery time. The effects of digoxin administered after atropine could be antiadrenergic, direct, or both, and are opposite to those induced by atropine alone. Because these effects are similar to those of vagotonia yet are not apparent when the vagi are unblocked, digoxin may have direct excitatory, adrenergic or previously unrecognized vagolytic effects on sinus nodal function in man and their manifestation may be dependent on heart rate or autonomic tone.

Influence of plasma drug level and the presence of conduction disease on the electrophysiologic effects of procainamide

Electrophysiologic measurements were made in 16 patients before and after the intravenous administration of procainamide. The drug was administered at two different dose levels. The lower plasma procainamide level (6 to 7 μg/ml) caused small decreases in cycle length (848 ± 13 versus 799 ± 42 msec), sinus nodal recovery time (1,166 ± 81 versus 1,024 ± 90 msec at a paced rate of 120 beats/min) and sinoatrial conduction time (105 ± 11 to 90 ± 9 msec). Sinus or atrial echo zones, whether or not they caused supraventricular tachyarrhythmia, were abolished by procainamide in 11 of 13 instances. The higher plasma level of procainamide (10 to 11 μg/ml) generally caused greater changes in electrophysiologic measurements. Atrial refractory periods tended to increase but changed significantly only at higher plasma levels. The latter effect was blunted in patients with a prolonged sinoatrial conduction time. The A-H interval and atrioventricular nodal functional refractory period tended to decrease at higher plasma levels, but not significantly. The H-V interval increased slightly from 48 ± 2 to 52 ± 2 msec; this effect was blunted in patients with bundle branch block. It is concluded that procainamide could be useful in managing supraventricular tachyarrhythmia because it abolishes atrial and sinus echo zones that trigger supraventricular tachyarrhythmia and because its widespread effects make it capable of blocking reentry at several sites. The electrophysiologic effects or procainamide are less predictable in patients with conduction disease, and some effects occur only at high plasma levels.

Electrophysiologic effects of disopyramide phosphate on sinus node function in patients with sinus node dysfunction.

The electrophysiologic effects of intravenously administered disopyramide (2 mg/kg) on three parameters of sinus node function were examined in 16 symptomatic patients with sinus node dysfunction. Based on their ECG data before study, patients were subdivided into group A (n = 8), those with sinus pauses and/or sinoatrial (SA) exit block; and group B (n = 8), those with sinus bradycardia. Disopyramide shortened spontaneous cycle length in 10 of 16 patients and lengthened it in six--markedly so (91%) in one patient. Estimated SA conduction time decreased in seven of 14 patients and increased in seven. Two patients developed second degree SA exit block after disopyramide. Maximum sinus node recovery time was prolonged by disopyramide in 11 of 16 patients and markedly so in four. For the group as a whole there was no significant difference in spontaneous cycle length, maximum sinus node recovery time or estimated SA conduction time. P-wave and QRS durations and H-V intervals were significantly lengthened by disopyramide. Marked depression of the three parameters of sinus node function occurred in three group A patients and in one group B patient who had persistent severe sinus bradycardia. These four patients also had secondary pauses after termination of rapid atrial pacing under control conditions. Disopyramide should be administered cautiously to patients with sinus node dysfunction, particularly those with sinus pauses, SA exit block or secondary pauses.

Comparative study of two methods of estimating sinoatrial conduction time in man

Programmed premature atrial stimulation has been widely used to estimate sinoatrial conduction time in man. A proposed new approach uses continuous atrial pacing just above the spontaneous cycle length. Sinoatrial conduction time is represented by the difference between the first cycle after pacing and the spontaneous cycle length, assuming that sinus nodal automaticity is undisturbed by continuous atrial pacing. Both techniques were compared in 23 consecutive patients. Mean (± standard deviation) sinoatrial conduction time was 113 ± 27 msec estimated with the premature stimulus technique and 96 ± 48 msec when estimated with the continuous pacing technique. In about 30 percent of cases the two values corresponded well with each other. In the remaining patients sinoatrial conduction time estimated with the premature stimulus technique was longer than the time estimated with continuous atrial pacing. Additionally, the latter was estimated at two different rates of pacing in which the cycle length was 30 and 60 msec, respectively, shorter than the previous cycle length. The estimate then increased to 119 ± 39 and 136 ± 40 msec, respectively. Sinoatrial conduction time estimated with continuous atrial pacing did not depend on spontaneous cycle length and did not correlate with sinus nodal recovery time. The cycles after the first pause were slightly longer than the spontaneous cycle length. The results suggest that data from the two techniques cannot be easily compared and that premature atrial stimulation may exert a more depressive effect on sinus nodal automaticity than continuous atrial pacing. The observed differences in results may also be due to a more pronounced delay of retrograde conduction during premature atrial stimulation than during continuous atrial pacing. It is also possible that continuous atrial pacing leads to some overdrive exciting effect on the sinus node, although the opposite effect is suggested by the response of the cycles after the first postpacing cycle. A final conclusion regarding the validity of each technique cannot be reached on the basis of these clinical data.

Evaluation of sinus node automaticity and sinoatrial conduction in children with normal and abnormal sinus node function

AbstractSinus node recovery time (SNRT) and sinoatrial conduction time (SACT) were determined in each of 28 children. Eighteen children (ages 2 to 14 years) had electrocardiographically normal sinus node function and served as controls. Ten children (ages 4 to 13 years) had electrocardiographic evidence of sinus node dysfunction, consisting of inappropriate sinus bradycardia, periods of sinus arrest or sinoatrial exit block. Mean control SNRT was 133% of the sinus cycle length with an upper normal limit of 151% (mean + 2 SD). Control SACTs ranged from 45‐105 ms with mean and mean + 2 SD values of 71 ms und 105 ms.In the patients with SND, SNRTs averaged 168% and five patients had abnormally prolonged values of 158 to 256%. Mean SACT was 101 ms with four children having values greater than 105 ms. Seven of the 10 patients with SND had at least one electrophysiologic abnormality.This study defines normal sinoatrial conduction in children and validates the data by demonstrating a close correlation with similar data obtained from adult populations. Although abnormal electrophysiologic data confirms the presence of sinus node dysfunction, normal values for SNRT and SACT do not insure normal sinus node function.

Sinus node response to premature atrial stimulation in the rabbit studied with multiple microelectrode impalements.

In this study we investigated the response of the isolated rabbit sinus node to ectopic atrial premature beats elicited late in the atrial cycle. In three experiments the response of at least 45 different fibers of the sinus node was recorded, whereas, in other experiments, investigation was less extensive. In this way the spread of activation of the total pacemaker area could be mapped accurately both during spontaneous beating and the induction of ectopic atrial beats of different degrees of prematurity. We found that: (1) The conduction of an impulse from the dominant pacemaker area to the atrium during spontaneous rhythm (antegrade conduction) is slower than the conduction of an ectopic atrial impulse towards the center of the sinus node (retrograde conduction). (2) The action potential of the dominant pacemaker fibers in the sinus node is shortened because of premature activation caused by an ectopic impulse from the atrium. Late premature beats had no effect on diastolic depolarization. If the retrograde activation wave did not reach the area of the dominant pacemaker before the spontaneous discharge of these fibers, there was electrotonic influence demonstrable over a distance of about 0.5 mm. (3) Comparison of the true sinoatrial conduction time with the estimated sinoatrial conduction calculated indirectly from the length of the postextrasystolic atrial cycle revealed that, in the isolated rabbit heart, the calculated value is a serious underestimation of the true antegrade sinoatrial conduction time.

A new method for measurement of sinoatrial conduction time.

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.

Electrophysiological effects of verapamil.

Previous studies have demonstrated that verapamil possess potent anti-arrhythmic effects. The present study has been designed to define the cardiovascular effects of this drug. Isolated tissue studies performed in rabbit right atrium demonstrated that prompt and prominent slowing of the sinus rate even at a dose of 1 X 10(-7) mol . litre-1. This dose produced significant decrease in action potential amplitude and phase 4 slope, shifted the 'threshold potential' to a less negative value, prolonged action potential duration but did not change maximum diastolic potential. At this dose of verapamil, sinoatrial conduction time prolonged significantly (control: 40.0 +/- 4.8 ms; 1 X 10(-7) mol . litre-1 verapamil: 50.0 +/- 6.4 ms). Purkinje fibre studies demonstrated decreases in dV/dt, resting potential, total amplitude, action potential duration at 75, 95% of recovery and effective refractory period only after exposure to greater than or equal to 1 X 10(-5) mol . litre-1 verapamil. Electrophysiological studies in conscious dogs demonstrated, after bolus administration of verapamil, progressive increases in the A-H interval and heart rate, but no changes in H-V and QRS intervals. Anaesthetised dog studies showed the lack of significant effect on A-H and H-V intervals or QRS duration regardless of the bolus dose of verapamil. However, verapamil produced statistically significant increases in heart rate after 0.025 mg . kg-1. Verapamil administration did not produce a statistically significant change in escape pacemaker rate in vagal stimulation experiments or with spontaneously beating isolated Purkinje fibres. Finally, the effect of increasing intravenous bolus does of verapamil on ischaemic arrhythmias was studied in five conscious dogs 24 h following LAD ligation. Only one dog with ventricular tachycardia and another dog with junctional escape rhythm were converted to sinus rhythm after the 0.05 mg . kg-1 and 0.2 mg . kg-1 doses, respectively. In conclusion, these studies demonstrated that administration of verapamil specifically depresses tissue with electrophysiological dependence on slow channel current. Therefore, sinus and A-V nodal events would be suppressed and slow-channel mediated events in ischaemic ventricle also would be inhibited. Clinically, acute administration of verapamil would lead to depression of sinus and A-V nodal function as well as potentially eliminate slow current mechanisms in ischaemic arrhythmias.

Human electropharmacology of tocainide, a lidocaine congener

The electropharmacology of tocainide, an orally active congener of lidocaine, was evaluated in 10 patients with coronary artery disease. Electrophysiologic measurements including sinus nodal recovery time, sinoatrial conduction time, intraatrial conduction time, atrial, atrioventricular (A–V) nodal and ventricular refractory periods and intraventricular conduction time were obtained before and after intravenous infusion of tocainide. At blood levels shown to be effective against ventricular arrhythmias, tocainlde produced no statistically significant changes in the electrophyslologlc measurements, although occasional marked individual effects were observed. No side effects were observed during these studies. No adverse effects on A–V conduction were observed in patients with an intraventrlcular conduction disturbance or a prolonged control H–V interval. Thus, plasma tocainide concentrations effective in the therapy of ventricular arrhythmias exert no adverse effects on cardiac electrophysiologic properties in patients with coronary artery disease.