Improved sinus node sensing after atropine.

Although atropine is known to increase sinus rate through its vagolytic effect, the effects of atropine on sinus node sensing are unknown. The purpose of this study was to investigate alterations in sinus node sensing produced by atropine. Measurement of the zone of sinus node reset and sinoatrial conduction time was performed in 10 patients by programmed premature atrial stimulation. The zone of sinus node reset was determined as the transition point where premature atrial stimuli were followed by a less than compensatory pause. Sinoatrial conduction time was calculated from sinus node return cycles in the area where sinus node reset occurred. Atropine administration produced a significant increase in the percentage of the sinus cycle length at which premature atrial contractions penetrated and reset the sinus node. Sinus node reset occurred at a mean percentage of the sinus cycle of 71 +/- 8 per cent before atropine and 83 +/- 5 per cent after atropine (P less 0.01). The sinoatrial conduction time was significantly reduced from 109 +/- 29 to 62 +/- 23 msec. (P less than 0.01) from atropine as sinus cycle length was reduced from 909 +/- 118 to 642 +/- 75 msec. after atropine. Sinus node echoes were observed in two patients. In one patient atropine abolished the appearance of sinus node echoes. In the second patient atropine reduced the coupling interval necessary to produce sinus node echoes but appeared to facilitate sinus node re-entry by the appearance of an additional sinus node echo and a reduction in the echo cycle length. This study demonstrates that atropine produces significant improvement of sinus node sensing in man.     

Sinus node pacemaker shift: a phenomenon induced by premature atrial stimulation in man?

The aim of this study was to investigate whether premature atrial stimulation is able to induce a shifting of the sinus node pacemaker. For this purpose we compared, in 18 patients, the curve of sinus node function obtained with Strauss' method with that resulting from the scanning, with premature atrial stimulation, of the first returning cycle following a single premature induced atrial beat. We found that the length of the compensatory phase (zone I) evaluated on the curve resulting from the scanning of the first returning cycle following the single premature induced atrial beat was shorter (15%) than that observed with the original Strauss method. In addition, an inverse relationship between the shortening of the compensatory zone and the estimated sinoatrial conduction time was observed. This result could be accounted for by one of the following explanations: 1) a change in the sinoatrial conduction or in the sinus pacemaker automaticity; 2) sinus node reentry; 3) sinus node pacemaker shift. Even if there is no direct evidence either to prove or to exclude one or more of these explanations, sinus node pacemaker shift seems to be the most convincing explanation.     

Atrial stimulation and intranodal migration of sinus pacemaker in man (author's transl)

In order to demonstrate, in man, sinus node pacemaker shift following atrial stimulation, we compared, in 26 patients, the curve of sinus node function obtained with Strauss' method with that resulting by the scanning with premature atrial stimulation of the first returning cycle following either a single premature atrial induced beat (140 ms shorter than the basic cycle) (group A), or a train of 8 consecutive atrial beats induced with a rate slightly faster (10 beats/m) than the control sinus rhythm (group B). Assuming that no changes in sinus pacemaker automaticity or in sinoatrial conduction occur owing to atrial stimulation, curves with the same shape should be observed if the site of the dominant pacemaker remains unchanged: whereas, different lengths of the compensatory phase (zone I) should be expected if an intranodal pacemaker shift occurs. For evaluating the length of the compensatory zone (zone I), we calculate, on the curve of the sinus node function, the mean value of the relation points included in the first third of the reset zone (zone II). According to our results, the length of the compensatory phase (zone I) evaluated on the curve resulting by the scanning of the first returning cycle following either a single premature atrial induced beat (group A), or eight consecutive atrial beats (group B) was shorter than that observed with the original Strauss' method (10% and 18% respectively). However, only in the group B, this difference was statistically significant. In addition, a significant inverse relationship between the shortening of the compensatory zone and the sinoatrial conduction index was also observed. Considering that our results have been corrected in such way as to repeal eventual changes in sinus pacemaker automaticity or sinoatrial conduction following atrial stimulation, the shortening of the compensatory zone, we have observed in our patients, strongly suggests an intranodal sinus pacemaker shift. If we assume that this result could represent an indirect evidence of this phenomenon, some clinical implications may follow: 1) another limitation, in addition to others known (intraatrial conduction delay, sinus arrhythmia, changes in sinus node automaticity, difference between retrograde and antegrade conduction time) could decrease the accuracy of atrial stimulation techniques in the estimation of the sinoatrial conduction time; 2) sinus pacemaker shift following atrial stimulation, may induce an understimulation of the true sinoatrial conduction time; however, according to our results, the error is generally small, so that it does no preclude the usefulness of atrial stimulation techniques in the evaluation of sinoatrial conduction; 3) the more evident and significant shortenings of the compensatory phase occurred with atrial pacing technique: this finding could explain why shorter sinoatrial conduction times are generally observed with Narula's method in comparison with Strauss' method.     

Sinus node electrogram recording in 59 patients. Comparison with simultaneous estimation of sinoatrial conduction using premature atrial stimulation.

Directly measured sinoatrial conduction time was compared with sinoatrial conduction time assessed simultaneously by the single premature atrial stimulus technique in 59 patients: 20 with normal sinus function, 35 with sinus dysfunction, and four with sinus bradycardia but negative indirect methods. In patients with normal sinus function direct sinoatrial conduction time was 102.5 +/- 34 ms (mean +/- 2 SD) and was identical to indirect sinoatrial conduction time. Neither direct sinoatrial conduction time in the basal and return cycle, nor post-return and basal cycle lengths were different. Sinoatrial and atriosinus conduction durations were similar. In sinus dysfunction direct sinoatrial conduction time (average 160 +/- 47 ms) was longer than in normal sinus function. Prolonged direct sinoatrial conduction time may therefore be considered as a criterion of sinus dysfunction. In sinus dysfunction no significant correlation was observed between direct and indirect sinoatrial conduction times. Direct sinoatrial conduction time was equal to (17 patients), longer than (12 patients), or shorter than (six patients) indirect sinoatrial conduction time. These differences can be explained by delayed or incomplete premature depolarisation penetration into the sinus node rather than by the classical pacemaker shift.     

Programmed atrial stimulation in the study of sinoatrial conduction in normal subjects (author's transl)]

Sinoatrial conduction was investigated in 18 normal subjects, using premature atrial depolarizations. The results obtained in this investigation were evaluated plotting the test cycle (expressed as difference between the basic sinus cycle and the test cycle as a percentage of the basic sinus cycle) as a function of the return cycle (expressed as difference between the return cycle and the basic cycle as a percentage of the basic sinus cycle). In normal subjects, premature atrial depolarizations elicited in the last 10-20% of the spontaneous sinus cycle, produced a progressive prolongation of the return cycle and the points correlating the return cycle index to the test cycle index fell above the diagonal of the plotting system. After earlier premature atrial stimulations, the return cycle stayed the same length, and the points correlating the return cycle index to the test cycle index fell along a line parallel to "y" axis (plateau). The mean value of the returning cycle (expressed as above) corresponding to the test cycles (evaluated as above) included in the first 5% of the "plateau" can be defined as the "sinoatrial conduction index". This index, the sum of conduction into and out of the sinus node, ranged from 79 msec to 187 msec. By assuming similar anterograde and retrograde conduction, the sinoatrial conduction time ranged from 39.5 msec to 97.5 msec (mean value 70 msec).     

Indirectly estimated sinoatrial conduction time by the atrial premature stimulus technique: Patterns of error and the degree of associated inaccuracy as assessed by direct sinus node electrography

The atrial premature stimulus method for estimating sinoatrial conduction time (SACT) is commonly used. When the stimulated atrial premature depolarization (APD) does not appear to affect sinus node automaticity or conduction, the indirectly estimated SACT (SACT_I) is quite accurate. That is, SACT_I correlates quite highly with SACT measured directly (SACT_D) on sinus node electrograms (SNE). In this study we used direct SNE recordings in 17 patients to assess SACT_I when factors thought to produce inaccuracy in SACT_I were present. Three patients had sinoatrial entrance block, which might make some expect sinoatrial exit delay to be present. However, SACT_D was normal in two (60 and 70 msec) and prolonged (130 msec) only in the one who had other evidence of sinus node dysfunction. Therefore, sinoatrial entrance block does not necessarily indicate sinoatrial exit delay. Thirteen patients had apparent depression of sinus node automaticity by the induced APD (A₃A₄ > A₁A₁). In all 13, SACT, overestimated SACT_D. One patient had apparent sinoatrial conduction delay induced by the APD and/or vagal transmitter release induced by the APD. In this patient, too, SACT_I exceeded SACT_D. Thus when sinoatrial automaticity or conduction are depressed by the stimulated APD, SACT_I will overestimate SACT_D. if SACT_I is normal, SACT_D will be normal; however, if SACT_I is prolonged, SACT_D may or may not be prolonged.     

Postextrasystolic sinoatrial exit block in human sick sinus syndrome: demonstration by direct recording of sinus node electrograms.

Ten patients with sick sinus syndrome having repetitive sinus node electrograms during long postpacing pauses were studied during programmed atrial stimulation. Sinus node activity was recorded using a percutaneous catheter electrode. A sinus node electrogram was recorded before the return atrial beat in seven patients; it was similar to the sinus node electrogram observed during postpacing pauses and is clearly identified because sinoatrial conduction time was markedly prolonged following the atrial extra beat. Complete sinoatrial exit block occurred in four patients. (1) Sinus node electrograms were thus validated both during postpacing pauses and during programmed atrial stimulation in most patients with sick sinus syndrome. (2) Sinoatrial conduction time was markedly prolonged after one extrasystole, accounting for supracompensatory atrial return cycles. (3) If it were cumulative following multiple extrasystoles, this effect could constitute the electrophysiologic link between an abnormal response during programmed atrial stimulation and the complete sinoatrial block recorded during the pauses that follow rapid atrial pacing.     

Comparative study of sinoatrial conduction time and sinus node recovery time.

Atrial stimulation were performed in 5 normal patients (group A) and 4 patients with electrocardiographic evidence of sinoatrial disease (group B). The technique of premature atrial stimulation was used to calculate sinoatrial conduction time. Rapid atrial pacing was applied to measure maximum sinus node recovery time. In 4 cases both stimulation methods were repeated after intravenous administration of atropine Group A had a sinoatrial conduction time of 56 ms +/- 11 (SD) and a maximum sinus node recovery time of 1122 ms +/- 158. In 3 out of 4 patients with sinus node dysfunction a prolongation of sinoatrial conduction time could be demonstrated (145, 105, and 150 ms). In addition, one showed probable sinus node exit block after premature atrial stimulation. Sinus node recovery time was excessively prolonged in 2 (3880 and 3215 ms) and normal in the other 2 patients with sinoatrial disease (1330 and 1275 ms). Atropine leads to a decrease of sinoatrial conduction time. Results indicate that sinus node recovery time may not be a reliable indicator of sinus node automaticity if sinoatrial conduction is disturbed. The premature atrial stimulation technique makes it possible to study the pattern of sinoatrial conduction and to evaluate its reaction to therapeutic drugs.     

Comparative study of sinoatrial conduction time and sinus node recovery time.

Atrial stimulation were performed in 5 normal patients (group A) and 4 patients with electrocardiographic evidence of sinoatrial disease (group B). The technique of premature atrial stimulation was used to calculate sinoatrial conduction time. Rapid atrial pacing was applied to measure maximum sinus node recovery time. In 4 cases both stimulation methods were repeated after intravenous administration of atropine Group A had a sinoatrial conduction time of 56 ms +/- 11 (SD) and a maximum sinus node recovery time of 1122 ms +/- 158. In 3 out of 4 patients with sinus node dysfunction a prolongation of sinoatrial conduction time could be demonstrated (145, 105, and 150 ms). In addition, one showed probable sinus node exit block after premature atrial stimulation. Sinus node recovery time was excessively prolonged in 2 (3880 and 3215 ms) and normal in the other 2 patients with sinoatrial disease (1330 and 1275 ms). Atropine leads to a decrease of sinoatrial conduction time. Results indicate that sinus node recovery time may not be a reliable indicator of sinus node automaticity if sinoatrial conduction is disturbed. The premature atrial stimulation technique makes it possible to study the pattern of sinoatrial conduction and to evaluate its reaction to therapeutic drugs.     

Atrial rhythms in response to an early atrial premature depolarization in man

The effect of an early atrial premature depolarization (APD) on spontaneous atrial rate was assessed in 16 patients in sinus rhythm. At close coupling intervals (range 27 to 48 per cent of the preceding sinus cycle), atrial acceleration was observed for several beats following the APD in 13 patients. On the basis of P wave configuration and the intra-atrial activation sequence, the accelerated beats appeared to originate from the sinus node. Furthermore, this “sinus” acceleration appeared regardless of the site at which the APD was introduced and was unrelated to latency or current strength. The findings are consistent with APD-induced sinus node re-entry, although sinus node pacemaker acceleration and shift is an alternative mechanism. Sinus node re-entry may explain certain instances of “interpolated” APD's and atrial tachyarrhythmias seen clinically.     

Sinoatrial pacemaker shift following atrial stimulation in man.

Indirect evidence of a sinoatrial pacemaker shift after programmed atrial stimulation in man is presented. Following electrically induced beats, time intervals and postextrasystolic morphology of atrial electrogram and P waves were scrutinized in 30 catheterization studies. Applying premature atrial stimulation, a decrease of the interval between the last basic atrial depolarization and the stimulus-produced atrial excitation (curtailed cycle) below a critical interval was followed by a sinoatrial pacemaker shift in three cases. This electrophysiologic event consisted of a concomitant change in shape of high right atrial electrogram and an increase of atrial cycle length. Simultaneous alteration of P waves could be detected in 2/3 patients. Assuming that the pacemaker shift indicates the arrival of ectopic activation in the sinus node, capture of the sinus node by the premature beat could be distinguished from failure to capture. Thus, pacemaker shift can be used for estimating sinoatrial conduction time in addition to present methods using measurement of postextrasystolic atrial intervals. The changes described could be seen both before and after atropine administration. Tracings of a pacemaker shift after cessation of rapid atrial pacing are also presented. In summary, we found a sinoatrial pacemaker shift underlying sinus node response to ectopic atrial activation in man, a phenomenon which contributes to our understanding of indirect assessment of sinoatrial conduction time by the premature stimulation technique.     

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.     

Study of the mechanism of an atrial pause using endocavitary recording of the sinus node potential in man

The aim of this clinical study was to determine the electrophysiological mechanism of spontaneous atrial standstill, defined as a sudden lengthening of the trial cycle to over 10 p. 100 of its basal value, by recording the sinus node potential by endocavitary electrocardiological techniques. Satisfactory recordings of the sinus potential were obtained for the study of 65 atrial pauses recorded in 31 patients (18 without sinus node dysfunction and 13 with sinus node disease). It was shown that atrial pauses, shorter than two basal atrial cycles correspond to a moderate slowing of the sinus rhythm and to a sometimes very significant lengthening of the sinoatrial conduction time when sinus rhythm resumed. Pauses longer than two basal atrial cycles were always due to sinoatrial block which sometimes occured in patients with clearly individualised sinus activity, and sometimes with a slow continuous sinus activity. The sinus period did not change during these long pauses and sinoatrial conduction was normal when sinus rhythm resumed. The increased duration of the sinus potential, a constant finding during these pauses, is related to an intrasinusal conduction defect. This suggest that the primum movens of sinoatrial block is intrasinusal block which prevents rapid recruitment of a sufficient number of elemental sinus potentials so that the resultant potential becomes subliminal and therefore incapable of passing the sinoatrial junction. Short-lasting atrial pauses with a normal response to extrastimulus or atrial stimulation and characterised electrophysiologically by an increased sinoatrial conduction time without block of the sinus potential may be opposed to long atrial pauses with the pathological response of sinus node dysfunction characterised electrophysiologically by block of the sinus impulse. In practice the ability to induce a long pause by atrial stimulation (sinoatrial block) revealing latent disease of intrasinusal or sinoatrial conduction, may constitute an essential physiological sign of sinus node dysfunction.     

The effect of atropine on calculated sinoatrial conduction time in man.

This study investigates the effect of atropine on the length of the return cycles after premature atrial stimulation in man. On the assumption that sinus node automaticity is not changed by premature depolarization of the sinus node, sinoatrial conduction time (SACT) was calculated from the differences between the length of the return cycles and the spontaneous cycle length. 11 patients were studied before and after the injection of atropine. In all cases atropine caused an increase in heart rate. In 8 patients the return cycles exhibited a typical behavior. In 6 patients without signs of sinus node dysfunction, the mean calculated SACT was 109 msec, whereas 2 patients with a sick sinus syndrome (SSS) had a mean calculated SACT of 190 and 225 msec, respectively. 3 patients with SSS demonstrated an atypical pattern of the postextrasystolic pauses. In 6 patients without sinus node dysfunction, atropine caused a reduction of calculated SACT about 35%. In 2 patients with SSS the reduction was 38 and 49% of the control value, respectively, whereas in the remaining 3 patients with SSS who had an atypical return cycle pattern, a normalization occurred after the administration of atropine. We conclude that, besides its effects on sinus node automaticity, atropine has also a marked effect on sinoatrial conduction, even in patients with the sick sinus syndrome.     

The sinus node electrogram in the evaluation of atrial pauses

The aim of this study was to establish the electrophysiological mechanism of atrial pauses, defined as a sudden lengthening of atrial cycle greater than or equal to 10% of its basal value. The sinus node electrogram (SNE) was recorded during electrophysiological study in 20 subjects. Satisfactory recordings of 64 pauses were obtained, 25 of which were spontaneous, 16 were induced by short periods of atrial pacing (AP) in normal subjects, whereas 23 atrial pauses were induced with the premature stimulation method. The basal sinus cycle and the one during the spontaneous pauses were measured from the upstroke slope on the SNE. The electrically induced pauses of the sinus cycle were measured from the artifact of the stimulus to the upstroke slope of the SNE of the first post-pacing beat. We have found that: 1-spontaneous atrial pauses correspond to a moderate slowing of the sinus cycle and to a depression of the sinoatrial conduction occasionally up to a second degree sinoatrial block. Only in subjects with sick sinus disease, the atrial pauses are induced by depression of the sinus automatism; 2-in normal subjects the AP results in a sinoatrial conduction delay; 3-the single extrastimulus regularly produces a moderate increase of the sinoatrial conduction time with variable but minimal effects on the sinus node automatism.     

Intracellular and extracellular recordings of sinus node activity: comparison with estimated sinoatrial conduction times during pacemaker shifts in rabbit 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.     

Sinus node sequences after atrial stimulation: similarities of effects of different methods

Sinoatrial conduction is commonly assessed from features of the initial cycle after a single atrial extrastimulus or eight beats atrial pacing. In contrast, sinus node automaticity is assessed by the duration of the first interval after prolonged atrial pacing. The return cycle and initial sequences after these different methods were compared in 10 subjects with normal sinus node function and 30 patients with sick sinus syndrome. Typically, sequences after all three methods showed a maximally prolonged first interval with a progressive decrease over five or more cycles. A model of recovery from overdrive suppression was used to compute the elements of conduction time and automaticity in the first interval. The sequences which followed a single extrastimulus and pacing were similar, the only index which increased significantly with prolonged pacing was associated with the degree of suppression of automaticity. The computed component of sinoatrial conduction in the return cycle was similar for all three methods. Thus all three conventional methods which consider only the initial post-stimulation interval measure both sinoatrial conduction and sinus node automaticity. The separate components of automaticity and conduction may be assessed by analysis of the total sequence.     

Sinus node sequences after atrial stimulation: similarities of effects of different methods.

Sinoatrial conduction is commonly assessed from features of the initial cycle after a single atrial extrastimulus or eight beats atrial pacing. In contrast, sinus node automaticity is assessed by the duration of the first interval after prolonged atrial pacing. The return cycle and initial sequences after these different methods were compared in 10 subjects with normal sinus node function and 30 patients with sick sinus syndrome. Typically, sequences after all three methods showed a maximally prolonged first interval with a progressive decrease over five or more cycles. A model of recovery from overdrive suppression was used to compute the elements of conduction time and automaticity in the first interval. The sequences which followed a single extrastimulus and pacing were similar, the only index which increased significantly with prolonged pacing was associated with the degree of suppression of automaticity. The computed component of sinoatrial conduction in the return cycle was similar for all three methods. Thus all three conventional methods which consider only the initial post-stimulation interval measure both sinoatrial conduction and sinus node automaticity. The separate components of automaticity and conduction may be assessed by analysis of the total sequence.     

The effect of premature atrial depolarization on sinus node automaticity in man.

Sino-atrial conduction time (SACT) may be calculated from the difference between the length of the return cycle and the spontaneous cycle, using programmed premature atrial stimulation during spontaneous sinus rhythm. This approach to sinoatrial conduction assumes that sinus node automaticity is not changed by premature depolarization. In order to validate this assumption, we compared the length of the post-return cycles to the spontaneous cycle length in 71 patients. Patients were grouped according to clinical diagnosis and the value of calculated SACT. At long coupling intervals at which no reset of the sinus node occurred there was only a small prolongation of the post-return cycles (less than 8.4 msec, on an average) compared to the spontaneous cycle length. This suggests no or only an insignificant effect of premature depolarization on the sinus node. However, during test stimuli leading to reset of the sinus node, the post-return cycles were significantly prolonged between 20 to 30 msec, on an average. The response of the individual cases sometimes varied to a great extent. In patients who demonstrated a progressive linear prolongation of the return cycles at decremental shortening of the test interval, there was no significant prolongation of the post-return cycles versus the spontaneous cycle length. We conclude that 1) premature depolarization of the sinus node may have a depressant effect on sinus node automaticity, which, if present, is usually small; 2) calculation of SACT using the extrastimulus technique may overestimate true SACT.     

Analysis of sino-atrial conduction in man using premature atrial stimulation.

Sino-atrial conduction was investigated using premature atrial depolarization in 25 patients seven of whom had sino-atrial block. The results obtained in this investigation were evaluated plotting the test cycle (expressed as difference between the basic sinus cycle and the test cycle as a percentage of the basic sinus cycle) as a function of the return cycle (expressed as difference between the return cycle and the basic cycle as a percentage of the basic sinus cycle). In normal subjects, premature atrial depolarizations elicited in the last 10-20% of the spontaneous sinus cycle, produced a progressive prolongation of the return cycle and the points correlating the return cycle index to the test cycle index fell above the diagonal of the plotting system. After earlier premature atrial depolarizations, the return cycle remained of the same length, and the points correlating the return cycle index to the test cycle index fell along a line parallel to the y-axis ('plateau'). The mean value of the returning cycles (as expressed above) corresponding to the test cycles (as evaluated above) included in the first 5% of the 'plateau' can be defined as 'the sino-atrial conduction index'. This index, the sum of conduction into and out of the sinus node, was found to range from 79 to 185 ms. By assuming similar anterograde and retrograde conduction, the sino-atrial conduction time ranged from 39.5 to 97.5 ms (mean value=70 ms). In the patients with sino-atrial block, fully compensatory pauses were observed for atrial premature depolarizations elicited up to the last 25-35% of the atrial cycle, and a slow and progressive divergence from the diagonal of the plotting system was seen instead of the 'plateau'. In these patients the sino-atrial conduction index ranged from 151 to 297 ms (mean 253 ms). By assuming similar antegrade and retrograde conduction, the sino-atrial conduction time ranged from 75.5 to 148.5 ms (mean value=126.5 ms) with a statistically significant difference with respect to normal subjects (P=0.001).