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).     

A second zone of compensation during atrial premature stimulation: Evidence for decremental conduction in the sinoatrial junction

125 consecutive patients with premature atrial stimulation were studied. Three demonstrated sinus node return cycles that were fully compensatory following premature atrial stimuli delivered early in diastole. This second zone of compensation was unaccompanied by significant alterations in the post-return cycle lengths or in P-wave morphology of the return cycle. To account for the occurrence of a complete compensatory pause following very early premature atrial depolarizations, we consider the possibility that retrograde conduction of the early atrial premature depolarization (APD) in the sinoatrial junction was delayed for a sufficient length of time to allow the sinus node to depolarize spontaneously on schedule. Collision between the APD and sinus beat would then occur despite the marked prematurity of the APD. Thus, the early APD had encountered the relative refractory period of the sinoatrial junction, suggesting that decrementai conduction takes place within the sinoatrial region in man. These findings imply that there is the potential for reentry in the region of the human sinoatrial junction.     

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.     

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.     

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.     

The measurement of sinus node refractoriness in man

We recently described a method for measuring sinus node refractoriness in the rabbit heart. Atrial premature beats either may result in reset return responses or may become interpolated because of encroachment on sinus node refractoriness. In previous studies with rabbits we defined the effective refractory period of the sinus node (SNERP) as the longest premature interval that is interpolated. This study presents results on the extension of this technique to the measurement of sinus node refractoriness in man. Out of 30 patients (12 with and 18 without sinus node dysfunction), SNERP could be measured in 26 at one or more basic cycle lengths. At a basic pacing cycle length of 600 msec, SNERP ranged from 250 to 380 msec (mean 325 +/- 39) in patients without sinus node dysfunction and from 500 to 550 msec (mean 522 +/- 20) in patients with sinus node dysfunction. This clear differentiation of patients with and without sinus node dysfunction by SNERP is in contrast to various results obtained by assessing sinus node function from sinus node recovery time and sinoatrial conduction time. Thus this study suggests the possible use of the measurement of SNERP in the assessment of sinus node function in man and its possible value in identifying patients with sinus node dysfunction.     

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.     

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.     

Right atrial versus left atrial echo zones: A proposed new criterion for determining the atrial site of retrograde preexcitation

In a patient whose electrocardiogram (ECG) initially (1966) showed a Type A Wolff-Parkinson-White pattern, recurrent supraventricular tachycardia (SVT) developed but never subsequently showed antegrade bypass conduction. Intracardiac pacing studies (1975) revealed that premature high right atrial (induced 250–450 msec after atrial depolarization) or coronary sinus depolarization (250–550 msec) resulted in SVT. Late coronary sinus depolarization resulted in SVT without A-H prolongation. During SVT, P wave morphology changed and the coronary sinus atrial electrogram preceded that from the low right atrium; retrograde ventriculoatrial conduction time was 240 msec. Neither pacing the high right atrium or coronary sinus up to rates of 200 beats/min nor progressive atrial premature depolarizations from the high right atrium or coronary sinus resulted in antegrade bypass conduction. Failure of antegrade bypass conduction does not preclude SVT due to retrograde pre-excitation and must be distinguished from atrioventricular (A-V) nodal reentry. Atrial effective refractory period (200 msec) was shorter than the minimal time required for an atrial impulse to return to the atrium (380 msec), suggesting concealed antegrade bypass conduction. Stimulation of the atrium linked to the A-V bypass results in earlier bypass activation and recovery and explains the differing high right atrial vs coronary sinus echo zones.     

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.     

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.     

Premature atrial stimulation during regular atrial pacing: A new approach to the study of the sinus node

Using an induced premature atrial depolarization after atrial pacing for 8 beats to scan the postpacing cycle, sinus node (SN) response was studied in 23 patients and the results were compared with those obtained using the Strauss method. Late extrastimuli resulted in compensatory return cycles (zone I), increasing prematurity gave rise to less-than-compensatory return cycles (zone II or “plateau”) and interpolation or echo responses occurred at shorter coupling Intervals (zone III). The sinoatrial (SA) conduction time was defined as the difference between return cycle and postreturn cycle lengths that fell in the latter portion of zone II. The SA conduction time was similar to those derived from the Strauss method (r = 0.91, n = 17, p < 0.01) and remained similar at the 2 pacing cycles, 172 ± 52 ms (mean ± standard deviation) at 739 ± 71 ms (cycle 1) and 170 ± 60 ms at 596 ± 57 ms (cycle 2). In 4 patients, the atrial pacing method could unmask zone II. The SN refractory period was defined as the longest coupling interval at which zone III was apparent. It was compared at cycles 1 and 2 in 14 patients. There was a significant increase in the SN refractory period with faster pacing rates, from 406 ± 104 ms (cycle 1) to 462 ± 112 ms (cycle 2) (p < 0.05). The atrial pacing method provides an alternative evaluation of SA conduction and may permit the study of drug effects at identical basic rates.     

Sinus node electric activity in prolonged atrial pauses in subjects with the sick sinus syndrome

Sinus node electrogram (SNE) was recorded in 15 patients with sick sinus syndrome (SSS) in which prolonged atrial pauses were observed. The aim of this study was clarify the physiopathological mechanisms underlying atrial pauses as well as to evaluate the sensitivity of sinoatrial conduction time (SACT) directly measured on SNE and of SACT estimated with the indirect Strauss method with respect to the detection of SSS. The following results were obtained: Sinus electrical activity was recorded during atrial pauses (greater than or equal to 2 basic sinus cycle length) in all the 9 patients in which the pauses spontaneously occurred and in the 2 patients in whom the pauses of 2860 and 3190 msec were induced by atrial pacing. In one of these latter two patients, moreover, a complete electrical desynchronization was observed. In the remaining 4 patients in whom, pauses (greater than or equal to 3 sec) were induced by carotid sinus massage of in 3 no sinus electrical activity was detected on SNE while in 1 advanced sinus node desynchronization was observed. Direct sinoatrial conduction time was abnormally prolonged in 6 patients with SSS and indirect sinoatrial conduction time in 9 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.     

Electrophysiologic effects of atropine on sinus node and atrium in patients with sinus nodal dysfunction

Electrophysiologic studies were conducted in 21 patients with sinus nodal dysfunction before and after intravenous administration of 1 to 2 mg of atropine. The mean sinus cycle length (± standard error of the mean) was 1,171 ± 35 msec before and 806 ± 29 msec after administration of atropine (P < 0.001). Mean sinus nodal recovery time determined at a paced rate of 130/min and maximal recovery time were, respectively, 1,426 ± 75 and 1,690 ± 100 msec before and 1,169 ± 90 and 1,311 ± 111 msec after atropine (P < 0.001 and < 0.001). Mean calculated sinoatrial conduction time, measured in 16 patients, was 113 ± 8 msec before and 105 ± 9.7 msec after atropine (difference not significant). Mean atrial effective refractory period, measured at an equivalent driven cycle length, was 262 ± 11.1 msec before and 256 ± 10.3 msec after atropine (not significant). Mean atrial functional refractory period was 302 ± 12.5 msec before and 295 ± 11.3 msec after atropine (not significant).

The shortening of sinus cycle length and sinus recovery time with atropine was similar to that noted in patients without sinus nodal dysfunction. In contrast, atropine had insignificant effects on sinoatrial conduction and atrial refractoriness in this group whereas it shortens both in normal subjects. This finding may reflect altered perinodal and atrial electrophysiologic properties in patients with sinus node disease.     

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.     

Comparison between intracellular and extracellular direct current recordings of sinus node activity for evaluation of sinoatrial conduction time

For evaluation of sinoatrial conduction time in humans, study of extracellular direct current (DC) electrograms from the sinus node has been proposed. To validate this method, we compared transmembrane potentials from multiple sites (40 to 60, "mapping" of sinoatrial activation by microelectrode technique) and extracellular DC electrograms of the sinus node in 12 isolated rabbit atria. Sinoatrial conduction time, measured by microelectrodes and by extracellular electrograms, was essentially the same if the DC electrode was positioned over the pacemaker center (35 +/- 15 and 33 +/- 15 msec, respectively; deviation less or equal to 2 msec). While in all experiments phase 4 and phase 0 depolarization of dominant pacemaker fibers was reflected in the DC electrogram, it shape was influenced by pacemaker location and duration of sinoatrial impulse propagation. If sinoatrial conduction time was long (greater than 25 msec) the transition from the diastolic to the upstroke slope was smooth and the sinus node potential was clearly separated from atrial activity. If sinoatrial conduction time was short (less or equal to 25 msec) the onset of the upstroke slope was well defined and the upstroke slope directly merged into atrial activity. Extracellular recordings 0.2 mm away from the pacemaker center were fairly unchanged in shape; however, sinoatrial conduction time was significantly underestimated. Underestimation also occurred when the tip size of the extracellular electrode was increased from 0.2 to 0.5 and 1.0 mm. Thus sinus node activity is reflected in extracellular DC recordings; however, measurement of sinoatrial conduction time by this technique requires exact localization of the electrode over the pacemaker center, which cannot be controlled in humans.     

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.     

Sinus nodal responses to atrial extrastimuli in patients without apparent sinus node disease.

In 36 patients without sinus node disease scanning with an atrial extrastimulus (A2) was performed during sinus rhythm with the sinus cycle length measured in milliseconds. Zones of nonreset due to interference, reset, interpolation and sinus echoes were defined by noting the timing of the first response after A2. Zones were defined in terms of their longest and shortest A1-A2 coupling intervals (in milliseconds). A zone of nonreset was found in 12 of 12 patients in whom A2 was delivered late. The mean cycle length in these 12 patients was 779 msec, with a mean zone of nonreset of 779 to 585 msec (25 percent of cycle length). All 36 patients (100 percent) had a zone of reset. The mean cycle length in these 36 patients was 803 msec with a zone of reset from 692 to 319 msec (46 percent of cycle length). Seven of 36 patients (19 percent) had a zone of interpolation. The mean cycle length in these seven patients was 754 msec, with a mean zone of interpolation of 344 to 279 (9 percent of cycle length). Four of 36 patients (11 percent) had a zone of sinus echoes. The mean cycle length in these four patients was 870 msec, with a mean zone of echoes from 350 to 313 msec (4 percent of cycle length). Calculated sinoatrial conduction time ranged from 40 to 153 msec (mean +/- standard deviation 92 +/- 30 msec). Shortening of the cycle length with atrial pacing increased the number of patients with zones of interpolation and echoes. In conclusion, zones of nonreset and reset are found in all patients with normal sinus nodal function, whereas zones of interpolation and echoes are much less common. Sinoatrial conduction time is surprisingly long in patients without apparent sinus node disease.