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.     

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.     

New application of direct sinus node recordings in man: assessment of sinus node recovery time

Sinus node recovery time (SNRT) is frequently used to assess sinus node function in patients with suspected sick sinus syndrome (SSS). Although SNRT is assumed to reflect sinus node automaticity, this assumption remains unproven. The purpose of this study was (1) to test the hypothesis that SNRT in patients with and without SSS reflects sinus node automaticity, and (2) to assess the role of sinoatrial conduction time in the measurement of SNRT. A total of 16 patients (mean +/- SD age 63 +/- 9 years), seven of which had SSS, form the basis of this report. An electrogram of the sinus node was obtained for each of the 16 patients, and overdrive pacing was performed in each at cycle lengths of 1000 to 300 msec. SNRT was measured (1) on the sinus node electrogram (direct method, measuring SNRTd) as the interval from the last pacing stimulus artifact to the onset of the upstroke slope of first postpacing sinus beat and (2) on the high right atrial electrogram (indirect method, measuring SNRTi). Results were as follows: (1) The longest SNRTd was significantly shorter than the longest SNRTi (989 +/- 304 vs 1309 +/- 356 msec, p less than .001). (2) For the first postpacing sinus beat there was a significant prolongation of sinoatrial conduction time as compared with that for sinus beats before pacing (319 +/- 152 vs 99 +/- 35 msec, p less than .001). Sinoatrial conduction time normalized within 3.6 +/- 0.96 postpacing sinus beats. (3) At the pacing cycle length that resulted in the longest recovery time, sinus node depression was seen in 56% of patients, sinus node acceleration was noted in 26%, and no appreciable change in sinus node automaticity was observed in 19%. (4) Sinoatrial conduction time for the sinus beat before pacing and that for the first postpacing beat was longer in patients with SSS when compared with in patients without SSS. (5) In patients with SSS the abnormal SNRTi, when corrected for the degree of prolongation of sinoatrial conduction time for the first postpacing beat, became normal in five of six patients. We conclude that (1) SNRTi reflects both sinus node automaticity and sinoatrial conduction time, whereas SNRTd reflects sinus node automaticity, (2) overdrive atrial pacing results in marked prolongation of sinoatrial conduction time for the first postpacing beat, which is longer in patients with SSS when compared with in those without SSS, and (3) in patients with SSS the inference of abnormal sinus node automaticity on the basis of a prolonged corrected SNRTi is usually incorrect.     

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.     

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.     

Mechanisms of cardiac arrhythmias after the Mustard operation for transposition of the great arteries

To determine the mechanisms of the cardiac arrhythmias frequently seen after the Mustard operation for transposition of the great arteries, intracardiac electrophysiologic studies were performed in 52 children 1 to 8 years after the Mustard operation. Sinus nodal automaticity as judged from the response to rapid atrial pacing was abnormal in 28 of the 52 children. Sinoatrial conduction (conduction of the sinus impulse to the atrium) was found to be abnormal in three of nine patients studied with the atrial extrastimulus method. Conduction of the sinus impulse from the high right atrium to the atrioventricular (A-V) node was abnormally delayed in only 2 of 41 subjects. The low lateral wall of the right atrium was depolarlzed late in 3 of 11 subjects (including the preceding 2). Two subjects showed delayed A-V nodal conduction and one delayed His-Purkinje conduction. The mechanism of supraventricular tachycardia induced in the laboratory was determined to be sinoatrial nodal reentry in four subjects and atrial muscle reentry in four. Two of the four with atrial muscle reentry had prolonged high right atrium to low lateral right atrium intervals during sinus rhythm.

Thus, damage to the sinus node remains the most common cause of arrhythmias after the Mustard operation. In addition, delayed atrial conduction may predispose to atrial muscle reentrant tachycardia.     

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.     

Assessment of sinus node function in patients with congenital long QT syndrome

Sinus node function was evaluated in 4 patients with congenital long QT syndrome suffering from recurrent episodes of syncope and ventricular arrhythymias. Three of the 4 patients had bradycardia at rest on a 24-hour ECG. Sinus node function was examined by the atrial overdrive suppression test and the atrial premature stimulation test. Corrected sinus node recovery time (CSNRT) was prolonged in all patients. Total sinoatrial conduction time was also prolonged in 2 of the 4 patients. In all patients with abnormally high values, these values returned to normal after atropine administration, except in one patient. His prolonged CSNRT remained high after atropine administration, indicating abnormal automaticity such as that seen in sick sinus syndrome. These results show that sinus node function in congenital long QT syndrome is often associated with autonomic dysfunction, and sometimes with intrinsic disturbances of sinoatrial conduction.     

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.     

Electrophysiologic manifestations in so-called "sick sinus syndrome"

Electrophysiologic disorders in 17 patients with sick sinus syndrome (SSS) were assessed by recording of intracardiac electrograms, atrial overdrive pacing and extrastimulus technique. Significant suppression of the sinoatrial node (SAN) by overdrive pacing (maximum corrected SAN recovery time of longer than 560 msec) was noted in 14 or 16 patients studied. In nine patients, scanning with atrial extrastimuli, sinus rest was defined in all. In one patient there was a longer interpolation zone. Calculated sinoatrial conduction time (SACT) in individual patients varied considerably. The mean SACT was over 110 msec in 5 of 9 patients (56%). Sinus echo was demonstrated in 3; one manifested SAN- re-entrant tachycardia with rates of 72 to 77 beats/min. AV nodal echo was demonstrated in 3, two of them manifested AV nodal re-entrant tachycardia. Intracardiac electrograms revealed prolonged AV conduction time in 2 of 15 patients and prolonged His-Purkinje system conduction time in 2 of 17 patients studied. Two patients disclosed what we thought to be manifestation of intraatrial conduction disturbance. Both had considerable time interval between pacing impulse and atrial response. In one of them Mobitz type 1 and 2:1 intraatrial blocks were observed on atrial pacing and a possible internodal tract depolarization was also recorded. It is concluded that the electrophysiologic manifestations of patients with SSS cover a wide spectrum. The machanism of tachycardia can be due to either SAN or AV nodal re-entry.     

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.     

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.     

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.     

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.     

Assessment of sinus node function in asymptomatic subjects with sinus bradycardia and in symptomatic patients with sino-atrial disease.

Sinus node function was evaluated in 18 patients with sinus bradycardia without complaints (Group I), in 16 patients with sinus bradycardia and/or sinoatrial block with complaints (subgroup IIa) and in 14 patients with the bradycardia-tachycardia syndrome (subgroup IIb). Mean values of corrected sinus node recovery time (CSRT), atrial effective refractory period (AERP) and atrial functional refractory period (AFRP) differentiated significatively asymptomatic subjects of group I from the two subgroups of patients with sinoatrial disease, but failed to differentiate each subgroup from the other one. There was no significative difference in mean sinoatrial conduction time (SACT) between group I and each of the two subgroups. Three patients of subgroup IIa and 1 patient of subgroup IIb had a false negative response after both overdrive and premature programmed atrial pacing. Spontaneous cycle length was directly correlated with the sinus node recovery time and the atrial refractoriness in group I, and with the only sinus node recovery time in subgroup IIb. No direct correlations were observed in subgroup IIa. This suggests a less disturbed sinus node automaticity in bradycardia-tachycardia syndrome.     

Sinus automaticity and sinoatrial conduction in severe symptomatic sick sinus syndrome.

Electrophysiologic studies with recordings of sinus node electrograms were performed in 38 patients with severe symptomatic sick sinus syndrome. Thirty-two of the 38 patients had episodic tachyarrhythmias and 17 presented with syncope. The clinically documented sinus or atrial pause was 5.6 +/- 2.8 s (mean +/- SD). Patients were divided into three groups according to electrophysiologic findings. Group I consisted of nine patients with complete sinoatrial block. Sinus node electrograms were recorded during the episodes of long pauses. Seven patients had unidirectional exit block, with the atrial impulse being capable of retrograde penetration to the sinus node causing suppression of sinus automaticity; two had bidirectional sinoatrial block. Group II consisted of 22 patients with either 1:1 sinoatrial conduction (group IIa = 13 patients) or second degree sinoatrial exit block (group IIb = 9 patients) during spontaneous sinus rhythm. Sinoatrial exit block, ranging from 1 to greater than 14 sinus beats, was observed during postpacing pauses that ranged from 1,650 to 37,000 ms (mean 7,286 +/- 6,989). The maximal sinus node recovery time ranged from 770 to 5,580 ms (mean 3,004 +/- 1,686) and was normal in 5 patients and prolonged in 17. Group III consisted of seven patients with no recordable sinus node electrogram, reflecting either a technical failure or a quiescence of sinus activity. The sinus node recovery time in these seven patients ranged from 1,190 to 4,260 ms (mean 2,949 +/- 1,121). Thus, abnormalities in both sinus node automaticity and sinoatrial conduction are responsible for the long sinus or atrial pauses in the sick sinus syndrome. However, complete sinoatrial exit block can occur and cause severe bradycardia with escape rhythm; repetitive sinoatrial exit block plays a major role in producing posttachycardia pauses.     

Sinus node automaticity during atrial fibrillation in isolated rabbit hearts.

BACKGROUND. It is still unclear what role the sinus node may play in the genesis or perpetuation of atrial fibrillation. Therefore, we studied the electrical activity in different regions of the sinus node during atrial fibrillation. METHODS AND RESULTS. In Langendorff-perfused rabbit hearts, paroxysms of atrial fibrillation were induced by burst pacing. Standard microelectrode techniques were used to record transmembrane potentials from different regions of the sinus node. We found that during atrial fibrillation, a high degree (5:1) of sinoatrial entrance block was present that protected the pacemaker fibers in the center of the sinus node against the high rate of fibrillatory impulses. As a result, the true pacemaker fibers in the center of the node were activated with only a slightly higher average rate than during sinus rhythm. Spontaneous diastolic depolarization was still present but was modulated by electrotonic depolarizations due to intranodal conduction block of atrial fibrillatory impulses. Incidentally, phase 4 depolarization resulted in the generation of spontaneous action potentials in the sinus node. However, the high activation rate in the sinoatrial border during atrial fibrillation prevented these spontaneous impulses to exit from the sinus node. Because of the minimal degree of sinus node overdrive suppression (9%) and the presence of concealed automaticity during atrial fibrillation, spontaneous termination of atrial fibrillation was promptly followed by resumption of normal sinus rhythm. CONCLUSIONS. During atrial fibrillation, sinus automaticity still is present in the center of the sinus node and hardly overdrive suppressed due to a high degree of sinoatrial entrance block.     

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.     

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.