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.     

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.     

Intra-sinus echo: demonstration using direct intracavitary recording of the sinus potential

The authors searched for intra-sinusal echos during electrophysiological investigation of 53 patients (41 men, 12 women, average age: 61 +/- 12 years). Cycles of sinus echos were recorded in 8 patients (15 per cent). The period during which sinus echos could be recorded was 125 ms (average 40.6 +/- 34 ms). Indirect assessment of sinus node function in patients with sinus echos was normal (corrected sinus node recovery time, estimated atrio-sino atrial conduction times using Narula's technique). A valid and reproducible direct recording of the sinus node potential was only possible in one patient. In this case the echo cycles were provoked by stimulation periods of between 440 and 320 ms (echo zone of 120 ms). All the echos obtained were preceded by a sinus node potential with a different duration and morphology to that observed during basal sinus cycles (respective sino-atrial conduction times 105 and 115 ms). In this patient we were also able to induce sinus echos after a single extrastimulus during the spontaneous rhythm. the echo zone was 130 ms and with a shorter coupling interval (310 ms) two successive sinus echos were recorded. The demonstration of intrasinusal echos by direct recording of the sinus node potential supports the experimental data of Allessie and Bonke on isolated right atrial tissues of the rabbit. Improvements in the technique of endocavitary direct recording of the sinus node potential in man should complete this data by showing the possibility of sinoatrial tachycardias due to reentry.     

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.     

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.     

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.     

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.     

Measurement of sinoatrial conduction time

A prolonged sinoatrial conduction time (SACT) is one of the electrophysiologic characteristics of sick sinus syndrome. Because conduction from the sinus node to the atrium can not be assessed directly, an indirect method for estimating the SACT was developed by Strauss et al.: the premature atrial stimulation technique. The theoretical basis of the method is reviewed and the use of atrial spontaneous premature beats is proposed to estimate the SACT instead of electrical premature atrial stimulation.     

Indirect measurement of sinoatrial conduction time in patients with sinoatrial disease and in controls.

Clinical recognition of sinoatrial disease currently depends on the presence of transient sinus bradycardia, sinoatrial block, or supraventricular tachyarrhythmias. The value of clinical electrophysiological assessment in these patients is not clear. Using intracardiac electrophysiological recordings and programmed stimulation we have examined 14 patients with sinoatrial disease and 11 control patients undergoing investigation for chest pain. Intracardiac conduction times were normal in all patients. There was no significant difference of sinus node recovery times between the sinoatrial disease and control groups. Sinoatrial conduction times were measured by the indirect method and two populations were identified. However, the mean values of 128 +/- 27 ms in patients and 112 +/- 30 ms in controls were not significantly different and major overlap rendered this measurement clinically valueless. It is concluded that no current electrophysiological measurement has diagnostic value in patients with sinoatrial disease.     

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.     

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.     

Electrophysiologic consequences of the arterial switch repair of d-transposition of the great arteries

Electrophysiologic studies were performed at 12.7 +/- 4 months postoperatively in 20 patients who had the arterial switch repair at 1 to 120 days (mean 13 +/- 26 [SD]) for d-transposition of the great arteries. Preoperative electrocardiograms (ECGs) at rest revealed an ectopic atrial rhythm in one patient. Postoperative rest ECGs revealed transient postoperative ectopic atrial or junctional rhythms in two patients, intermittent ectopic atrial rhythms in two and right bundle branch block in nine with a normal QRS axis. In addition, ambulatory monitor recordings revealed infrequent premature ventricular complexes in five patients. Catheter endocardial mapping revealed sinus rhythm in 18 patients and ectopic atrial rhythm in 1 patient. Atrial activation after the switch repair was comparable with normal atrial activation. Activation of all low atrial sites was significantly earlier after the switch repair than after the Mustard repair. Mild abnormalities of sinus node function were present and consisted of slight prolongation of corrected sinus node recovery time in six patients and slightly increased sinoatrial conduction time in four. The ratio of sinus node recovery time to sinus cycle length was normal in all 20 patients. Atrial effective and functional refractory periods were normal in all patients and no atrial arrhythmias could be induced by programmed stimulation. Atrioventricular (AV) node conduction was excellent with normal AV node effective and functional refractory periods. The only electrophysiologic abnormality of His-Purkinje function was distal right bundle branch block in nine patients. Programmed stimulation of the ventricle produced repetitive ventricular responses in four patients: bundle branch reentry in three and intraventricular reentry in one.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Identification of the sinus potential in man by endocavitary electrocardiography. Identification criteria, preliminary results]

The potential of the sinus node was recorded in 24 patients by endocavitary electrocardiography using the same equipment as for usual electrophysiological investigation. The sinus node potential is a slow wave which starts progressively, has a rounded peak and precedes the endocavitary atrial activation and the surface P wave, and is relayed at an acute angle to the high amplitude deflection of atrial depolarisation. In some specially selected recordings it is easy to confirm the sinus origin of this slow wave where its preatrial position may be defined by the fixed relation of the S-P interval and by the variability of the T-S interval. Usually it is necessary to use technical manoeuvres (vagal stimulation, premature atrial stimulation) to demonstrate the preatrial behaviour of a potential thought to be of sinus origin. The variability of the sinus potential and the apparent sinoatrial conduction time, is suggestive of a physiological instability of the intrasinus pacemaker. The sinoatrial conduction time measured directly does not seem to exceed 140 ms in normal subjects.     

Correlation between directly measured and indirectly estimated sinoatrial conduction time in children

The indirectly estimated sinoatrial conduction time has been widely used in children to assess sinus node (SN) function, but has never been validated in pediatric patients. Using a standard quadripolar catheter with high amplification and low-pass filters, SN electrograms were recorded in 11 of 26 (42%) pediatric cardiac patients (age range 10 months to 18 years) with normal SN function. The sinoatrial conduction time was measured directly from the SN electrogram and estimated indirectly by the premature stimulation and continuous pacing methods. The direct sinoatrial conduction time (15 to 91 ms) in these 11 patients (ages 1 to 18 years) correlated well with that estimated by the premature stimulation method (r = 0.81, n = 9, p less than 0.01). There was a poor correlation between the direct and continuous pacing methods (r = 0.53, n = 8, p = 0.17). It was concluded that SN electrograms can be recorded in children and that there is a good correlation between the directly measured sinoatrial conduction time and the indirectly estimated sinoatrial conduction time by the premature stimulation method.     

Association of sinus node dysfunction, atrioventricular node conduction abnormality and ventricular arrhythmia in patients with Kawasaki disease and coronary involvement.

BACKGROUND: This study was performed to investigate the incidence of arrhythmias in patients with Kawasaki disease (KD). METHODS AND RESULTS: Electrophysiologic studies (EPS) were performed in 40 patients (mean age: 10.3+/-5.1 years; 30 males, 10 females) with KD who had severe to moderate coronary artery disease. Clinical arrhythmias were documented in 4 patients (premature ventricular contractions, ventricular tachycardia, atrioventricular block, and ventricular fibrillation). Dual atrioventricular nodal pathways were demonstrated in 3 patients. Nonsustained atrial fibrillation was induced in 1 patient. The AH interval was prolonged in 2 patients. The Wenckebach rate was 164+/-37 beats/min, and 4 of the patients had a decreased Wenckebach rate. The maximum and corrected sinus node recovery times were 997+/-257 ms and 281+/-130 ms, respectively, and 7 patients were thought to be abnormal. The sino-atrial conduction time was 108+/-64 ms, and 2 patients had prolonged conduction times. CONCLUSIONS: Although there was no relationship between coronary stenosis or obstruction and the EPS parameters, the incidence of abnormal sinus node and atrioventricular node function is apparently higher in KD patients than in the normal population. These functional abnormalities may possibly be caused by myocarditis or an abnormal microcirculation in the sinus node and atrioventricular node artery. In some patients, myocardial ischemia may provoke malignant ventricular arrhythmia.     

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.     

Electrophysiologic evaluation of sinus node dysfunction in postoperative children and young adults utilizing combined autonomic blockade

Sinus node dysfunction is a recognized problem following surgery for congenital heart disease. Seven postoperative patients with sinus node dysfunction (5 Mustard, 1 tetralogy of Fallot, 1 Fontan) underwent electrophysiology study of sinus node function during combined autonomic blockade (CAB) utilizing propranolol 0.2 mg/kg i.v. and atropine 0.04 mg/kg i.v. to evaluate intrinsic sinus node function isolated from autonomic control. During CAB, intrinsic heart rate, intrinsic corrected sinus node recovery time, and intrinsic sinoatrial recovery time were measured. These results were compared with age-matched normal intrinsic data from our lab [normal (n = 7, mean age 9 years) IHR 128 +/- 24, intrinsic corrected sinus node recovery time 135 +/- 40 ms, intrinsic sinoatrial conduction time 86 +/- 19 ms]. Among postoperative Mustard patients (n = 5, mean age 13 years, mean years postoperative 11) 2 of 5 had clearly abnormal intrinsic sinus node function with nonsinus rhythm during CAB; 3 of 5 had sinus rhythm during CAB with normal or mildly abnormal intrinsic sinus node function. The postoperative case of tetralogy of Fallot (age 20 years, postoperative 14 years) had mildly abnormal intrinsic sinus node electrophysiology study. The postoperative case of Fontan (age 16 years, postoperative 1.5 years) had sinus rhythm at rest but left atrial rhythm during CAB. Different aspects of sinus node dysfunction may be expressed during resting electrophysiology study vs. electrophysiology study utilizing CAB. The pathophysiology of sinus node dysfunction among postoperative pediatric patients is not homogeneous with regard to the contribution of intrinsic sinus node dysfunction. In those patients with normal or mildly abnormal intrinsic sinus node function, an important pathophysiologic influence of the autonomic nervous system is implicated.     

Examination of sinoatrial conduction through premature atrial stimuli via the esophagus]

Sinoatrial (SA) conduction can be tested in man by premature atrial stimuli. The difference between the post-extrasystolic pause and the spontaneous sinus cycle is a sign of the sinoatrial delay. Extern atrial stimuli provoked over the esophagus showed analogous results to intracardiac tests. The sinoatrial conduction time estimated by the esophagus method is about 20 ms higher. In 30 normal persons it was 95 +/- 36 ms (x +/- 2 SX). 7 patients with sick sinus syndrome showed aberrations as in the intracardiac test. Different types of sinoatrial block should be distinguished. Type I measured by the esophagus method had a "SAE time" over 130 ms. Type II always had compensating postextrasystolic pauses due to higher SA delay. Type III of other authors could not be observed; there are doubts about the rightness of this type. In 2 patients SA blocks over several sinus cysles could be induced by premature stimuli. This feature osberved for the first time has been declared as type IV. In 28 patients with different diseases of the heart type I could be found 12 times and type II 6 times; SA block was not known previously. The calculation of the SA time by atrial stimuli via the esophagus offers a riskless and simple method for the further differential diagnosis of disturbances of the cardiac rhythm.     

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.