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.     

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.     

Electrophysiologic effects of ethmozin on sinus node function in patients with and without sinus node dysfunction

To compare the effects of ethmozin on sinus node (SN) function in the presence (9 patients) and absence (17 patients) of SN dysfunction, sinus cycle length (SCL), maximal corrected sinus recovery time (CSRT), paced cycle length yielding peak SN suppression, and indirect sinoatrial SA conduction time (SACT) were determined before and after intravenous administration of ethmozin in the dose 2 mg/kg. The mean +/- SD SCL were significantly shortened in patients with normal SN and were not changed in patients with SN dysfunction after ethmozin administration. The mean maximal CSRT was 252 +/- 72 before and 284 +/- 86 ms after ethmozin administration in patients with normal SN function (p less than 0.05). In patients with SN dysfunction (p less than 0.1) the mean maximal CSRT was found to be 1016 +/- 434 before and 2170 +/- 1756 ms after ethmozin administration. The mean SACT was 158 +/- 41 before and 174 +/- 51 ms after drug administration in patients with normal SN (p less than 0.05). Four out of nine patients with SN dysfunction developed second degree SA exit block after ethmozin administration, whereas SACT increased significantly in the remaining group of patients (180 +/- 35 to 210 +/- 32 ms; p less than 0.05). The PR, PA, AH, and HV intervals significantly lengthened and the valves of QRS and QT were not changed after ethmozin administration in either group. The conclusion is drawn that ethmozin should be administered cautiously to patients with SN dysfunction, particularly to patients with SA exit block, sinus pauses, or secondary pauses (in particular, with bradycardia-tachycardia syndrome).     

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

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

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.     

Sinoatrial and intra-atrial conductive disorders. The value of recording the sinus node potential

Direct recording of the sinus node potential in the bipolar mode using two electrodes of a quadripolar recording catheter positioned in the region of the sinus node at the junction of the superior vena cava to the right atrium was performed in 24 patients. Asynchronous overdrive atrial pacing was carried out using Strauss 'technique. Pharmacological denervation was carried out using intravenous propranolol (0,02 mg/kg) and atropine (0,04 mg/kg) using Jose's technique. An intravenous injection of a bolus of 20 mg of ATP was given in 3 cases. The sinus potential was identified by morphological criteria and confirmed after carotid sinus compression and atrial extrastimuli to exclude artefacts, especially the end of ventricular repolarisation of the preceding complex. The sinoatrial conduction time measured directly under basal conditions was considered normal when within 80 to 150 ms. Direct measurement of the sinus potential in the diagnosis of sinus node dysfunction seems to be less useful than the indirect techniques. On the other hand, it does confirm the diagnosis of sinoatrial block: five cases of special interest are described; in four cases the degree of sinoatrial block was variable: a significant increase of sinoatrial conduction time under basal conditions in 1 case; paroxysmal 3rd degree sinoatrial block revealed by programmed atrial stimulation in 2 cases; 2nd degree 2/1 sinoatrial block after injection of ATP in which the direct sinoatrial conduction time and sinus node function had been considered to be normal (1 case).(ABSTRACT TRUNCATED AT 250 WORDS)     

Measured and estimated sinoatrial conduction during variations in rhythm. Microelectrode study of the isolated rabbit atrium

Strips of isolated atrium were obtained from 10 rabbits to study the validity of indirect methods of estimating sinoatrial conduction time during variations of the sinus rhythm. Direct recordings of the trans-membrane action potential of the sinus node were made. Mapping of the sinus region was undertaken to determine the site of the dominant pacemaker. A quadripolar surface electrode was positioned on the lower part of the crista terminalis for stimulation and recording of the atrial potential. This enabled a comparison to be made between the indirect estimated and the directly measured conduction times. An intrasinusal shift of the dominant pacemaker was obtained by cooling from 38 degrees C to 35 degrees C. This shift occurs progressively in the cranino-candal direction. The estimated and measured conduction times were compared under basal conditions and after cooling. The sinus cycle was significantly longer (p less than 0.001) at 35 degrees C (318 +/- 68 ms) than at 38 degrees C (255 +/- 48 ms). The mean measured anterograde conduction time also decreased from 36 to 31 ms (p less than 0.01) and the mean measured retrograde conduction time also decreased from 39 to 33 ms (p less than 0.02); the total conduction time decreased from 75 to 64 ms (p less than 0.001). The results of the total estimated conduction times were discordant. The associated effects of stimulation and cooling can cause conduction defects and an overestimation of the conduction time.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of various indirect methods for evaluation of sinus function

Sinus node function was evaluated by Mandel, Strauss and Narula's methods in 60 consecutive patients: 20 females, 40 males; average age 59 +/- 17 years. Three had second degree sinoatrial block, 2 had bradycardia-tachycardia syndromes and 10 had sinus bradycardia. The corrected sinus node recovery time was 414 +/- 417 ms. It exceeded 520 ms in 8 cases, 5 where the two other methods confirmed sinus node dysfunction, 1 where the two other methods showed no abnormality. In the last two patients pathological results with Narula's method coincided with normal values with Strauss' method but the basal sinus cycle and the post return cycle differed from one method to the other. The atriosinoatrial conduction time estimated by Narula's method was 274 +/- 117 ms. In the thirteen cases where it exceeded 300 ms abnormal results were also recorded with Strauss' (11 cases) and/or Mandel's method (7 cases). The atriosinoatrial conduction time assessed by Strauss' method was 239 +/- 106 ms. It exceeded 300 ms in 18 patients. In these patients the results of Narula and Mandel's methods were normal in 7 cases. This discordance cannot be explained either by variations in the catheter position, or by the duration of the basal sinus or the post return cycles. This raises the question of penetration of the sinus node by the last stimulus when Narula's technique is used. A significant linear correlation was observed between the atriosinoatrial conduction time assessed by Narula's method and the atriosinoatrial time assessed by Strauss' method (N = 60; r = 0,59) and with the corrected sinus node recovery time (N = 60; r = 0,43) and a double linear correlation was found with these two parameters (N = 60; r = 0,62). There was no significant linear correlation between the atriosinoatrial conduction time assessed by Strauss' method and the corrected sinus node recovery time (N = 60; r = 0,27). The atriosinoatrial conduction time evaluated by Narula's method seems to be intermediary between the two other parameters which seem to be independent of each other.     

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.     

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.     

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.     

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.     

Electrophysiologic effects of flecainide acetate on sinus node function, anomalous atrioventricular connections, and pacemaker thresholds

The acute electrophysiologic effects of i.v. flecainide acetate (2 mg/kg body weight) were assessed in 71 patients undergoing electrophysiologic study. Ten patients underwent investigation for sinus node dysfunction. Sinus cycle length shortened slightly, from 980 +/- 292 to 931 +/- 276 ms (p less than 0.01). Uncorrected or corrected sinus node recovery times or sinoatrial conduction time (according to the methods of Strauss and Narula) did not change in 6 patients with normal sinus node function and in 3 of 4 patients with abnormal sinus node function at rest. In the remaining patient maximal sinus node recovery time increased from a value at rest of 5,185 ms to 23,460 ms after flecainide. In the same patient sinoatrial conduction times at rest increased from 159 ms (Strauss method) and 143 ms (Narula method) to 1,398 and 1,455 ms, respectively, after flecainide. Thirty-three patients underwent electrophysiologic evaluation of anomalous atrioventricular (AV) pathways and reentrant tachycardias. Flecainide significantly prolonged accessory AV pathway anterograde and retrograde refractoriness. Anterograde accessory pathway block occurred in 33% of patients and retrograde accessory pathway block in 44%. Flecainide was successful in the acute termination of 86% of orthodromic atrioventricular reentrant tachycardias. In 15 patients with dual AV nodal pathways, only retrograde "fast" AH pathway refractoriness was significantly increased by flecainide, which was successful in the acute termination of 88% of intra-AV nodal reentrant tachycardias. In 28 patients who underwent endocardial pacing threshold assessment before and after i.v. flecainide, the acute threshold rose by a maximum of 117%, whereas the chronic threshold rose by a maximum of 83%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiologic effects of lidocaine on sinus node and atrium in patients with and without sinoatrial dysfunction

Electrophysiological studies were conducted in 13 patients with normal sinus node function and 14 with sinus node dysfunction before and after intravenous lidocaine. Mean +/- SEM sinus cycle length significantly shortened from 810 +/- 34.3 to 774 +/- 34.3 msec in patients with normal sinus node (P less than 0.001) and from 1061 +/- 67.6 to 1016 +/- 64.5 msec in patients with sinus node dysfunction (P less than 0.025) after lidocaine. Mean sinus recovery time was 1027 +/- 49.4 before and 1026 +/- 52.5 msec after lidocaine in patients with normal sinus node (NS) and 1269 +/- 97.7 before and 1170 +/- 73.8 msec after lidocaine in patients with sinus node dysfunction (P less than 0.05). Mean calculated sinoatrial conduction time was 87 +/- 9.5 before and 90 +/- 9.2 msec after lidocaine in patients with normal sinus node (NS) and 80 +/- 10.3 before and 96 +/- 10.2 msec after lidocaine in patients with sinus node dysfunction (P less than 0.001). Mean atrial effective and functional refractory periods were not significantly changed with lidocaine. Thus lidocaine shortened sinus cycle length in both groups, without affecting atrial refractoriness. Lidocaine appeared to depress perinodal tissue only in patients with sinus node dysfunction. The abbreviation of sinus recovery time in patients with sinus node dysfunction could reflect increased sinus automaticity and/or increased perinodal refractoriness, allowing entrance block to occur. This mechanism may explain why sinus arrest has been noted in some patients during lidocaine administration.     

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.     

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.     

Electrophysiologic effects of oral diltiazem before and after beta blockade

We conducted electrophysiologic (EP) studies and estimated the sinus node function and atrioventricular (AV) conduction in 10 patients with suspected coronary arterial disease (age range 35-55 years) before and during diltiazem therapy (60 mg thrice daily for 5-7 days). The effect of beta blockade (0.1 mg/kg of intravenous propranolol) was evaluated in both EP studies. The mean spontaneous sinus cycle length (SCL) and the AV nodal Wenckebach cycle lengths (AVWB) were significantly higher (p less than 0.05) after propranolol alone (913 +/- 131 and 504 +/- 197 ms, respectively) compared with baseline values (SCL: 827 +/- 149 ms, AVWB: 439 +/- 173 ms). Diltiazem alone failed to influence the SCL and AVWB significantly. Following the combination (diltiazem + propranolol), SCL (945 +/- 147 ms) and AVWB (533 +/- 148 ms) were significantly higher (p less than 0.05) than baseline and post diltiazem values (SCL: 840 +/- 150 ms; AVWB 457 +/- 103 ms). None of the other parameters (sinoatrial conduction time, corrected sinus node recovery time, AH and HV intervals, AV nodal and atrial effective refractory periods) were significantly influenced by propranolol, diltiazem, or the combination. No patient developed AV block, sinus arrest/sinoatrial exit block, or symptomatic sinus bradycardia following beta blockade after diltiazem administration. Oral diltiazem therapy alone and after beta blockade does not appear to adversely influence the sinus node function and AV conduction in patients below the age of 55 years. The combination of diltiazem and beta blocker thus appears safe in selected patients with coronary arterial disease.     

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.     

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.