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.     

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.     

Transvenous technique of human sinus node electrogram recording. Its significance and applications

Experience with intracardiac recording of sinus node electrograms (SNE) in 27 patients is described. Under fluoroscopic monitoring the poles of a tri- or quadripolar catheter were positioned at the superior vena cava--right atrium junction. For recording, high amplification of 100 microV/cm and low-pass filters of 0.2-70 Hz were used. SNE was verified by simultaneously recording electrograms from two pairs of poles at the same filter setting and the application of carotid sinus massage. SNE was obtained in 17 patients (63%). It was recognized as a smooth, low-frequency upstroke slope before rapid atrial depolarization. Its amplitude range was 30-90 microV. Directly recorded sinoatrial conduction time (SACT) ranged from 55 to 120 ms (mean 88 +/- 20). In 4 patients with sick sinus syndrome SACT varied from 90 to 220 ms. SACTs calculated by the premature stimulation method and measured directly from SNE were in good correlation (r = 0.61, p less than 0.05).     

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

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

Direct stimulation of the sinus node in man. A possible explanation for an unusual finding during premature atrial stimulation.

An atypical behavior of the postextrasystolic pauses was observed in a 19-yr-old patient studied by His bundle electrography and programmed premature atrial stimulation. In the normal case there is a prolongation of the postextrasystolic pauses compared to the spontaneous cycle length allowing calculation of sinoatrial conduction time (SACT). In this case there were constant postextrasystolic pauses during the whole range of prematurity which were identical to the spontaneous cycle length. It is suggested that the catheter tip was accidentally positioned at the sinus node itself. The lengths of the spontaneous cycles, of the return cycles, and of the postreturn cycles showed no significant differences. Thus, one may assume that sinus node automaticity was not influenced in this case.     

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.     

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 function in patients with sinus node dysfunction.

Twenty patients of mean age 66.2 years, with suspected sinus node dysfunction, underwent extensive electrophysiologic study. Sinus bradycardia (18), sinus pauses (3), and sinoatrial block (1) were identified in their ECGs prior to study. Also 11 patients had some abnormality of atrioventricular nodal and/or intraventricular conduction prior to study. At the time of electrophysiological study, 10/20 patients (50%) had a mean cycle length exceeding 1000 msec, and mean P-V interval exceeded 210 msec in 7/20 (35%). The estimated "sinoatrial conduction time" exceeded 215 msec in 6/16 (38%) patients. The maximum first escape cycle following pacing at six different rates exceeded a value equal 1.3 X the mean value of the control cycle length + 101 msec (slope of regression line + Y intercept + 1 SD) in 13/9 (68%) patients. Nineteen patients received 1 mg atropine intravenously and mean cycle length decreased by 19%, from 891 +/- 175.8 msec to 718 +/- 182.9 msec. Graded infusion of isoproterenol was employed in 19 patients; four patients required an infusion rate greater than 28.3 ng/kg/min to produce a 20% decrease in spontaneous sinus cycle length. These data would indicate that a variety of interventions are required to characterize the disturbance of sinus node automaticiy and sinoatrial conduction in patients with sinus node dysfunction.     

Complete sinoatrial block in two patients with bradycardia-tachycardia syndrome

Electrophysiologic studies with recordings of sinus node electrograms were performed in two patients with bradycardia-tachycardia syndrome. In both patients, the rest electrocardiogram showed apparent sinus bradycardia. Patient 1 had frequent paroxysms of atrial tachycardia with long pauses of up to 10 seconds; Patient 2 had paroxysmal atrial flutter and atrial pauses of up to 8 seconds. Multiple, repetitive, low frequency deflections, with a cycle length ranging from 730 to 960 ms in Case 1 and 570 to 750 ms in Case 2, suggestive of sinus node electrograms, were recorded at a critical area at the junction between the superior vena cava and the right atrium. These low frequency deflections had no relation to spontaneous junctional beats or the spontaneous atrial beats that showed high frequency deflections on the atrial electrogram. However, they could be suppressed by spontaneous or paced atrial beats. Pharmacologic interventions in Case 2 showed that the cycle length of the low frequency deflections shortened after administration of isoproterenol and did not change after propranolol or atropine. Thus, complete sinoatrial exit block with intact entrance conduction can occur in patients with bradycardia-tachycardia syndrome. Under such circumstances, the surface electrocardiographic manifestation of sinus bradycardia may not be of sinus origin.     

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

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

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

Sinoatrial conduction times, estimated by premature atrial stimulation, were compared with direct measurement of the sinoatrial conduction time in 15 isolated rabbit sinus node preparations before and after intrasinusal pacemaker shifts induced by cooling. Transmembrane potentials and surface electrograms were recorded from the sinus node and crista terminalis. Extracellular sinus node activity was recorded in five preparations. Mapping was performed at 38 degrees C and 35 degrees C to determine the site of the dominant pacemaker. The sinus cycle was significantly longer at 35 degrees C (319.4 ms vs 258.1 ms). Intracellular measured conduction time was significantly shorter (63.8 ms vs 70.4 ms) because of caudal shift of the dominant pacemaker. Estimated sinoatrial conduction time was significantly longer (110.3 ms vs 85.4 ms) owing to the depression of automaticity by the extrastimulus. Extracellular measured conduction time did not differ significantly from intracellular measured conduction time. These results suggest that intrasinusal pacemaker shift may explain inaccuracies in indirect estimations of sinoatrial conduction time by atrial pacing techniques. Extracellular recordings appear to be a better method of evaluating sinoatrial conduction times.     

Sinus node 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.     

Evaluation of sino-atrial function using the method of extrasystole induced by constant-relative premature impulses. 1. Method and normal results]

Atrial pacemaking under conditions of relative constancy (40 or 50% of the preceding cycle) enables us to calculate the immediate sino-atrial conduction time (retrograde and antegrade) (SACT). 17 patients were chosen for their normal sino-atrial function under spontaneous changes of the sinus cycle (SC). In each case, a significant inverse linear relationship was found between SACT and the corresponding SC. The mean correlation slope was -0.36 in 10 patients with no post-pacing depression (PPD). The slope was greater in 7 patients with a PPD (-0.89); if this depression is taken into account when the SACT is calculated, the slope decreases. In 5 patients, atropine (1 mg I.V. reduced the mean value of SC, and shortened (constant relative value) the SACT. The mechanisms for the spontaneous and induced variations in the sinus output are discussed; it may be that there are substitute pacemakers within the cells of the sino-artrial node, which are affected by variations in sympathetic or parasympathetic activity or by pacing. In clinical practice, automatism and conduction with the sinus node should be interpreted as inter-related functions, both under normal conditions and after vagal block.     

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.     

Method for recording electrical activity of the sinoatrial node and automatic atrial foci during cardiac catheterization in human subjects

A method for recording electrical activity of the sinoatrial (S-A) node and automatic atrial foci in human subjects is described. To record S-A nodal electrograms, an electrode catheter was inserted percutaneously into the femoral vein and advanced under fluoroscopic control to the superior vena caval-right atrial junction. The distal terminal of the catheter was placed in the area of the S-A node and the proximal terminal on the free right atrial wall or in the right atrial lumen. Polarity was reversed from the conventional electrocardiographic recording; high amplification (about 100 μV/cm) and selective filters (0.1 to 20 hertz) were used.S-A nodal electrograms recorded with this method in human subjects were similar to electrograms obtained previously from the dog and rabbit and revealed negatively directed diastolic and upstroke slopes preceding the P wave of the electrocardiogram. Sinoatrial conduction time measured from the S-A nodal electrograms in 15 cases was 34.9 ± 2.1 ms (mean ± standard error of the mean) for a sinus cycle length of 736.4 ± 38.6 ms. The coronary sinus electrograms in a patient with coronary sinus rhythm were recorded by the same technique except that the distal terminal of the catheter was placed at the coronary sinus ostium. A negatively directed diastolic slope preceding the P wave was consistently recorded.This method for recording electrograms of the S-A node and ectopic automatic atrial foci should prove useful in (1) assessment of both normal and abnormal S-A nodal function, (2) direct determination of conduction time from the S-A nodal pacemaker to the atrium, and (3) localization of automatic atrial foci.     

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

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

Influence of intravenous clonidine on normal and pathological sinus and atrioventricular nodes and carotid sinus sensitivity

A number of clinical observations have suggested that clonidine may be responsible for dizziness and even syncope. The aim of this study was to assess the effects of this drug on normal and pathological sinus and AV nodes and on carotid sinus sensitivity. 19 patients were investigated (average age: 73 years). 14 patients complained of dizziness or syncope, including 3 patients with spontaneous sinus node dysfunction. 5 patients were asymptomatic; 3 were investigated for severe sinus bradycardia (1 on clonidine); 1 patient had sinoatrial block and 1 patient underwent pre-operative assessment for intraventricular block. The sinus node was studied using Mandel's method at 100, 120 and 150/min; the AV node was studied by the extrastimulus method with fixed atrial cycle of 600 ms. The following parameters were measured: Wenckebach point, AH interval in spontaneous and paced cycle length of 600 ms, effective refractory periods. Carotid sinus sensitivity was tested by right and left carotid sinus massage. These parameters were measured under basal conditions and 15 and 30 minutes after IV injection of 0.150 mg of clonidine. Two groups of patients were identified from the results under basal conditions: group 1:11 patients with corrected post-stimulation pauses less than 525 ms, and group 2:8 patients with at least one corrected post-stimulation pause of over 525 ms. Clonidine influenced the post-stimulation pauses significantly in both groups. However, the number of pathological pauses increased much more in group 2 than in group 1.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Physiopathology of the sinus node and sinoatrial conduction

New information about the pathophysiology of the sinus node and sino-atrial conduction has been published in the last few years. The sinus node consists of cells separated by a network of collagen fibres. This anatomical disparity explains the different electrophysiological characteristics of the node; the morphology of cellular action potentials depends on the site of recording. The dominant and most automatic pacemaker cells are situated in the cephalic region and the latent pacemaker cells in the caudal region. However, synchronisation of these different cellular activities is possible and results in a coherent signal. This complex synchronisation has been the object of several recent papers. The phenomenon of intrasinusal pacemaker shift and the stimuli which induce it have been studied in depth. In general, positive chronotropic stimuli tend to shift the dominant pacemaker towards the cephalic part and negative chronotropic stimuli towards the caudal part of the node. It is possible to assess pacemaker shift clinically and this phenomenon must be taken into consideration when studying sinus node function. Intercellular conduction and especially electrotonic conduction does not play a role in the genesis of the flux, which represents spontaneous cellular automatism, but in its mode of expression, that is to say the sinus rhythm. The pathophysiology of sinoatrial block is complex because it may be situated within and/or around the sinus node. The extrinsic or intrinsic mechanisms of these blocks may be interrelated. Variations in sinus rhythm must be taken into account in the genesis of sinoatrial block; an acceleration in rhythm may block conduction in the perisinusal region. Finally, our knowledge of the ionic fluxes underlying sinus automatism has also improved with individualization of the pacemaker current (if).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.