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.     

First-degree sinoatrial heart block: sinoatrial block in the sick-sinus syndrome.

Sinoatrial conduction time (SACT) was estimated from the delay in the atrial recovery period after premature depolarization applied in that portion of atrial diastole when increasing prematurity resulted in a constant recovery interval. In 20 normal patients SACT was 169 msec. +/- 91 (2 S.D.). At least nine of 19 patients with "sick-sinus syndrome" (SSS) demonstrated SACT that were longer than seen in these normal subjects. SACT was prolonged in seven of nine SSS patients with abnormal A-V nodal conduction. Among 10 SSS patients with normal A-V conduction, only two had prolonged SACT. This study identifies first-degree sinoatrial block as a frequent manifestation of SSS associated with the presence of A-V node conduction abnormalities.     

Electrophysiologic effects of propranolol on sinus node function in children

Little is known regarding the effects of propranolol (P) on sinus node function in children. In this study, corrected sinus node recovery time (CSNRT) and estimated sinoartial conduction time (SACT) were measured in 10 children (ages 3 to 16 years; mean 8.3 years) without clinical evidence of sinus node dysfunction before and after intravenous P. The spontaneous sinus cycle length (SCL) increased after P(0.1 mg/kg) in all patients. Mean SCL increased 13.4% from 635 ± 200 msec (± SD) to 720 ± 202 msec (p < 0.01). Maximum CSNRT increased in nine patients after P and mean CSNRT increased 63% from 203 ± 61 msec to 330 ± 190 msec (p < 0.05). SACT changed in a random fashion after P. Mean SACT did not change significantly. We conclude that P significantly suppresses sinus node automaticity in children with normal sinus node function but has little or no effect on sinoatrial conduction.     

The effect of premature atrial depolarization on sinus node automaticity in man.

Sino-atrial conduction time (SACT) may be calculated from the difference between the length of the return cycle and the spontaneous cycle, using programmed premature atrial stimulation during spontaneous sinus rhythm. This approach to sinoatrial conduction assumes that sinus node automaticity is not changed by premature depolarization. In order to validate this assumption, we compared the length of the post-return cycles to the spontaneous cycle length in 71 patients. Patients were grouped according to clinical diagnosis and the value of calculated SACT. At long coupling intervals at which no reset of the sinus node occurred there was only a small prolongation of the post-return cycles (less than 8.4 msec, on an average) compared to the spontaneous cycle length. This suggests no or only an insignificant effect of premature depolarization on the sinus node. However, during test stimuli leading to reset of the sinus node, the post-return cycles were significantly prolonged between 20 to 30 msec, on an average. The response of the individual cases sometimes varied to a great extent. In patients who demonstrated a progressive linear prolongation of the return cycles at decremental shortening of the test interval, there was no significant prolongation of the post-return cycles versus the spontaneous cycle length. We conclude that 1) premature depolarization of the sinus node may have a depressant effect on sinus node automaticity, which, if present, is usually small; 2) calculation of SACT using the extrastimulus technique may overestimate true SACT.     

The 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.     

Different determination of sinoatrial conduction time (SACT) in man

Summary Using intracardiac recordings of electrical activity and programmed electrical right atrial stimulation of the human heart, the sinoatrial conduction time (SACT) in the method of Strauß et al. 1973 (SACTc) was calculated in 80 patients with and without disturbances of rhythm and compared to the modified measurement of the SACT in the method reported by Narula et al. in 1978 (SACT_N). The number of continuously stimuli varied from 4, 8 and 16 stimuli with a frequency of 10% just above the averaged spontaneous frequency.The best correlation was found between the SACTc and the SACT_N16 (r=0.74; p<0.001) with a regression line of: SACT_N16=1.04 SACTc+28.6.Under these conditions, as opposed to SACT_N4 or SACT_N8, the most favourable reproducibility and relative coefficient of variation (rVk) could be observed: SACT_N16; rVk=9.5%; r=0.91; SACT_N8. rVk=12.3%; r=0.89; SACT_N4: rVk=24.3%; r=0.53.Higher individual values for SACT_N16 were found by continuous atrial stimulation as compared to other methods of determination indicating mainly a higher depression of sinus node automaticity due to overdrive suppression.Under parasympathicolysis (1 mg atropine)_the lowest values of SACT were found for SACT_N4 (45.9±20.7 ms) coming closest the true SACT, since under these conditions neither an increase of the refractory period nor an overdrive suppression exert an influence.     

Sinus node electrogram recording in complete atrioventricular block

Surface electrocardiogram (ECG), sinus node electrogram (SNE), His bundle electrogram (HBE), and intracardiac electrogram of high right atrium (HRA) were recorded synchronously in 11 of the 14 consecutive cases with complete atrioventricular block (CAVB). SNE showed the presence of a pre-P wave that preceded in all the P wave on the ECG and had no relationship to QRS complex or TU repolarization. This confirmed that the pre-P wave arose from the sinus node. Direct sinoatrial conduction time (SACTd) in nine cases was within the normal range (less than 120 msec). SACTd in another two cases was prolonged to 185 msec and 210 msec, respectively, suggesting their abnormal sinus node conduction.     

The sinus node electrogram in the evaluation of atrial pauses

The aim of this study was to establish the electrophysiological mechanism of atrial pauses, defined as a sudden lengthening of atrial cycle greater than or equal to 10% of its basal value. The sinus node electrogram (SNE) was recorded during electrophysiological study in 20 subjects. Satisfactory recordings of 64 pauses were obtained, 25 of which were spontaneous, 16 were induced by short periods of atrial pacing (AP) in normal subjects, whereas 23 atrial pauses were induced with the premature stimulation method. The basal sinus cycle and the one during the spontaneous pauses were measured from the upstroke slope on the SNE. The electrically induced pauses of the sinus cycle were measured from the artifact of the stimulus to the upstroke slope of the SNE of the first post-pacing beat. We have found that: 1-spontaneous atrial pauses correspond to a moderate slowing of the sinus cycle and to a depression of the sinoatrial conduction occasionally up to a second degree sinoatrial block. Only in subjects with sick sinus disease, the atrial pauses are induced by depression of the sinus automatism; 2-in normal subjects the AP results in a sinoatrial conduction delay; 3-the single extrastimulus regularly produces a moderate increase of the sinoatrial conduction time with variable but minimal effects on the sinus node automatism.     

The estimation of sinoatrial conduction time in rabbit heart by the constant atrial pacing technique.

This study compared estimates of sinoatrial conduction time (SACT) obtained by constant atrial pacing (CAP) and premature atrial stimulation (PAS) with measured SACT in isolated rabbit right atrial preparations. Transmembrane potentials and surface electrograms were recorded from the sinus node and crista terminalis, respectively. The crista terminalis was paced 5, 10 and 15 beats/min faster than the spontaneous sinus rate with a train of eight pulses. Estimate of SACT by CAP was taken as the difference between the first atrial return cycle and the mean spontaneous cycle length. SACTs at 5, 10 and 15 beats/min faster were 76 +/- 10, 86 +/- 10 and 96 +/- 10 msec (mean +/- SEM; n = 12), respectively; correlation coefficients with the true SACT were 0.7, 0.54 and 0.4. Consecutive determinations of SACT by PAS and CAP in the same preparation (n = 6) at 10 beats/min faster gave SACTs of 86 +/- 13 and 79 +/- 14 msec, respectively, compared with true SACTs of 79 +/- 10 msec. Shortening of sinus node action potential, depression of automaticity and shifts in the site of the primary pacemaker contributed to the errors in both techniques. Estimation of SACT by CAP may be further complicated by failure of sinus node capture. Principles to minimize some of these errors are also presented.     

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.     

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).     

Influence of drugs on the relationship between sinus node recovery time and calculated sinoatrial conduction time in man

Summary Sinus node recovery time (SRT), the pacing rate with the maximal SRT, and calculated sinoatrial conduction time (SACT) were studied by overdrive atrial pacing and programmed premature atrial stimulation in 78 patients before and after the application of several antiarrhythmic drugs or of atropine.The maximu SRT was usually observed at lower rates of atrial pacing after application of a drug that prolonged SACT, whereas the opposite behaviour was observed in the majority of cases in whom the drug tested shortened calculated SACT. However, this relationship was not observed in all cases which may be due to random changes of sinus node automaticity or sinoatrial conduction, or to the inability of programmed premature atrial stimulation to detect changes of SACT.The results of this study further substantiate the importance of the properties of sinoatrial conduction for achieving a maximal depression of sinus node activity during high rate atrial pacing.

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Wirkung von Pharmaka auf das Verhalten von Sinusknotenerholungszeit und sinuatrialer Leitungszeit

Zusammenfassung Bei 78 Patienten wurden Sinusknotenerholungszeit, die Stimulationsfrequenz mit der maximalen Sinusknotenerholungszeit und die sinuatriale Leitungszeit mittels hochfrequenter und programmierter vorzeitiger atrialer Stimulation vor und nach Applikation verschiedener Antiarrhythmika oder von Atropin bestimmt.Nach Gabe eines Pharmakons, das die sinuatriale Leitungszeit verlängerte, wurde die maximale Sinusknotenerholungszeit gewöhnlich bei einer niedrigeren Stimulationsfrequenz beobachtet als während der Kontrollmessung. Dagegen fand sich ein entgegengesetztes Verhalten der Stimulationsfrequenz mit maximaler Sinusknotenerholungszeit nach Gabe von Substanzen, die die sinuatriale Leitungszeit verkürzten. Dieses gegensinnige Verhalten wurde jedoch nicht bei allen Patienten beobachtet. Dies kann an spontanen Schwankungen der Sinusknotenautonomie liegen oder auf methodischen Problemen bei der Bestimmung der sinuatrialen Leitungszeit beruhen.Die Ergebnisse weisen auf die Bedeutung der sinuatrialen Leitung hin, die das Ausmaß der Sinusknotendepression während hochfrequenter Vorhofstimulation mitbestimmt.

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With 5 figures     

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.     

Comparison of indirect and direct methods for determination of sinoatrial conduction time

We have performed an electrophysiologic study (EPS) in 18 subjects(mean age 21 ± 17 years) with normal sinus node function(group A) and in 15 patients (mean age 43 ± 26 years)with sinus node dysfunction (group B). Three extrastimulus methods(both Strauss and Kirkorian methods and our modification ofthe extrastimulus method) were carried out in 31 patients ofboth groups and sinoatrial conduction times (SACT_STR, SACT_KIR,SACT_MOD) could be estimated in 27 of them. SACT by the Narulamethod (SACT_NAR) was assessed in 25 patients of both groups.Sinus node electrograms (SNEs) were attempted in 22 patientsand were obtained in 17 of them. Among the indirect methods, by comparison with SACTSTR in groupA the best correlation was for SACT_MOD (r = 0.81) and the weakestfor SACT_KIR (r = 0.67); there was no significant differencebetween SACTs estimated by Strauss and other methods. In groupB the weakest correlation was also for SACT_KIR (r = 0.68), whereasthe correlations for both SACT_MOD and SACT_NAR were similar (r= 0.72 and r = 0.74, respectively); in this group SACT was significantlyunderestimated only by the Kirkorian method (P<0.01; sensitivityof 45%). By our method sensitivity was 82%, similar to boththe Strauss and Narula methods (92 and92%, respectively). By comparison of indirect methods with the direct measurementof SACT we have found similar good correlations for the Strauss,our own, and the Narula methods in group A (r = 0.81, r = 0.75,r = 0.79, respectively) and in group B (r=0.81, r = 0.86, andr = 0 72, respectively); here too the weakest correlation was,in both groups, for the Kirkorian method (r = 0.67, and r =0.68, respectively). The SACT in group B was the more significantlyunderestimated (P < 0.001). Significant underestimation ofSACT occurred also by our method and the Strauss method (P <0.01,and P <0.001, respectively), whereas the Narula method didnot significantly underestimate the directly measuredSACT. From the SNEs after atrial pacing we have shown the limitationof the Kirkorian method and observed the conspicuous beat-to-beatvariability of SACT_direct as the possible explanation of chaoticpattern of return cycles by the extrastimulus methods in somepatients of group B. We conclude that: (i) SACTs were not significantly distinguishedin controls by all indirect methods used, whereas in patientswith sinus node dysfunction the Kirkorian method was shown tobe incorrect; the chaotic pattern of atrial return cycles wasthe main limitation of all the extrastimulus methods; (ii) theresults of our modified extrastimulus method correlated wellwith both the Strauss and direct methods; (iii) the direct recordingsof SNE have allowed the elucidation of some peculiarities relatedto the difficulties of indirect estimation of SACT.     

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.     

Electrophysiological effects of lorcainide in sinoatrial disease and in Wolff-Parkinson-White syndrome

The influence of lorcainide on sinus node function and intracardiacconduction was studied in 34 patients, including seven patientswith sinoatrial disease and 14 patients with Wolff-Parkinson-Whitesyndrome. Programmed cardiac stimulation and His bundle electrographywere undertaken. Lorcainide, 2 mg/kg body weight, was givenintravenously over a period of 10 min. In normal subjects, aslight increase of sinus rate was observed; lorcainide did notchange corrected sinus node recovery time (CSNRT) and sinoatrialconduction time (SACT), calculated by use of the premature stimulustechnique. In sinoatrial disease, however, three out of sevenpatients demon-strated a decrease of heart rate due to sinusnode exit block, and CSNRT was markedly prolonged under theinfluence of the drug. Sinus node entrance block to prematureatrial beats was observed in two controls and two patients withsinoatrial disease. Spontaneous sinus node exit block developedin two patients with sinoatrial dysfunction after administrationof lorcainide. Refractory periods of the right atrium, rightventricle and conduction through the A V node (AH intervals)were unaffected by lorcainide, while HQ, QRS and QT intervalswere prolonged. In Wolff-Parkinson-White syndrome, antegradeconduction via the accessory pathway was blocked in six outof 12 patients. After lorcainide, refractory periods of theaccessory pathway increased in both the antegrade and retrogradedirection. The ventricular rate during reciprocating tachycardiaand during atrial fibril-lation was decreased by lorcainide.The results identify slowing of intraventricular conductionas the main action oflorcainide. In sinoatrial disease, lorcainidemay aggravate sinus node dysfunction.     

Latent abnormalities of sinus node function in patients with organic heart disease and normal sinus node on clinical basis

Sinus node (SN) function was analyzed in 22 patients (mean age: 46.2±12.9 years) with organic heart disease and normal SN on clinical basis (group I) and in 20 normal subjects (mean age: 43.9±15.6 years), (control group). Sinus cycle length (SCL), corrected sinus node recovery time (CSRT) and sinoatrial conduction time (SACT) were analyzed. After the control study, autonomic blockade (AB) was induced by i.v. propranolol (0.2 mg/Kg) and atropine (0.04 mg/Kg). Measurements of SCL, CSRT and SACT were then repeated. The mean SCL values were very similar in the two groups during the control state and after AB. There were no significant differences in SACTs between the two groups during the control state or after AB. On the contrary, the CSRT of group I was significantly longer than that of control group during the control state (344.8±78.9 versus 262.2±46.3 msec, P<0.001) and after AB (238.9±72.8 versus 166.8±39.3 msec, P<0.001). The analysis of real depression of SN automaticity (CSRT minus SACT) in the two groups shows that prolongation of CSRT in group I during the control study and after AB is related to an intrinsic abnormality of SN automaticity; on the contrary, no dysfunctions of the autonomic nervous system appear. These data indicate that the intrinsic abnormality of SN automaticity represents the earliest in volvement of the SN in subjects with organic heart disease and normal SN on clinical basis, although this conclusion is speculative and requires experimental verification.     

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.     

Effect of nifedipine on the sick sinus syndrome

The effect of nifedipine (N) on sinus node (SN) function was studied in 15 patients (9 males, 6 females) sixty-two to seventy-six (mean 68.1 +/- 11) years old, with sick sinus syndrome (SSS). SSS was characterized electrophysiologically by a prolonged corrected sinus node recovery time (CSNRT greater than 535 msec) and/or prolonged sinoatrial conduction time (SACT greater than 125 msec), assessed by applying premature atrial stimulation. Ten mg N was given sublingually, and CSNRT and SACT were again evaluated sixty minutes after N administration, and again ten minutes after 1.5 mg atropine (A) was given IV. Heart rate increased significantly after N (p less than 0.005), systolic blood pressure (SBP) diminished significantly (p less than 0.005), and CSNRT and SACT shortened significantly (p less than 0.005, p less than 0.005) and became normal in 7 and 5 patients respectively. After A administration, a further significant increase of heart rate (p less than 0.005) and decrease of CSNRT (p less than 0.005) and SACT (p less than 0.005) were observed. CSNRT and SACT became normal in 8 and 7 patients respectively. SBP remained stable.