Parameters Of Sinus Node Function Research Articles

Hypervagotonic binodal dysfunction in children. Features of the natural course

Aim. To evaluate the clinical and electrophysiological picture of binodal disease in children, as well as studying the clinical course of this disease.
 Methods. To study the clinical and electrophysiological picture of autonomic binodal disease, 426 patients under 18 years old were examined; the average age was 15.35±2.43 years (3-17.9). Patient’s complaints, medical history were examined, ECG, 24-hour ECG, stress ECG (treadmill or bicycle test), echocardiography, transesophageal electrophysiologic study were performed. In the case of a combination with pathological signs of sinus node dysfunction and atrioventricular node conduction disorders with the normalization of all parameters after the atropine administration, hypervagotonic binodal dysfunction was diagnosed. To assess the clinical course of the disease, a group of 72 children was selected, who were monitored repeatedly. Mean follow-up duration was 33 months.
 Results. During the study period, sinus node dysfunction and atrioventricular blocks completely resolved in 14 (19.44%), seen as normal clinical picture with no complaints, normal heart rate, no signs of sinoatrial block or atrioventricular block, normalization of Wenckebach point position. Another 35 (48.62%) had only one node dysfunction resolved (either sinoatrial or atrioventricular - Wenckebach point position within the age normal values and/or atrioventricular block resolved). In 23 (31.94%) - deterioration of the sinus node and atrioventricular node dysfunction was observed.
 Conclusion. There are significant differences in the frequency characteristics of heart rhythm and electrophysiological parameters of sinus node function in children with a favorable clinical course of binodal disease and progressive course of the disease.

Electrophysiological features in patients with sinus node dysfunction and vasovagal syncope

IntroductionSyncope is a common presentation of sinus node dysfunction (SND). Some patients who receive a permanent pacemaker due to SND do not benefit from it and further diagnostic workup leads to the diagnosis of vasovagal syncope (VVS). The aim of the study was to identify electrophysiological criteria that can be used for identification of patients with SND and concurrent VVS.Material and methodsTransoesophageal atrial pacing (TAP) was performed in 100 patients divided into four groups depending on symptoms and TAP results. Standard electrophysiological parameters of sinus node function and their variability were obtained in the basal state and after pharmacological autonomic blockade (AB).ResultsPatients with concurrent SND and VVS had a greater variability of sinoatrial conduction time assessed by Strauss’ method than patients without incidents of syncope (83.2 ±53.9 vs. 34.1 ±19.6, 47.8 ±33.6 and 32.1 ±22.99). Apart from abnormal sinus node recovery time and second pause, patients with SND had bigger basal state variability of these parameters. In patients with SND and concurrent vasovagal syncope the variability of sinus node recovery time (SNRT), corrected SNRT (cSNRT) and second pause (IIP) decreased after autonomic blockade.ConclusionsPatients with concurrent SND and VVS have distinct electrophysiological features – greater sinoatrial conduction time (SACT) variability and the decrease of SNRT, cSNRT and IIP variability after AB. However, further studies in larger study groups are needed to validate our findings. Transoesophageal atrial pacing is a useful procedure in patients with syncope, especially when the coexistence of more than one cardiac cause is suspected.

Electrophysiologic evaluation of sinus node function and atrioventricular conduction in patients with prolonged ventricular asystole during obstructive sleep apnea

In 15 patients with ventricular asystole of 8.5 ± 3.5 seconds (range 5.0 to 16.8) occurring exclusively during obstructive sleep apnea, electrophysiologic study of sinus node function and atrioventricular conduction before and after administration of intravenous atropine (0.02 mg/kg) was performed. Electrophysiologic parameters of sinus node function were normal in 12 of 15 patients (80%) and atrioventricular (AV) nodal function was normal in 7 patients (47%). Almost all abnormal findings of sinus node function and AV nodal function were reversible by administration of atropine. The HisPurkinje system function was normal in 6 patients (40%). Prolonged HV intervals (57 to 73 ms) were found in 9 patients (60%). Intra- or infra-His block was not observed in any patient. In summary, electrophysiologic parameters of sinus node function and AV conduction were normal or only slightly abnormal in all 15 study patients, which suggests that prolonged ventricular asystole during obstructive sleep apnea is not due to fixed or anatomic disease of the sinus node or the AV conduction system.

Electrophysiological effects of glucose-insulin-potassium on sinus node function in patients with and without sinus node dysfunction.

The electrophysiological effects of glucose (100 g)-insulin (20 U)-potassium (10 mmol X litre-1) infusion (GIK) on three parameters of sinus node function were studied in 14 control subjects (mean age 53 +/- 14 yr) and 11 patients (mean age 50 +/- 17 yr) with sinus node dysfunction (SND). In a first series of experiments the response to GIK was examined in nine control and 11 SND patients. Following GIK, the mean spontaneous cycle length decreased by 17% (671 to 560 ms; P less than 0.01) in the control group and by 33% (1066 to 715 ms; P less than 0.001) in the SND patients; this difference between both groups was statistically significant (P less than 0.01). In the control group mean corrected sinus node recovery time (CRST) and calculated sinoatrial conduction time (SACT; n = 6) were not significantly altered after GIK. In SND patients GIK decreased the mean value of CSRT by 40% (693 to 416 ms; P less than 0.05) and of calculated SACT (n = 6) by 27% (130 to 95 ms; P less than 0.05); prolonged secondary pauses following termination of rapid atrial pacing in SND patients were also shortened. In a second series of experiments, mannitol (100 g, iv) was administered in five control patients but had no significant effect on the electrophysiological parameters tested. Plasma levels of glucose were significantly increased, by 500% (P less than 0.01), after GIK; plasma potassium and sodium concentrations decreased by 7 and 5% (P less than 0.05). The results indicate that GIK had a beneficial effect on sinus node dysfunction.

Altered Autonomic Mechanisms in the Sick Sinus Syndrome and Diurnal Variations in the Parameters of Sinus Node Function : Symposium on Sinus Node Function and Its Abnormality

The role of two divisions of autonomic nervous system was investigated and the variations of the sinus cycle length after autonomic blockade (the intrinsic cycle length, ICL) and the sinus node recovery time (SNRT) were tested in 26 patients with symptomatic sinus bradycardia. Three groups of patients were recognized from the responses of sinus rate to autonomic blocking with propranolol followed by atropine, comparing with the healthy controls. In 9 patients (group A) with normal responses to cholinergic and beta-adrenergic blockades, reactions to the autonomic stimulations with barorefiexe and Valsalva maneuver and to isoproterenol were all normal. Reduced automaticity of sinus node and normal autonomic regulation are conceivable in these patients. In some of this group, sinoatrial disease was evident from abnormal ICL. In other I 7 patients with reduced response to atropine, reactions to the autonomic stimulations and to isoproterenol were blunted. With propranolol, enhanced prolongation of sinus cycle length was observed in 7 patients (group BI) and normal or reduced response in 10 (group BII). Severe clinical symptoms were more prevalent in group BI and BII patients than group A and SNRT and ICL was abnormal in most of Group B. Sinoatrial disease is evident in these patients, and reduced cholinergic control and partial beta-adrenergic compensation in group BI and disturbed regulation by both of cholinergic and beta-adrenergic system in group BII are suggested. Difference between ICL at 4 pm and O am was more than 200 msec in 8 and exceeded 300 msec in 5 of I 7 patients whose ICL were determined twice. Measurement of SNRT was repeated more than three times at O, 6 and 10 am and 4 and 10 pm in I 8 patients. SNRT fluctuated more than 2 seconds in 10 and the ratio of the longest SNRT to the shortest was 2 or more in 7 patients. We conclude that different and altered autonomic mechanisms exist in the patients with the sick sinus syndrome. Sinus node automaticity free from autonomic influence is fluctuating and the clinical parameters of sinus node function are non-reproducible in some of the sick sinus patients.

Sinus node responses to various factors. The effects of pH, antiarrhythmic drugs, stimulation sites, etc.

The role of two divisions of autonomic nervous system was investigated and the variations of the sinus cycle length after autonomic blockade (the intrinsic cycle length, ICL) and the sinus node recovery time (SNRT) were tested in 26 patients with symptomatic sinus bradycardia. Three groups of patients were recognized from the responses of sinus rate to autonomic blocking with propranolol followed by atropine, comparing with the healthy controls. In 9 patients (group A) with normal responses to cholinergic and beta-adrenergic blockades, reactions to the autonomic stimulations with barorefiexe and Valsalva maneuver and to isoproterenol were all normal. Reduced automaticity of sinus node and normal autonomic regulation are conceivable in these patients. In some of this group, sinoatrial disease was evident from abnormal ICL. In other I 7 patients with reduced response to atropine, reactions to the autonomic stimulations and to isoproterenol were blunted. With propranolol, enhanced prolongation of sinus cycle length was observed in 7 patients (group BI) and normal or reduced response in 10 (group BII). Severe clinical symptoms were more prevalent in group BI and BII patients than group A and SNRT and ICL was abnormal in most of Group B. Sinoatrial disease is evident in these patients, and reduced cholinergic control and partial beta-adrenergic compensation in group BI and disturbed regulation by both of cholinergic and beta-adrenergic system in group BII are suggested. Difference between ICL at 4 pm and O am was more than 200 msec in 8 and exceeded 300 msec in 5 of I 7 patients whose ICL were determined twice. Measurement of SNRT was repeated more than three times at O, 6 and 10 am and 4 and 10 pm in I 8 patients. SNRT fluctuated more than 2 seconds in 10 and the ratio of the longest SNRT to the shortest was 2 or more in 7 patients. We conclude that different and altered autonomic mechanisms exist in the patients with the sick sinus syndrome. Sinus node automaticity free from autonomic influence is fluctuating and the clinical parameters of sinus node function are non-reproducible in some of the sick sinus patients.

Electrophysiologic effects of disopyramide phosphate on sinus node function in patients with sinus node dysfunction.

The electrophysiologic effects of intravenously administered disopyramide (2 mg/kg) on three parameters of sinus node function were examined in 16 symptomatic patients with sinus node dysfunction. Based on their ECG data before study, patients were subdivided into group A (n = 8), those with sinus pauses and/or sinoatrial (SA) exit block; and group B (n = 8), those with sinus bradycardia. Disopyramide shortened spontaneous cycle length in 10 of 16 patients and lengthened it in six--markedly so (91%) in one patient. Estimated SA conduction time decreased in seven of 14 patients and increased in seven. Two patients developed second degree SA exit block after disopyramide. Maximum sinus node recovery time was prolonged by disopyramide in 11 of 16 patients and markedly so in four. For the group as a whole there was no significant difference in spontaneous cycle length, maximum sinus node recovery time or estimated SA conduction time. P-wave and QRS durations and H-V intervals were significantly lengthened by disopyramide. Marked depression of the three parameters of sinus node function occurred in three group A patients and in one group B patient who had persistent severe sinus bradycardia. These four patients also had secondary pauses after termination of rapid atrial pacing under control conditions. Disopyramide should be administered cautiously to patients with sinus node dysfunction, particularly those with sinus pauses, SA exit block or secondary pauses.

Sinus node dysfunction: An overview with emphasis on autonomic and pharmacologic consideration

Sinus node dysfunction is a disorder of impulse generation and Impulse conduction. Previous works have emphasized that the dysfunction occurs not only within the sinus node but also within the escape pacemaker. Adrenergic and cholinergic mechanisms, as well as pulsations and pressure within the sinus node artery, play an important role in normal sinus node activity. Although perinodal fibers act as a buffer zone for sinoatrial conduction, their role in man is yet to be clarified. During normal sinus node activity, pacemaker shifts from the sinus node to the crista terminalis have been shown to occur. Following sinus node destruction, similar shifts do occur. Clinical methods of determining sinus node function, such as the sinus node recovery time and sinus atrial conduction time, are useful but have limitations. Dynamic electrocardiographic monitoring provides the best Clinical method available for detecting sinus node dysfunction. Digitalis appears to improve the parameters of sinus node function by increasing the automaticity of latent atrial pacemakers. The atrial arrhythmia of sinus node dysfunction appears to be related to the characteristics of latent atrial pacemaker and “enhanced” cholinergic tone.

Electrophysiologic effects of propranolol on sinus node function in patients with sinus node dysfunction.

The electrophysiologic effects of intravenously administered propranolol (0.1 mg/kg) on three parameters of sinus node function were examined in ten symptomatic patients with sinus node dysfunction. The patients ranged in age from 26 to 79 years. Symptoms ranged from fatigue to frank syncope. Sinoatrial (SA) block and sinus pauses were observed in one patient; sinus pauses alone were observed in three patients. Five (5/10) patients had intraatrial block; three (3/10) patients had atrioventricular block; four (4/10) patients had an intraventricular conduction disturbance. At the time of electrophysiologic study, two patients had a control spontaneous sinus cycle length that exceeded 1000 msec. Following propranolol, the mean spontaneous cycle length increased by 17.4% (924 to 1085 msec, P less than 0.005) and spontaneous second degree SA block reappeared in the one patient. The maximum escape cycle ranged from 116% to 229% of the prepacing spontaneous cycle length and was considered to be prolonged in two of ten patients. Propranolol had no significant effect on the maximum escape cycle/prepacing cycle length X 100 (%). The estimated sinoatrial conduction time (SACT) was determined in seven patients and ranged in value from 120 to 238 mes. Propranolol increased the mean value of the estimated SACT from 179 to 213 msec, P less than 0.025. Propranolol may cause marked bradyarrhythmias in some patients with sinus node dysfunction, and should be used with caution in these patients.