Key result
Patients with sick sinus syndrome exhibit altered autonomic mechanisms, with fluctuating sinus node automaticity and non-reproducible clinical parameters of sinus node function.
Why the study?
Do autonomic mechanisms and diurnal variations in sinus node function differ in patients with symptomatic sinus bradycardia compared to healthy controls?
Observational (n=26)
Do autonomic mechanisms and diurnal variations in sinus node function differ in patients with symptomatic sinus bradycardia compared to healthy controls?
Patients with sick sinus syndrome demonstrate heterogeneous autonomic dysfunction and significant diurnal variability in sinus node function parameters, suggesting that single clinical measurements may be non-reproducible.
Answers are grounded in this paper and cite their sources.
Single sinus node measurements may be unreliable in sick sinus syndrome due to autonomic fluctuations; leaves open whether repeated or diurnal testing improves diagnosis.
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.
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Kontani et al. (1980) conducted an observational in Symptomatic sinus bradycardia (sick sinus syndrome) (n=26). Autonomic blockade (propranolol followed by atropine) vs. Healthy controls was evaluated on Variations of the sinus cycle length after autonomic blockade (intrinsic cycle length) and sinus node recovery time. Patients with sick sinus syndrome exhibit altered autonomic mechanisms, with fluctuating sinus node automaticity and non-reproducible clinical parameters of sinus node function.
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