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Sinus node dysfunction during long-term lithium treatment
M Rosenqvist1, L Bergfeldt, H Aili
1Department of Cardiology, Karolinska Institute, at Karolinska Hospital, Stockholm, Sweden.
Insights
Long-term lithium treatment can cause sinus node dysfunction, affecting heart rhythm. While common, clinically significant issues are rare, and the effect appears intrinsic, not due to increased nervous system activity.
Area of Science:
- Cardiology
- Pharmacology
- Electrophysiology
Background:
- Lithium is occasionally linked to sinus node bradyarrhythmias.
- The prevalence and mechanisms of lithium-induced arrhythmias during long-term use remain unclear.
- This study investigates lithium's cardiac effects, focusing on sinus node function.
Purpose of the Study:
- Evaluate lithium's systemic effects on cardiac conduction in healthy individuals.
- Determine lithium treatment prevalence in pacemaker patients.
- Assess the interaction between the parasympathetic nervous system and sinus node cells during lithium therapy.
Main Methods:
- Long-term electrocardiography on 45 lithium-treated patients (>12 months) without cardiovascular or metabolic disorders.
- Comparison with an age-stratified reference group.
- Carotid sinus pressure and sinus cycle length analysis before and after atropine in 21 patients.
- Prevalence assessment in 650 pacemaker patients.
Main Results:
- Moderate sinus node dysfunction observed in 56-78% of lithium users versus 30% in controls (p < 0.01).
- Severe dysfunction was similar between groups.
- Lithium treatment found in 0.46% of pacemaker patients.
- Abnormal sinus cycle variations occurred in 14% at baseline and 52% post-atropine in lithium users.
Conclusions:
- Lithium treatment is associated with significantly increased sinus node dysfunction compared to controls.
- Clinically significant bradyarrhythmias due to lithium are uncommon.
- Lithium's effect on the sinus node appears intrinsic, independent of parasympathetic tone.
Background And Objective:
Lithium has occasionally been reported to cause symptomatic sinus node bradyarrhythmias. The prevalence and mechanism of these arrhythmias during long-term treatment are unknown. The aims of this study were (a) to evaluate the systemic effects of lithium treatment on cardiac conduction in individuals who were free from cardiovascular disorders; (b) to assess the prevalence of lithium treatment in a group of patients with pacemakers; and (c) to evaluate the interaction between the parasympathetic limb of the autonomous nervous system and the sinus node cells during long-term lithium treatment.
Patients And Methods:
45 patients who had been treated with lithium for > 12 months were investigated in a long-term electrocardiography study. Only patients without cardiovascular disease, or concomitant chronotropic medication, or metabolic disorders known to cause rhythm disturbances were included. An age-stratified population was used as a reference group. 21 patients also underwent analysis of carotid sinus pressure and sinus cycle length before and after atropine to clarify whether neural mechanisms were involved. The prevalence of lithium treated patients was determined in 650 patients with pacemakers.
Results:
(a) Signs of moderate sinus node dysfunction (sinus arrest > 1.5 s, minimum heart rate < 50 beats/min) were found in 56% and 78% respectively in the lithium-treated group compared with 30% and 30% respectively in the reference group (p < 0.01). Severe sinus node dysfunction was equally common in both groups. (b) The prevalence of chronic lithium treatment in the pacemaker population was 0.46%. (c) Sinus cycle variations were abnormal in the basal state in three (14%) patients and in 11 (52%) patients after atropine despite signs of intact and normal parasympathetic innervation.
Conclusions:
Depressed sinus node function was significantly more common in a lithium-treated population than in an age-stratified reference group. Clinically significant dysfunction, however, was uncommon. The effect of lithium on the sinus node seemed to be intrinsic and was not caused by increased parasympathetic tone.