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Published on: April 29, 2013
Reduced 24-h Sodium Excretion Is Associated With a Disturbed Plasma Acylcarnitine Profile in Vasovagal Syncope
Jinqing Song1, Chunyan Tao1, Guozhen Chen1,2
1Department of Pediatrics, Peking University First Hospital, Beijing, China.
Insights
Low sodium intake in children with vasovagal syncope (VVS) is linked to altered plasma acylcarnitine levels. This suggests that changes in carnitine metabolism due to restricted sodium may contribute to VVS development.
Area of Science:
- Biochemistry
- Pediatrics
- Cardiology
Background:
- Vasovagal syncope (VVS) is a common cause of syncope in children.
- Dietary factors, including sodium intake, may influence VVS pathophysiology.
- Carnitine and acylcarnitine profiles are crucial indicators of cellular energy metabolism.
Purpose of the Study:
- To investigate the association between low sodium intake and plasma carnitine/acylcarnitine profiles in children with VVS.
- To explore the potential role of disturbed carnitine metabolism in VVS pathogenesis.
Main Methods:
- Twenty-six children with VVS were categorized based on 24-hour urinary sodium excretion (low <3g, normal 3-6g).
- Plasma carnitine and acylcarnitine levels were quantified using tandem mass spectrometry.
- Head-up tilt tests were performed, and clinical/hemodynamic data were compared between groups.
Main Results:
- Children with low urinary sodium excretion reported more fatigue.
- Significantly higher plasma concentrations of tiglylcarnitine (C5:1), hydroxyhexadecanoylcarnitine (C16OH), hydroxyoctadecanoylcarnitine (C18OH), and carnitine C22 were observed in the low sodium group.
- These elevated acylcarnitines were negatively correlated with 24-hour urinary sodium levels.
Conclusions:
- Reduced 24-hour urinary sodium excretion correlates with an altered plasma acylcarnitine profile in pediatric VVS patients.
- Disturbances in plasma acylcarnitines, potentially induced by restricted sodium intake, may play a role in the development of VVS in children.
- Further research into the link between sodium, carnitine metabolism, and VVS is warranted.
Abstract:
Objective: To investigate if the low sodium intake is associated with the plasma carnitine and acylcarnitine profile in children with vasovagal syncope (VVS). Materials and Methods: Twenty-six children suffering from VVS were recruited in the present study and divided into a group of low urinary sodium excretion or a group of normal urinary sodium excretion according to the excretion of 24-h urinary sodium <3 or 3-6 g, respectively. The excretion of 24-h urinary sodium was detected with ion-selective electrode approach. Plasma carnitine and acylcarnitine concentrations were measured with tandem mass spectrometry. Each participant completed the head-up tilt test. The demographics, clinical characteristics, hemodynamic parameters and plasma carnitine and acylcarnitine concentrations were compared between the two groups. A bivariate correlation between plasma acylcarnitine profiles and the excretion of 24-h urinary sodium was conducted with Spearman's correlation coefficients. Results: Of the enrolled VVS patients, 14 patients were assigned to the group of low urinary sodium excretion and the remaining 12 patients were assigned to the group of normal urinary sodium excretion. Symptoms of fatigue were more prevalent in the group of low urinary sodium excretion than in the group of normal urinary sodium excretion (p = 0.009). Aside from fatigue, no other differences in the demographics, clinical characteristics or hemodynamic parameters during the head-up tilt test were found between the two groups (p > 0.05). Concentrations of plasma tiglylcarnitine (C5:1), hydroxyhexadecanoylcarnitine (C16OH), hydroxyoctadecanoylcarnitine (C18OH), and carnitine C22 were significantly higher in the group of low urinary sodium excretion than in the group of normal urinary sodium excretion (all p-values = 0.048); moreover, they were all negatively correlated with 24-h urinary sodium levels (all p-values = 0.016). There were no differences between the two groups in other acylcarnitines or free carnitine. Conclusions: Reduced excretion of 24-h urinary sodium is associated with a disturbed plasma acylcarnitine profile in children with VVS. The findings suggest that restricted sodium intake-induced disturbance of plasma acylcarnitines and related cellular energy metabolism might be involved in the pathogenesis of VVS in children.
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