Why the study?
Low HRV is linked to cardiac death in haemodialysis patients, while LC n-3 PUFA may exert anti-arrhythmic effects, prompting investigation of relationships between HRV and LC n-3 PUFA status in new haemodialysis patients.
Is LC n-3 PUFA status associated with heart rate variability in patients with CKD stage 5 on haemodialysis?
Is LC n-3 PUFA status associated with heart rate variability in patients with CKD stage 5 on haemodialysis?
In patients commencing haemodialysis, higher EPA to DHA ratios are associated with lower vagally-mediated HRV, suggesting potential compromised conversion of EPA to DHA that may impair cardiac autonomic function.
Low heart rate variability (HRV) is independently associated with increased risk of sudden cardiac death (SCD) and all cardiac death in haemodialysis patients. Long chain n-3 polyunsaturated fatty acids (LC n-3 PUFA) may exert anti-arrhythmic effects. This study aimed to investigate relationships between dialysis, sleep and 24 h HRV and LC n-3 PUFA status in patients who have recently commenced haemodialysis. A cross-sectional study was conducted in adults aged 40–80 with chronic kidney disease (CKD) stage 5 (n = 45, mean age 58, SD 9, 20 females and 25 males, 39% with type 2 diabetes). Pre-dialysis blood samples were taken to measure erythrocyte and plasma fatty acid composition (wt % fatty acids). Mean erythrocyte omega-3 index was not associated with HRV following adjustment for age, BMI and use of β-blocker medication. Higher ratios of erythrocyte eicosapentaenoic acid (EPA) to docosahexaenoic acid (DHA) were associated with lower 24 h vagally-mediated beat-to-beat HRV parameters. Higher plasma EPA and docosapentaenoic acid (DPAn-3) were also associated with lower sleep-time and 24 h beat-to-beat variability. In contrast, higher plasma EPA was significantly related to higher overall and longer phase components of 24 h HRV. Further investigation is required to investigate whether patients commencing haemodialysis may have compromised conversion of EPA to DHA, which may impair vagally-mediated regulation of cardiac autonomic function, increasing risk of SCD.
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Pinto et al. (2021) studied this question.
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