Effect of propranolol on heart rate variability in patients with end-stage renal disease

A double-blind, placebo-controlled, randomized crossover pilot trial

K. Tory, E. Horváth, Z. Süveges, A. Fekete, P. Sallay, K. Berta, T. Szabó, A. J. Szabó, T. Tulassay, G. Reusz

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Background: Low heart rate variability (HRV) is an independent risk factor of cardiac mortality in patients with end-stage renal disease (ESRD). It has been explained by uremic parasympathetic neuropathy. Sympathetic overactivity can also reduce HRV. Our aim was to determine whether there is vagal activity in ESRD patients that is masked by sympathetic activity. Methods: The effect of propranolol on HRV was examined in 13 patients with ESRD, aged 20.1 ± 7.6 years without diabetes. All patients were given intravenous propranolol (0.05 mg/kg) once and placebo once in a randomized, double-blind way, with an interval of 6.6 days (mean, range: 2 - 9). Propranolol was administered before hemodialysis treatment, after 40 minutes supine resting period. HRV was registered for 10 minutes, during supine, before and after the injection. Patients' HRV data were compared to that of 29 age-matched healthy controls. Results: Initially, both high-(HFV) and low-frequency (LFV) bands of heart rate variability were lower in ESRD patients compared to controls (p <0.001 for both). Propranolol resulted in a significant increase of HFV (propranolol: ΔlgHFV = 0.182 (0.027 - 0.337), placebo: ΔlgHFV = -0.029 (-0.128 - +0.070); p = 0.032). Elevation of LFV was not significant. Six patients had an elevated plasma norepinephrine and/or epinephrine level. Plasma dopamine level was elevated in all but 1 patient (mean: 432 pmol/l, 95% CI: 320 - 543) and showed an inverse relationship with the increase of lgHFV secondary to propranolol (r = -0.66, p = 0.014). Conclusions: Low HFV of ESRD patients can be improved by β -adrenergic blockade. It demonstrates that there is some vagal activity in ESRD that is masked by sympathetic activity. Therefore, altered sympathovagal balance of ESRD patients should be taken into consideration in the assessment of vagal uremic neuropathy.

Original languageEnglish
Pages (from-to)316-323
Number of pages8
JournalClinical Nephrology
Volume61
Issue number5
Publication statusPublished - May 2004

Fingerprint

Propranolol
Cross-Over Studies
Chronic Kidney Failure
Heart Rate
Placebos
Adrenergic Agents
Epinephrine
Renal Dialysis
Dopamine
Norepinephrine
Injections
Mortality

Keywords

  • Autonomic nervous system
  • Heart rate variability
  • Renal failure
  • Sympathetic overactivity
  • Uremia

ASJC Scopus subject areas

  • Nephrology

Cite this

Effect of propranolol on heart rate variability in patients with end-stage renal disease : A double-blind, placebo-controlled, randomized crossover pilot trial. / Tory, K.; Horváth, E.; Süveges, Z.; Fekete, A.; Sallay, P.; Berta, K.; Szabó, T.; Szabó, A. J.; Tulassay, T.; Reusz, G.

In: Clinical Nephrology, Vol. 61, No. 5, 05.2004, p. 316-323.

Research output: Contribution to journalArticle

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abstract = "Background: Low heart rate variability (HRV) is an independent risk factor of cardiac mortality in patients with end-stage renal disease (ESRD). It has been explained by uremic parasympathetic neuropathy. Sympathetic overactivity can also reduce HRV. Our aim was to determine whether there is vagal activity in ESRD patients that is masked by sympathetic activity. Methods: The effect of propranolol on HRV was examined in 13 patients with ESRD, aged 20.1 ± 7.6 years without diabetes. All patients were given intravenous propranolol (0.05 mg/kg) once and placebo once in a randomized, double-blind way, with an interval of 6.6 days (mean, range: 2 - 9). Propranolol was administered before hemodialysis treatment, after 40 minutes supine resting period. HRV was registered for 10 minutes, during supine, before and after the injection. Patients' HRV data were compared to that of 29 age-matched healthy controls. Results: Initially, both high-(HFV) and low-frequency (LFV) bands of heart rate variability were lower in ESRD patients compared to controls (p <0.001 for both). Propranolol resulted in a significant increase of HFV (propranolol: ΔlgHFV = 0.182 (0.027 - 0.337), placebo: ΔlgHFV = -0.029 (-0.128 - +0.070); p = 0.032). Elevation of LFV was not significant. Six patients had an elevated plasma norepinephrine and/or epinephrine level. Plasma dopamine level was elevated in all but 1 patient (mean: 432 pmol/l, 95{\%} CI: 320 - 543) and showed an inverse relationship with the increase of lgHFV secondary to propranolol (r = -0.66, p = 0.014). Conclusions: Low HFV of ESRD patients can be improved by β -adrenergic blockade. It demonstrates that there is some vagal activity in ESRD that is masked by sympathetic activity. Therefore, altered sympathovagal balance of ESRD patients should be taken into consideration in the assessment of vagal uremic neuropathy.",
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T2 - A double-blind, placebo-controlled, randomized crossover pilot trial

AU - Tory, K.

AU - Horváth, E.

AU - Süveges, Z.

AU - Fekete, A.

AU - Sallay, P.

AU - Berta, K.

AU - Szabó, T.

AU - Szabó, A. J.

AU - Tulassay, T.

AU - Reusz, G.

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N2 - Background: Low heart rate variability (HRV) is an independent risk factor of cardiac mortality in patients with end-stage renal disease (ESRD). It has been explained by uremic parasympathetic neuropathy. Sympathetic overactivity can also reduce HRV. Our aim was to determine whether there is vagal activity in ESRD patients that is masked by sympathetic activity. Methods: The effect of propranolol on HRV was examined in 13 patients with ESRD, aged 20.1 ± 7.6 years without diabetes. All patients were given intravenous propranolol (0.05 mg/kg) once and placebo once in a randomized, double-blind way, with an interval of 6.6 days (mean, range: 2 - 9). Propranolol was administered before hemodialysis treatment, after 40 minutes supine resting period. HRV was registered for 10 minutes, during supine, before and after the injection. Patients' HRV data were compared to that of 29 age-matched healthy controls. Results: Initially, both high-(HFV) and low-frequency (LFV) bands of heart rate variability were lower in ESRD patients compared to controls (p <0.001 for both). Propranolol resulted in a significant increase of HFV (propranolol: ΔlgHFV = 0.182 (0.027 - 0.337), placebo: ΔlgHFV = -0.029 (-0.128 - +0.070); p = 0.032). Elevation of LFV was not significant. Six patients had an elevated plasma norepinephrine and/or epinephrine level. Plasma dopamine level was elevated in all but 1 patient (mean: 432 pmol/l, 95% CI: 320 - 543) and showed an inverse relationship with the increase of lgHFV secondary to propranolol (r = -0.66, p = 0.014). Conclusions: Low HFV of ESRD patients can be improved by β -adrenergic blockade. It demonstrates that there is some vagal activity in ESRD that is masked by sympathetic activity. Therefore, altered sympathovagal balance of ESRD patients should be taken into consideration in the assessment of vagal uremic neuropathy.

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KW - Heart rate variability

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