Saudi Journal of Kidney Diseases and Transplantation

LETTER TO THE EDITOR
Year
: 2016  |  Volume : 27  |  Issue : 5  |  Page : 1057--1058

Beta-blockers control pulse rate during hemodialysis


Kiyonori Ito, Susumu Ookawara, Yuichiro Ueda, Kaoru Tabei 
 Division of Nephrology, First Department of Integrated Medicine, Saitama Medical Center, Jichi Medical University, Saitama City, Japan

Correspondence Address:
Dr. Susumu Ookawara
Division of Nephrology, First Department of Integrated Medicine, Saitama Medical Center, Jichi Medical University, Saitama City
Japan




How to cite this article:
Ito K, Ookawara S, Ueda Y, Tabei K. Beta-blockers control pulse rate during hemodialysis.Saudi J Kidney Dis Transpl 2016;27:1057-1058


How to cite this URL:
Ito K, Ookawara S, Ueda Y, Tabei K. Beta-blockers control pulse rate during hemodialysis. Saudi J Kidney Dis Transpl [serial online] 2016 [cited 2020 Dec 4 ];27:1057-1058
Available from: https://www.sjkdt.org/text.asp?2016/27/5/1057/190901


Full Text

To the Editor,

Tachycardia and bradycardia are signs of cardiac abnormalities. Hemodialysis (HD) patients have cardiac complications although the pulse rate (PR) of approximately 90% of HD patients is maintained within normal limits (60-99 beats/min) at the start of dialysis. [1] Furthermore, HD patients have a much higher risk of sudden cardiac death (SCD) and lethal arrhythmia than the general population. [2] These events occur between 0-12 and 60-72 h from the start of dialysis. [3] Although later events may be explained by fluid retention and hyperkalemia, the mechanisms triggering adverse events at the start of dialysis remain unclear. Beta-blocker (βB) usage over this time frame is lower than during other time points during dialysis. [3] There are few reports on the effect of βBs on PR during HD. Here, we investigated the differences in PR during HD in patients on treatment with or without βBs.

We conducted a cross-sectional study on maintenance HD patients (n = 85; mean age, 66 ± 10 years; mean HD duration, 5.4 ± 6.9 years). Inclusion criteria were a reduction in blood volume (BV) of more than 5% using a BV monitor on a Nikkiso DCS-27 dialysis machine (Tokyo, Japan) to confirm water removal to achieve adequate dry weight and no usage of digoxin. Patients were divided into two groups: 46 patients were receiving βB agents, whereas 39 persons were not. There was no difference in the clinical parameters examined including BV reduction (with βB, −10.9± 3.5%; without βB, −10.4 ± 3.6%), ultrafiltration rate (with βB, 630 ± 180 mL/h; without βB, 596 ± 209 mL/h), and total water removal (with βB, 2.1 ± 0.7 L/HD session; without βB, 2.0 ± 1.0 L/HD session). The prevalence rate of diabetes mellitus in the groups on treatment with or without βB group was 58% and 46%, respectively. The βBs used included carvedilol (74%), bisoprolol (20%), and metoprolol (6%).

Blood pressure (BP) and PR were monitored hourly. There was no significant difference in systolic and diastolic BP. However, PR between the two groups was significantly different during HD. In addition, PR was significantly lower during HD compared to the start of HD, in the group receiving βBs [Figure 1]. {Figure 1}

PR is influenced by many factors, especially sympathetic hyperactivity due to an increase in circulating plasma volume before HD. Water removal during HD often induces an increase in PR and various arrhythmias. Our results suggest that βB usage prevents cardiac sympathetic hyperactivity induced by HD, even in patients experiencing a BV reduction from water removal. These results may explain how βB usage could prevent SCD and arrhythmia during HD. Cice et al reported that carvedilol, a βB, can control PR over long periods of time, improve the two-year survival rate, and prevent adverse cardiac events. [4] Therefore, βB may have a cardioprotective effect in HD patients. However, we cannot conclude whether there are any beneficial effects on arrhythmia frequency or prognosis of HD patients. A larger longitudinal study is needed to clarify the role of βB agents in preventing SCD and lethal arrhythmia during HD.

Conflict of interest: None declared.

References

1Nakai S, Masakane I, Akiba T, et al. Overview of regular dialysis treatment in Japan (as of 31 December 2005). Ther Apher Dial 2007;11: 411-41.
2Myerburg RJ, Mitrani R, Interian A Jr., Castellanos A. Interpretation of outcomes of antiarrhythmic clinical trials: Design features and population impact. Circulation 1998;97: 1514-21.
3Bleyer AJ, Hartman J, Brannon PC, ReevesDaniel A, Satko SG, Russell G. Characteristics of sudden death in hemodialysis patients. Kidney Int 2006;69:2268-73.
4Cice G, Ferrara L, D'Andrea A, et al. Carvedilol increases two-year survival in dialysis patients with dilated cardiomyopathy: A prospective, placebo-controlled trial. J Am Coll Cardiol 2003;41:1438-44.