Saudi Journal of Kidney Diseases and Transplantation

ORIGINAL ARTICLE
Year
: 2010  |  Volume : 21  |  Issue : 3  |  Page : 460--465

Changes in QT intervals in patients with end-stage renal disease before and after hemodialysis


Mahmoud Malhis, Sami Al-Bitar, Saleh Farhood, Khair Al-Deen Zaiat 
 Department of Internal Medicine, Faculty of Medicine, Aleppo University Hospitals, Aleppo, Syrian Arab Republic, Syria

Correspondence Address:
Saleh Farhood
Department of Internal Medicine, Faculty of Medicine, Aleppo University Hospitals, Aleppo, Syrian Arab Republic
Syria

Abstract

Increased dispersion of QT intervals is known to predispose to ventricular arrhyth­mias and sudden cardiac death. To assess the effect of hemodialysis (HD) on QT and corrected QT (QTc) intervals and their dispersions in chronic hemodialyzed patients we studied 85 patients (male/female = 48/37; mean age 44 ± 17 year) on chronic hemodialysis. Simultaneous 12-lead ECG was recorded before and after HD in a standard setting. The QT intervals for each lead were measured manually by one observer using calipers. Each QT interval was corrected for heart rate: QTc= QT √ R-R/ (in milliseconds [ms]). ECG parameters, body weight, blood pressure, heart rate, electrolytes (Na + , K + , Ca ++ , phosphate), urea, and creatinine were measured before and after HD. The mean of pre and post dialysis cycle intervals was 828 ± 132 ms and 798 ± 122 ms respec­tively; the difference was not significant. The mean of QT max intervals changed significantly from 446 ± 47 to 465 ± 72 ms (P< 0.05). The mean of corrected QT cmax intervals increased significantly from 472 ± 38 to 492 ± 58 ms (P< 0.05). The mean of QT dispersions and the corrected QT interval dispersions changed from 60 ± 29 to 76 ± 32 ms (P< 0.05) from 72 ± 46 to 98 ± 56 ms (P< 0.05), respectively. During HD, the serum potassium and phosphate levels decreased whereas the calcium levels increased. We conclude that QT and QTc interval and dispersion increase in HD patients.



How to cite this article:
Malhis M, Al-Bitar S, Farhood S, Zaiat KA. Changes in QT intervals in patients with end-stage renal disease before and after hemodialysis.Saudi J Kidney Dis Transpl 2010;21:460-465


How to cite this URL:
Malhis M, Al-Bitar S, Farhood S, Zaiat KA. Changes in QT intervals in patients with end-stage renal disease before and after hemodialysis. Saudi J Kidney Dis Transpl [serial online] 2010 [cited 2021 May 17 ];21:460-465
Available from: https://www.sjkdt.org/text.asp?2010/21/3/460/62727


Full Text

 Introduction



Despite improvements in dialysis therapy, pa­tients with end-stage renal disease (ESRD) have a significantly decreased life expectancy. Mor­tality on dialysis averages 28% within the first year regardless of dialysis modality, and me­dian survival without transplantation is only five to six years. [1] Although this marked dec­rease in life expectancy may be explained par­tially by concomitant malnutrition, impaired immunity, bleeding diathesis, and comorbid diseases [2] such as cardiac disease.

The QT interval is a measure of the duration of ventricular depolarization and repolariza­tion, and prolongation of the QT interval can predict cardiovascular death. [3],[4] QT dispersion (maximum minus minimum QT interval on standard 12-lead ECG) is a marker of varia­bility of ventricular repolarization and is known to be increased in various 'high-risk' groups, such as diabetics, [5] and patients with cardiac failure [6] or essential hypertension. [7] Increased QT dispersion can predict cardiac death following myocardial infarction or cardiac failure. [6],[8]

The purpose of our study was to assess the effect of hemodialysis (HD) on QT and correc­ted QT (QTc) interval and QT and QTc inter­val dispersion.

 Materials and Methods



We studied 94 chronic HD patients randomly selected for this study. The dialyses were ca­rried out in a standard setting (Fresenius 2008 A device; Fresenius 4008B & S) with F6 and F7 polysulfone filters (Fresenius) for 4 hours 2 times per week. Bicarbonate dialysate contai­ning (in mmol/L) 131 Na + , 2.0 K + , 1.75 Ca ++ ,and 0.5 Mg ++ was used. The age of the patients ranged from 18 to 76 (mean 44 ± 17) years, and the duration of HD therapy ranged from 8 to 118 month (mean 24 ± 18 months). Exclu­sion criteria were:



unmeasurable T waves;atrial fibrillation;bundle branch block;pacemaker; andantiarrhythmic drugs that lengthen the QT interval.There were 85/94 (90%) patients fulfilled all the entry criteria, and participated in the study. Before and after HD session, the subjects were weighed, and serum electrolytes Na + , K + , Ca 2+ , phosphate, urea, and creatinine were obtained.

Twelve-lead electrocardiographs were perfor­med at 10 mm/mv and 25 mm/s, before and immediately after HD sessions. The ECGs were performed with the patients lying comfortably in the supine position, and the V1-V6 leads were obtained from fixed chest landmarks made, using a skin marker. The QT intervals for each lead were measured manually with a caliper by one observer from the onset of the QRS com­plex to the end of the T wave. When T waves were inverted, the end was taken at the point where the trace returned to the T-P baseline. However, when U waves were present, the end of the T wave was taken as the nadir between the T and U waves. If the end of the T wave was not clear in a particular lead then it was excluded from analysis; for any particular ECG, no more than three leads were excluded.

Each QT interval was corrected for heart rate using Bazett's formula: QTc= QT [INSIDE:1] (ms), where QTc is the corrected QT interval. QT and QTc dispersions were defined as diffe­rences between the minimal and maximal QT and QTc values in each of the 12 leads.

 Statistical Analysis



Statistical analysis was performed using SPSS for Windows (Statistical program for social sciences version 12.0, 2005). The means and standard deviations (SD) of all variables were calculated. The relationship of the mean of differences between intervals and disper­sions in groups (pre-HD and post-HD) and differences among subgroups (ischemic heart disease, hypertension, gender, diabetes) were analyzed using ANOVA. Analysis employed the student's t-test for paired data to determine the significance of differences. Univariate cor­relation coefficients were examined to assess the effects of electrolyte, and BP changes, and on QT dispersion. A value of PP> 0.05). The maximal QT interval changed signi­ficantly from 446 ± 47 to 465 ± 72 ms (P> 0.05). Both QT and QTc intervals and disper­sions increased significantly at the end of hemodialysis (P> 0.05), [Figure 1] and [Figure 2].

During hemodialysis, the mean of serum po­tassium levels decreased from 5.7 ± 0.7 to 3.9 ± 0.8 meq and the mean of phosphate levels from 6.2 ± 0.6 to 5.8 ± 0.5 mg/dL (P [9]

The normal range for QT dispersion is 40 to 50 ms with a maximum of 65 ms and if the QT dispersion values are greater than 65 ms the patients are at risk for serious ventricular ar­rhythmias or sudden death. [10] Our study found a basal increase of pre-HD QTmax and QTcmax intervals, and QT and QTc dispersions with a significant further increase in these intervals post-HD.

Because QT dispersion reflects a non homo­geneous recovery of ventricular excitability, the results suggest that dialysis patients may be at higher risk of reentrant arrhythmias, and that this risk rises in the immediate post dialysis period. The incidence of ventricular arrhyth­mias among HD patients has been shown to be elevated, [11] which may be life threatening, al­though their predictive power for mortality in the HD population has not yet been shown. [12] Currently, one of the noninvasive ways of asse­ssing ventricular repolarization is based on the measurement of the QT interval and QTd. The QTd has been suggested to reflect regional variation in action potential duration. [13],[14] In patients with ESRD, the cardiac structural and functional changes can alter the repolarization and are at least partly responsible for the high overall incidence of cardiac arrhythmias. [10],[15] However, although the arrhythmogenic effect of HD is well known, the exact cause of HD­induced arrhythmias has remained elusive.

In our study, the patients with pre-existing coronary artery disease had significantly longer QTc intervals and greater QTc dispersion pre and post HD so this group of patients may be at higher risk for ventricular fibrillation and sudden death.

In diabetics; cardiac autonomic neuropathy is well known and is associated with QT pro­longation. [16] we found such correlation in our study. Hyperglycemia per se can affect QT in­ terval. [17]

We conclude that non-homogeneity of regio­nal ventricular repolarization in patients with chronic end-stage renal failure receiving hemo­dialysis may be suggested by the increase in QT and QTc interval or increase in QT and QTc dispersion. The prolongation of these parameters may be a further noninvasive mar­ker of susceptibility to ventricular arrhythmias.

 Acknowledgement



The authors thank Dr. Riad Asfari for assis­tance with study design and Dr. Ahmad Husam Al-Ahmad for his assistance in QT interval measurement.

References

1Agodoa LY, Jones CA, Held PJ. End-stage renal disease in the USA: Data from the United States Renal Data System. Am J Nephrol 1996; 16:7-16.
2Mailloux LU, Bellucci AG, Wilkes BM, et al. Mortality in dialysis patients: Analysis of the causes of death. Am J Kidney Dis 1991;18: 326-35.
3Jervell A, Lange-Nielson F. Congenital deaf mutism, functional heart disease with prolon­gation of the QT interval, and sudden death. Am Heart J 1957;54:59-68.
4Schouten EG, Dekker JM, Meppelink P, Kok FJ, Vandenbroucke JP, Pool J. QT interval prolongation predicts cardiovascular mortality in an apparently healthy population. Circulation 1991;84:1516-23.
5Wei K, Dorian P, Newman D, Langer A. Asso­ciation between QT dispersion and autonomic dysfunction in patients with diabetes mellitus. J Am Coll Cardiol 1995;26:859-63.
6Barr CS, Naas A, Freeman M, Lang CC, Struthers AD. QT dispersion and sudden un­expected death in chronic heart failure. Lancet 1994;343:327-9.
7Mayet J, Shahi M, McGrath K, et al. Left ventricular hypertrophy and QT dispersion in hypertension. Hypertension 1996;28:791-6.
8Higham PD, Campbell RW. QT dispersion. Br Heart J 1994;71:508-10.
9Ritz E, McClellan WM. Overview. Increased cardiovascular risk in patients with minor renal dysfunction: an emerging issue with far reaching consequences. J Am Soc Nephrol 2004;15:513-7.
10Abe S, Yoshizawa M, Nakanishi N, et al. Electrocardiographic abnormalities in patients receiving hemodyalysis. Am Heart J 1996;131: 1137-44.
11Sforzini S, Latini R, Mingardi G, et al. Ventri­cular arrhythmias and four year mortality in hemodialysis patients. Lancet 1992;339:212-3.
12Zabel M, Portnoy S, Franz MR. Electrocardio­graphic indexes of dispersion of ventricular repolarization: An isolated heart validation study. J Am Coll Cardiol 1995;25:746-52.
13Higham PD, Hilton CJ, Aitchesou JD, et al. Does QT dispersion reflect dispersion of ven­tricular recovery? Circulation 1992;86:1392.
14Van De Loo A, Arendts W, Hohnloser SH. Variability of QT dispersion measurements in the surface electrocardiogram in patients with acute myocardial infarction and in normal subjects. Am J Cardiol 1994;74:1113-8.
15Ichkhan K, Molnar J, Somberg J. Relation of left ventricular hypertrophy and QT dispersion in patients with systemic hypertension. Am J Cardiol 1997;79:508-11.
16Sivieri R, Veglio M, Chinaglia A et al. Prevalence of QT prolongation in a type-1 diabetic population and its association with autonomic neuropathy. Diabetic Med 1993;10:920-4.
17Marfella R, Nappo F, DeAngelis L et al. The effect of acute hyperglycemia on QTc duration in healthy men. Diabetologia 2000;43:571-5.