Haemodialysis increases QTc interval but not QTc dispersion in ESRD patients without manifest cardiac disease

Background. HD has been reported to determine an increase in QTc interval and QTc dispersion (QT(max)-QT(min))-risk factors that predispose to severe ventricular arrhythmias and sudden death. However, most studies have included end-stage renal disease (ESRD) patients with significant heart pathology. We therefore aimed to study the impact of a single HD session in subjects without manifest cardiac disease. Methods. Sixty-eight stable, non-diabetic HD patients (47.1% males, age 40.2 +/- 12.7 years, HD duration 57 +/- 36 months and 37% hypertensive), with normal maximal ECG stress test and sub-endocardiac viability index and without ECG left ventricular hypertrophy were included. QT interval was calculated 10 min pre- and post-HD, as an average of three consecutive complexes, and corrected for heart rate using Bazett's formula (QTc = QT/(R-R)(1/2)). Na+, K+, Ca2+, PO4, pH and BP levels were also determined pre- and post-HD. Results. The QTc interval increased significantly post-HD to 434 +/- 29 from 421 +/- 26 ms pre-HD (P = 0.005); an abnormally prolonged QTc (> 440 ms) was recorded in 34% cases pre-HD and in 46% post-HD, i.e. 1.5-2.3 times higher than in the high risk EURODIAB IDDM population. However, this effect was not homogeneous. Only 47 subjects had an increase in QTc duration after a dialysis session, while in 21 a decrease in QTc duration was recorded. The increase in QTc post-HD correlated with Ca2+ homeostasis. Patients with greater increases in QTc after dialysis had higher baseline plasma calcium levels (r = 0.47, P < 0.001); also, a larger decrease in Ca2+ post-HD correlated with higher increases in QTc interval (r = 0.33, P < 0.05). In contrast with QTc behaviour and with data from the literature, in this young HD population without manifest cardiac disease and with a low prevalence of HTA, post-HD QTc dispersion was similar to pre-HD values, increasing in only 39 patients. Furthermore, changes in QTc dispersion were not related to changes in electrolytes and BP following dialysis. However, changes in QTc dispersion and in QTc interval were directly correlated (r = 0.37, P = 0.42). There were no relationships between pre-HD measured echocardiographic variables, including: LV ejection fraction, internal diameters, wall thickness, mass and mass index and baseline or changes in QTc or QTc-d. Conclusions. Haemodialysis increases the QTc interval in ESRD patients, mainly related to rapid changes in electrolyte plasma concentrations. However, the impact on QTc dispersion is less important in the absence of significant coexisting cardiac disease.