Background: Arrhythmia and sudden death represent striking features in patients with end-stage renal disease (ESRD). Increased QT dispersion has been shown to be associated with arrhythmias. Abnormal excitability and heterogeneous cardiac iron deposition may cause the arrhythmogenesis of human siderotic heart disease. Iron overload and precipitation with its toxicity in cardiac muscles may, therefore, cause QT prolongation in dialysis patients.
Methods: A total of 102 (65 women, 37 men; mean age, 47.7 +/- 13.4 years) nondiabetic patients undergoing peritoneal dialysis (PD) were enrolled in this study. Another 102 subjects with a serum creatinine level less than 1.5 mg/dL (133 micromol/L) were used as matched control subjects. The PD patients were divided into 2 groups according to whether their computerized measurements of corrected QT (QTc) dispersion were longer than 74 ms. A value of 74 ms has been associated with risk for serious arrhythmias related to sudden death in dialysis patients.
Results: The QTc dispersion of PD patients was significantly longer than that of the control subjects (69.8 +/- 40.0 versus 55.2 +/- 33.6 ms; P < 0.01). Thirty-eight PD patients with QTc dispersion longer than 74 ms had lower blood pressure ( P = 0.01), fewer left ventricle masses ( P = 0.036), and lower serum albumin levels (P = 0.046) but higher levels of serum calcium (P = 0.038) and transferrin saturation (TSAT; P = 0.022) than the other patients. Multivariate analysis identified TSAT as an independent factor for QTc dispersion (r = 0.432, P < 0.001). A linear relationship showed that at 74 ms of QTc dispersion, TSAT was 35.2%.
Conclusion: Long-term PD patients have longer QTc dispersion than subjects with normal renal function. The high body iron stores in these patients increase the risk of increased QT dispersion. The concern over iron overload in dialysis patients is not only because of its oxidative toxicity, but also its precipitation of arrhythmias, which may be measured by the surrogate marker of QTc dispersion.