Article contents
Heart rate variability in β-thalassaemia major with or without cardiac siderosis
Published online by Cambridge University Press: 12 February 2013
Abstract
Iron cardiomyopathy remains the major cause of death in β-thalassaemia major. Excessive iron loading could lead to cardiac dysfunction and arrhythmias. Reduced heart rate variability is associated with a higher risk of arrhythmia and sudden death after myocardial infarction and heart failure. Previous data have reported on reduced heart rate variability in patients with marked cardiac iron accumulation. In this study, we compared heart rate variability among β-thalassaemia major (TM) patients with or without cardiac siderosis.
Out of 70 β-thalassaemia major patients with preserved ejection fractions, 38 patients with cardiac T2* magnetic resonance imaging assessment were included in our study. Time domain heart rate variability parameters were analysed from 24-hour recorded electrocardiograms and were compared with the control group.
The mean T2* magnetic resonance imaging value was 22.9 ± 13.3 (4.7–47.5). In 21 patients with β-thalassaemia major, the T2* magnetic resonance imaging values were greater than 20 ms and these patients were considered to be in the early stage of the disease. When we compare these patients with control subjects, the standard deviation of all NN intervals was still significantly lower (133.0 ± 32.2 versus 162.8 ± 32.9, p = 0.001) in β-thalassaemia major patients despite normal T2* magnetic resonance imaging values. On the contrary, the standard deviation of all NN intervals was not correlated with haemoglobin levels in these patients (p > 0.05).
Heart rate variability parameters were reduced even in β-thalassaemia major patients without evident cardiac siderosis, as specified by magnetic resonance imaging data. The results of this study show that reduction of heart rate variability may start before cardiac iron loading is demonstrated by T2* magnetic resonance imaging in β-thalassaemia major.
- Type
- Original Articles
- Information
- Copyright
- Copyright © Cambridge University Press 2013
References
- 7
- Cited by