Spectral features of heart rate variability in Williams syndrome during sleep
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Aims
The study aims to reveal the spectral alterations of heart rate variability (HRV) in Williams syndrome (WS) during sleep, using a two-slope, broken power-law model, taking into account the multi-fractal properties of the RR-interval spectra, including effects of aging and associations with sleep structure indicators.
Methods & Results
Extracting ECG recordings from a polysomnography database of 20 subjects with WS and 20 age and sex matched typically developing (TD) controls, RR-interval time series were constructed, then the fractal and oscillatory power-spectral densities computed using the Irregular-Resampling Auto-Spectral Analysis (IRASA) method. The fractal component was parametrized with a piecewise-linear function, that allowed for a custom breaking point in the power spectral density (PSD), and separate slope and intercept values in the lower and higher frequency domains. The frequency and prominence of the dominant peak was extracted from the LF (0.04–0.15 Hz) and HF (0.15–0.4 Hz) bands.
Strong WS vs TD group differences were found in the frequency of the breaking point, high domain slope, intercept and HF peak prominence. Analysis of the LF peak frequency revealed age-dependent decrease in the TD, but not in the WS group, while generally decreased values in WS independent of age, potentially reflected accelerated aging, characteristic of the syndrome. As fractal parameters were correlated, a main component was identified using principal component analysis that described the typical alterations in the fractal spectrum in WS, and was correlated with sleep structure indices as well.
Conclusions
The broken power-law model proved to be successful in characterizing the fractal component of HRV spectra, furthermore it captured alterations in cardiac regulation in WS. A main spectral feature of WS was identified in the fractal component, being associated with sleep quality indicators, a possible biomarker of the degree of general autonomic deregulation inherent to the syndrome.
