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1 Dipartimento di Medicina Interna, University Tor Vergata, Roma, Italy; Divisione di Riabilitazione Cardiaca, IRCCS San Raffaele, Roma, Italy
2 Divisione di Riabilitazione Cardiaca, IRCCS San Raffaele, Roma, Italy
3 Neuroriabilitazione Pediatrica, IRCCS San Raffaele, Roma, Italy
* To whom correspondence should be addressed. E-mail: iellamo{at}med.uniroma2.it.
This study was designed to test the hypothesis that individuals with Down syndrome, but without congenital heart disease, feature an altered autonomic cardiac regulation. Ten subjects with Down syndrome (DS) and ten gender-and age-matched healthy subjects (NR) were studied at rest and during active orthostatism, which is known to induce reciprocal changes in sympathetic and parasympathetic traffic to the heart.. Autoregressive power spectral analysis was used to invesigate RR-interval variabilitiy. Baroreflex modulation of sinus node was assessed by the spontaneous baroreflex sequences method. No significant differences were observed in arterial blood pressure both at rest and in response to standing between DS and NR. Also RR-interval did not differ at rest. RR-interval decreased significantly less during standing in DS in comparison to NR. Normalized low-frequency (LFNU) and high-frequency (HFNU) component of RR-interval variability did not differ at rest between DS and NR. During standing, a significant increase in LFNU and decrease in HFNU was observed in NR, whereas no significant change in both LF and HF components of RR-interval variability was detected in DS. At rest, baroreflex sensitivity (BRS) did not differ between DS and NR, and underwent a significant decrease on going from supine to upright in both group. However, BRS was greater in DS than in NR during standing. These data indicate that subjects with DS exhibit reduced HR response to orthostatic stress associated with blunted sympathetic activation and vagal withdrawal and with a lesser reduction in BRS in response to active orthostatism. These findings suggest an overall impairment in autonomic cardiac regulation in DS and may help to explain the chronotropic incompetence tipically reported during exercise in subjects with DS without congenital heart disease.
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