Blood pressure and heart rate variability in autonomic disorders: a critical review

Spectral analysis (SA) of blood pressure (BP) and heart rate (HR) fluctuations has been proposed as a unique approach to obtain a deeper insight into cardiovascular regulatory mechanisms in health and disease. A number of studies performed over the last 15 years have shown that autonomic influences are involved in the modulation of fast BP and HR fluctuations (with a period <1 min), particularly at frequencies between 0.2 and 0.4 Hz [high frequency (HF) region or respiratory frequency] and around 0.1 Hz [mid frequency (MF) region]. In patients with secondary or primary autonomic dysfunction, SA of BP and HR signals recorded at rest or during orthostatic challenge in a laboratory environment have shown the occurrence of a reduction in the power of MF and/or HF, BP and HR components. Such a reduction is associated or may even precede the clinical manifestation of autonomic neuropathy. However, the above results collected in standardized laboratory conditions cannot reflect the features of neural cardiovascular control during daily life in ambulant individuals with autonomic failure. To investigate this issue, SA techniques have been applied to 24 h beat-to-beat intra-arterial and non-invasive finger BP recordings obtained in elderly subjects and in pure autonomic failure patients, respectively. In these conditions, HR powers displayed a reduction over a wide range of frequencies (from 0.5 to below 0.01 Hz). Conversely, BP powers underwent a complex rearrangement characterized by a reduction in the power around 0.1 Hz and by an increase in the powers at the respiratory frequency and at frequencies below 0.01 Hz. Dynamic quantification of the sensitivity of the baroreceptor-heart rate reflex by combined analysis of systolic BP and pulse interval (i.e. the interval between consecutive systolic peaks) powers around 0.1 Hz (alpha technique) has shown that in elderly subjects, and even more so in pure autonomic failure patients, baroreflex sensitivity is markedly reduced over the 24 h, and is no longer characterized by its physiological day-night modulation. In conclusion, although in some instances SA of cardiovascular signals may fail to fully reflect the features of autonomic cardiovascular control, the evidence discussed clearly demonstrates that this approach represents a promising tool for a dynamic assessment of the early impairment of neural circulatory control in autonomic failure. This is particularly the case when these analyses are performed on 24 h continuous BP and HR recordings in ambulant subjects.