Altered pattern of circadian neural control of heart period in mild hypertension.

We addressed the problem of the circadian changes in neural control of heart period in ambulant hypertensive subjects. A running spectral analysis of R-R variability from Holter tapes provided markers of sympathetic, i.e. low-frequency component (LF) almost equal to 0.10 Hz, and vagal, i.e. high-frequency component (HF) almost equal to 0.25 Hz, controlling activities for the 24-h period of the recording. Significant circadian differences were observed in LF between the two groups of subjects: during night-time rest (0300-0400 h), LF was greater in hypertensives than in normotensives (56 +/- 2 and 48 +/- 2 nu, respectively; P less than 0.05). Furthermore, the difference between daytime and night-time LF values was progressively reduced with increasing severity of the hypertensive state, as assessed by resting arterial pressure levels. Spectral analysis of R-R variability suggests that essential hypertension may be characterized by a reduced day-night oscillation in sympathetic activity than can be quantified non-invasively using this approach.

Altered dynamics of the circadian relationship between systemic arterial pressure and cardiac sympathetic drive early on in mild hypertension.

1. This study was designed to test the hypothesis that simultaneous non-invasive assessment of the circadian variations in both intermittent arterial pressure and the continuous 24 h changes of spectral markers of cardiac neural control could provide new information on cardiovascular regulatory mechanisms, in hypertensive patients and normotensive subjects. To test this hypothesis we studied 18 subjects with mild hypertension and 11 normotensive subjects in whom we recorded simultaneously non-invasive intermittent arterial pressure and Holter electrocardiogram for 24 h. We also studied the same subjects during resting and standing conditions in the clinical laboratory. 2. The normalized power of the low-frequency (approximately 0.1 Hz) spectral component of R-R interval variability, considered mainly a marker of sympathetic drive to the sino-atrial node, was, at rest, significantly higher in the hypertensive than in the normotensive subjects, as already reported. Moreover, the values of the low-frequency component at rest recorded in the clinical laboratory were significantly correlated with those obtained from ambulatory recording during night rest. The decrease in the values of arterial pressure during the night-time was accompanied by a reduction in the power of the low-frequency component only in the case of normotensive subjects. Accordingly, the slope of the regression of the low-frequency component as a function of systolic arterial pressure during ambulatory recordings was steep in normotensive subjects and flat in hypertensive subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Continuous 24-hour assessment of the neural regulation of systemic arterial pressure and RR variabilities in ambulant subjects.

In this study, we tested the hypothesis that the neural control of circulation in humans undergoes continuous but in part predictable changes throughout the day and night. Dynamic 24-hour recordings were obtained in two groups of ambulant subjects. In 18 hospitalized patients free to move, direct high-fidelity arterial pressures and electrocardiograms were recorded, and in an additional 28 nonhospitalized subjects, only electrocardiograms were obtained. Spectral analysis of systolic arterial pressure and of RR interval variabilities provided quantitative markers of sympathetic and vagal control of the sinus node and of sympathetic modulation of vasomotor tone. With this approach, the low-frequency (approximately 0.1 Hz) component of RR interval and systolic arterial pressure variabilities is considered a marker primarily of sympathetic activity, whereas the high-frequency (approximately 0.25 Hz) component of RR interval variability, related to respiration, seems to be a marker primarily of vagal activity. We observed a pronounced and consistent reduction in the markers of sympathetic activity and an increase in those of vagal activity during the night. In the invasive studies, while the subjects were still lying in bed after waking up, the markers of sympathetic activity rose rapidly and concomitantly with a simultaneous vagal withdrawal. Noninvasive studies confirmed the early morning rise of the markers of sympathetic activity and the circadian pattern of sympathovagal balance. These data indicate that the ominously increased rate of cardiovascular events in the morning hours may reflect the sudden rise of sympathetic activity and the reduction of vagal tone.