(Hypertension. 1995;26:808.)
© 1995 American Heart Association, Inc.
Articles |
Autonomic Nervous Function in Non-dipper Essential Hypertensive Subjects
Evaluation by Power Spectral Analysis of Heart Rate Variability
From the Second Department of Internal Medicine, Ehime University School of Medicine, Ehime, Japan.
Correspondence to Katsuhiko Kohara, MD, Second Department of Internal Medicine, Ehime University School of Medicine, Shigenobu-cho, Onsen-gun, Ehime 791-02, Japan.
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Abstract |
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Abstract Autonomic nervous function was evaluated by means of power spectral analysis of heart rate variability in hospitalized dipper (n=31) and non-dipper (n=31) essential hypertensive subjects. Twenty-four–hour blood pressure (BP) measurement was performed by the cuff-oscillometric method to evaluate the nocturnal decrease of BP. The non-dipper subjects were defined as those whose nocturnal decrease of systolic BP was <10% of daytime BP. Power spectral analysis of RR interval was performed from Holter ECG every 10 minutes by the maximum entropy method to obtain the low-frequency band (LFB, 0.04 to 0.15 Hz), which is an index of both parasympathetic and sympathetic nervous activities, and the high-frequency band (HFB, 0.15 to 0.4 Hz), which reflects parasympathetic nervous activity. LFB and HFB were averaged every hour to obtain hourly LFB and HFB values. Total LFB and total HFB were calculated as the mean values of 24 hourly averaged LFBs and HFBs. Both LFB and HFB were significantly lower in non-dipper hypertensives than in dipper subjects throughout the day. In dipper hypertensives, LFB showed a nocturnal decrease, whereas HFB was significantly increased during the nighttime. However, these diurnal changes in LFB and HFB were significantly blunted in non-dipper subjects. These findings indicate that non-dipper hypertensive subjects were characterized with a decreased physiological circadian fluctuation on autonomic functions compared with dipper subjects. This alteration in the autonomic nervous function may explain the non-dipper phenomenon in essential hypertension.
Key Words: blood pressure • autonomic nervous system • hypertension, essential
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The BP has diurnal variations.1 2 A decrease in the night and an increase in the morning show the circadian rhythm of BP.1 "Non-dipper" pattern refers to a diurnal change of BP in which the nocturnal decrease of BP is attenuated or absent.2 The clinical importance of alteration of the diurnal change of BP has been further proved by the fact that the non-dipper pattern of BP variation is associated with progression of end-organ damage.2 3 4
Although the mechanisms responsible for a nocturnal decrease of BP are not fully understood, withdrawal of sympathetic activity seems to play a pivotal role,1 because the circadian pattern of catecholamines is very similar to that of BP.5 6 7 Lack or attenuation of diurnal change in BP has been reported in secondary forms of hypertension associated with abnormal sympathetic nervous activities,8 9 and autonomic nervous failure10 11 further indicating that autonomic nervous abnormality is associated with non-dipper phenomenon. However, little information is available about the autonomic nervous function in the non-dipper phenomenon in essential hypertension.
Power spectral analysis of heart rate variability is a useful noninvasive method to provide practical information on autonomic nervous activity.12 In the present study, by use of power spectral analysis of RR intervals obtained from 24-hour Holter ECG, we evaluated the autonomic nervous function in dipper and non-dipper essential hypertensive subjects throughout the day.
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Methods |
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Subjects and Study Protocol
Sixty-two hospitalized essential hypertensive subjects (mean age, 57±2 years; 34 men and 28 women) participated in the study. Subjects with diabetes mellitus, congestive heart failure, renal failure, previous myocardial infarction, or cerebrovascular accident were excluded from the study. Informed consent for the procedure was obtained from each patient. Subjects received a diet containing 7 g (120 mmol) of NaCl per day, and their daily activities were controlled uniformly throughout the hospitalization period. All medications were discontinued on admission. After a stabilization period of 1 week, 24-hour urinary excretion of catecholamines, plasma levels of catecholamines, plasma renin activity, and plasma aldosterone concentration were determined.
Urine samples for catecholamine determination were collected in the presence of 6 mol/L HCl. Blood was withdrawn into ice-cold tubes containing EDTA-2Na early in the morning with subjects fasting and on bed rest for at least 30 minutes. Plasma and urine samples were stored at -20°C until assay. Catecholamine concentrations were determined by high-performance liquid chromatography.13 Plasma renin activity and plasma aldosterone concentration were measured using commercial kits: renin RIABEADS and Aldosterone RIAKIT II, respectively (Dainabot Company Ltd).
Twenty-four–Hour BP
Determination
Twenty-four–hour BP was measured by the
cuff-oscillometric method with the use of ABPM-630 (Nihon Colin
Electronics Co, Ltd) with CO2 gas–powered cuff
inflation. BP was measured every 30 minutes from 6 AM to 10
PM and every 60 minutes from 10 PM to 6
AM of the following day.13 14 Daytime and
nighttime BPs were obtained as the average values in the awake period
between 6 AM and 10 PM and in the sleeping
period between 10 PM and 6 AM,
respectively.
In the present study, all subjects were divided into two groups,
dipper and non-dipper, according to their nocturnal decrease of BP.
Subjects whose nocturnal decrease of SBP was 
10% of daytime SBP were
classified as dippers,2 and subjects whose nocturnal
decrease of SBP was <10% of daytime SBP were classified as
non-dippers. Time of awakening and falling asleep and the quality of
sleep was assessed by interview for each subject. A nocturnal decrease
of heart rate was observed in all participants.
Determination of LVMi
Echocardiographic study was performed with an
SSD-870 echocardiograph (Aloka Co, Ltd) with a 3.5-MHz
transducer. Recordings were made at a paper speed of 100 mm/s.
LV end-diastolic and end-systolic
dimensions and the thicknesses of the interventricular
septum and LV posterior wall were measured according to the
recommendations of the American Society of
Echocardiography.15 LV mass was
calculated by the formula of Devereux and Reichek16 and
was divided by the body surface area to obtain LVMi. All measurements
were performed with the use of a computerized graphic analyzer
(Cardio 500, Kontron).
Power Spectral Analysis of R-R Intervals
Two-channel 24-hour ECG monitoring (DMC-3252, Nihon Kohden)
was performed to record R-R intervals on magnetic tape. The tape of
the Holter system incorporated a phase-lock loop system that
corrects variations in the tape speed. R-R intervals recorded on
magnetic tape were converted to digital signals at 128 samples per
second (ambulatory ECG analysis system DMC-4000, Nihon Kohden).
R-R interval series were resampled at a constant interval of 300 ms. In
this process, ectopic beats and artifact were removed and interpolated
with the method of Berger et al.17 The DC component of
this time series was removed by subtracting mean values of the time
series in the analysis segment. Then, autoregressive
parameters were calculated, and power spectral densities
were computed with maximum entropy method with a commercially available
program (QP-413D, Nihon Kohden). In this method, "windowing" or
low-cut filtering, which is always used with fast Fourier transform
method, is not required, and good spectral fidelity can be
obtained.18 Subjects who had more than 100 ectopic beats
per day were excluded from the study. The effective frequency range of
this method is from 0.00158 to >0.4 Hz. Power spectral densities of
rhythmic oscillations over a frequency range of 0.04 to 0.4
Hz were obtained every 10 minutes. For each time segment, the power was
quantified in the LFB (0.04 to 0.15 Hz), which is an index of both
sympathetic and parasympathetic nervous activity, and in the HFB (0.15
to 0.4 Hz), which reflects parasympathetic nervous system
activity.12 19 20 The ratio of LFB to HFB, which is an
index of sympathovagal balance,21 was determined every 10
minutes and averaged every hour.
Fig 1 illustrates typical power spectrograms obtained from Holter ECG. LFB and HFB were averaged every hour to obtain hourly LFB and HFB. Total LFB and total HFB were calculated as the mean values of 24-hour averaged LFBs and HFBs. Daytime and nighttime power spectral densities were obtained in the same way as BP. Diurnal changes in power spectral densities were also determined in 10 normal control subjects matched for age and sex (mean age, 50±4 years; 6 men and 4 women) under hospitalization.
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Statistical Analysis
All values are expressed as mean±SEM. The significance of
differences among dipper and non-dipper hypertensive subjects and
normal control subjects was determined by ANOVA followed by Duncan’s
multiple-range test. The differences in diurnal changes in BP and
power spectral density between dipper and non-dipper hypertensive
subjects were analyzed by ANOVA with repeated measures. A value
of P<.05 was defined as significant.
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Results |
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Subjects’ Background and 24-Hour BP
Table 1 summarizes the characteristics of hypertensive subjects. On the basis of the profile of diurnal changes of BP, 31 subjects were classified as non-dipper hypertensive. Thirty-one dipper hypertensive subjects were matched in age, sex, and body mass index as well as office BP and heart rate. Subjects were either never treated with drugs or were free from drugs for at least 1 week at the time of the study. Nine of 31 dipper subjects and 9 of 31 non-dipper hypertensive subjects had never been treated before the study. Other subjects had been treated with one or two of the following antihypertensive agents: ß-blocker, diuretic, calcium channel blocker, angiotensin-converting enzyme inhibitor, or
1-blocker. The distribution of
these agents used for the treatment was not different between the two
groups. However, nondipper subjects had had hypertension for
significantly longer than dipper subjects.
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Fig 2 depicts the diurnal changes in BP and heart rate in dipper and non-dipper hypertensive subjects. Circadian variation of BP was significantly blunted in non-dipper subjects compared with that in dipper hypertensive subjects. However, there was no difference in heart rate changes between the two groups.
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Power Spectral Densities in Dipper and Non-dipper
Hypertensive Subjects
Fig 3 illustrates diurnal changes in power
spectral densities of R-R intervals and the ratio of LFB to HFB.
Repeated-measures ANOVA revealed that diurnal changes were
significantly different between dipper and non-dipper hypertensive
subjects in LFB, HFB, and LFB/HFB. Total, daytime, and nighttime
hemodynamic variables and power spectral densities
in dipper and non-dipper hypertensive subjects as well as normotensive
control subjects are summarized in Tables 2 and 3. Both LFB and HFB were significantly
low in non-dipper hypertensive subjects compared with those in dipper
hypertensive subjects, although there were no differences between
dipper hypertensive subjects and normotensive control subjects. To
further investigate the neuronal involvement in the non-dipper
phenomenon, the relationship between nighttime-to-daytime ratio of mean
blood pressure and those of power spectral parameters was
investigated (Fig 4). There were
significant positive correlations between the ratios of nighttime to
daytime of MBP and of LFB as well as the ratio of LFB to HFB.
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Humoral Variables in Dipper and Non-dipper Hypertensive
Subjects
Table 4 summarizes humoral variables. There
were no differences in these parameters between dipper and
non-dipper hypertensive subjects except for plasma level of
norepinephrine, which was significantly higher in
non-dipper hypertensive subjects.
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LVMi in Dipper and Non-dipper Hypertensive Subjects
LVMi in dipper and non-dipper hypertensive subjects is shown in
Fig 5. LVMi was significantly larger in non-dipper
subjects than in dipper hypertensive subjects (128±7 versus 106±4
g/m2, P<.01).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Ambulatory BP monitoring was developed from an esoteric technique to become a clinically useful tool by the wide use of the device.2 The Fifth Joint National Committee reported that clinical situations in which ambulatory blood pressure monitoring may be useful are white-coat hypertension, drug resistance, evaluation of nocturnal BP changes, episodic hypertension, hypotensive symptoms associated with antihypertensive medications or autonomic dysfunction, and carotid sinus syncope and pacemaker syndromes.22
A nocturnal decrease of BP is one of the characteristics of diurnal
changes of BP that was first demonstrated by Hill23 in
1898. As first described by Smirk24 as basal BP, the
nocturnal level of BP provides critical information, since the
influence of mental and physical activity is minimal during
sleep.24 25 It also has been shown that failure of BP to
decrease by 10% during sleep is associated with LV
hypertrophy3 and cerebrovascular damage
visualized by magnetic resonance imaging4 as well as
future cardiovascular events.26
Furthermore, subjects with a higher overall
cardiovascular risk such as those with diabetes have
shown lack of a normal decrease of BP during sleep.27 28
In the present study, hospitalized essential hypertension subjects
were analyzed under uniform conditions of time of rising,
meals, and sleep as well as physical activity, since these
parameters are known to affect diurnal change of
BP.8 Under these conditions, we confirmed that non-dipper
hypertensive subjects had larger LVMis than dipper hypertensive
subjects.
Plasma catecholamine levels decrease during sleep with diminished sympathetic nervous activity, suggesting that the sympathetic nervous system plays a pivotal role in diurnal change of BP.1 6 7 The close linkage between autonomic nervous dysfunction and absence of the nocturnal decrease of BP also has been shown in several studies. Recently, Chau et al29 reported that BP in diabetic subjects with severe autonomic neuropathy was less likely to decrease at night. Subjects with autonomic failure also showed a lack of nocturnal decrease of BP.10 11 In the present study, we first demonstrated that absolute power densities, both LFB and HFB, and their diurnal changes were significantly decreased in non-dipper hypertensive subjects.
Power spectral analysis of heart rate variability provides useful information on autonomic nervous function as well as the balance between its sympathetic and parasympathetic components.12 Autonomic imbalance in diabetes,30 31 in congestive heart failure,32 33 and in orthostatic hypotension34 has been investigated by power spectral analysis. There have been several studies reporting alteration of power spectral densities in essential hypertension subjects.35 36 Guzzetti et al36 observed that essential hypertension subjects had higher low frequency and lower high frequency than normotensive subjects. However, these alterations may depend on the stage of hypertension, since in the present study we found that power spectral densities of dipper subjects, both LFB and HFB, were not significantly different from those of normal control subjects.
The finding in the present study that HFB was significantly decreased in non-dipper hypertensive subjects indicates reduction in their parasympathetic nervous activity, since under physiological conditions the high-frequency component of the heart rate variability can to a certain degree be used as an estimate of the parasympathetic nervous activity.19 However, it is surprising that LFB in non-dipper hypertensive subjects was also low throughout the day, since plasma norepinephrine was higher in non-dipper hypertensive subjects. One of the possible explanations is that since the low-frequency component of the heart rate variability is governed by both sympathetic and parasympathetic nervous activity,19 20 a reduction in parasympathetic nervous activity may produce a profound reduction in LFB even if sympathetic drive is increased. It is also possible that pathologically increased sympathetic tone in non-dipper hypertensive subjects accounts for the decreased LFB in the non-dipper hypertensives, since saturation of the sinus node with sympathetic traffic may in fact produce a reduction in variability.19 20
The finding in the present study that the heart rate of non-dipper subjects was not different from that of dipper hypertensive subjects is consistent with previous studies.4 28 It is also noted that diurnal changes of heart rate of non-dipper hypertensive subjects was quite similar to that of dipper hypertensive subjects, despite the fact that diurnal variation of HFB and LFB was quite suppressed in non-dipper subjects. Recently, Panina et al33 demonstrated that 24-hour mean heart rate and power spectral densities of heart rate variability had no significant correlation in subjects with congestive heart failure, suggesting that these two parameters were governed by different mechanisms. They proposed to use the mean heart rate as a indicator of autonomic tone.
Low-frequency power density showed a nocturnal decrease and high-frequency power density showed a significant increase during nighttime in dipper hypertensive subjects. On the contrary, these diurnal changes in low-frequency and high-frequency power were significantly blunted in non-dipper subjects. These differences may represent the neuronal mechanisms of the observed dipper-non-dipper phenomenon in the present study. To support this hypothesis, we observed a significant positive correlation between the ratio of nighttime to daytime MBP and the nighttime/daytime ratio of LFB as well as the ratio of LFB to HFB, suggesting that the non-dipper phenomenon is due in part to the failure of withdrawal of sympathetic tone during nighttime. These findings together indicate that autonomic dysfunction including abnormal circadian variation contributes to non-dipper hypertension. However, the relatively weak correlation may indicate that factors other than autonomic nervous activity, such as structural damages of cardiovascular system,3 4 are also involved in the non-dipper phenomenon.
Recently, Veerman et al37 reported an age-dependent decrease in power spectral densities of R-R intervals and concluded that decreased vagal modulation and baroreceptor sensitivity accounted for the decreased power densities in the elderly. The elderly are also characterized as having higher plasma norepinephrine concentrations.38 Although the age distribution was not different between dipper and non-dipper hypertensive subjects in the present study, the non-dipper hypertensive subjects had lower power spectral densities associated with a higher level of plasma norepinephrine than dipper subjects. These findings indicate that the functional as well as the structural changes in the cardiovascular system in the non-dipper subjects might be the same as those in the elderly.
Ambulatory BP predicts the risk for target organ damage and future cardiovascular events better than casual or clinical BP.2 Power spectral density also predicts the severity of coronary artery disease39 as well as future cardiac events, including sudden death.40 41 In our previous report we showed that LVMi had a negative correlation with power spectral density, suggesting the involvement of autonomic dysfunction in the increased cardiac events, observed in subjects with LV hypertrophy.42 In the present study we further demonstrated that non-dipper hypertension was associated with higher LVMi and lower power density compared with dipper hypertension. These findings indicate that autonomic dysfunction may be involved in the increased cardiovascular events in non-dipper subjects.
In summary, power spectral analysis of heart rate variability showed that physiological circadian fluctuations on the autonomic nervous system were decreased in non-dipper essential hypertensive subjects with advanced end-organ damage. Autonomic nervous dysfunction including abnormal circadian variations may account for the non-dipper phenomenon.
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Selected Abbreviations and Acronyms |
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Received March 20, 1995; first decision April 26, 1995; accepted August 3, 1995.
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K. Kario, J. E. Schwartz, and T. G. Pickering Changes of Nocturnal Blood Pressure Dipping Status in Hypertensives by Nighttime Dosing of {alpha}-Adrenergic Blocker, Doxazosin : Results from the HALT Study Hypertension, March 1, 2000; 35(3): 787 - 794. [Abstract] [Full Text] [PDF]
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K. Kario, J. E. Schwartz, and T. G. Pickering Ambulatory Physical Activity as a Determinant of Diurnal Blood Pressure Variation Hypertension, October 1, 1999; 34(4): 685 - 691. [Abstract] [Full Text] [PDF]
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K. Kohara, Y. Jiang, M. Igase, Y. Takata, T. Fukuoka, T. Okura, Y. Kitami, and K. Hiwada Postprandial Hypotension Is Associated With Asymptomatic Cerebrovascular Damage in Essential Hypertensive Patients Hypertension, January 1, 1999; 33(1): 565 - 568. [Abstract] [Full Text] [PDF]
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G. Y. H. Lip, C. R. Gibbs, and D. G. Beevers Ambulatory Blood Pressure Monitoring and Stroke : More Questions Than Answers Stroke, August 1, 1998; 29(8): 1495 - 1497. [Full Text] [PDF]
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Y. Yamamoto, I. Akiguchi, K. Oiwa, M. Hayashi, and J. Kimura Adverse Effect of Nighttime Blood Pressure on the Outcome of Lacunar Infarct Patients Stroke, March 1, 1998; 29(3): 570 - 576. [Abstract] [Full Text] [PDF]
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K. Kario, K. Eguchi, Y. Nakagawa, K. Motai, and K. Shimada Relationship Between Extreme Dippers and Orthostatic Hypertension in Elderly Hypertensive Patients Hypertension, January 1, 1998; 31(1): 77 - 82. [Abstract] [Full Text] [PDF]
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K. Kario, K. Motai, T. Mitsuhashi, T. Suzuki, Y. Nakagawa, U. Ikeda, T. Matsuo, T. Nakayama, and K. Shimada Autonomic Nervous System Dysfunction in Elderly Hypertensive Patients With Abnormal Diurnal Blood Pressure Variation : Relation to Silent Cerebrovascular Disease Hypertension, December 1, 1997; 30(6): 1504 - 1510. [Abstract] [Full Text]
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