Download Daily Life Blood Pressure Changes Are Steeper in

Daily Life Blood Pressure Changes Are Steeper in
Hypertensive Than in Normotensive Subjects
Giuseppe Mancia, Gianfranco Parati, Paolo Castiglioni, Roberto Tordi, Elena Tortorici,
Fabio Glavina, Marco Di Rienzo
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Abstract—Target organ damage in hypertensive patients is related to their increased average blood pressure and greater
24-hour blood pressure variability. Whether the rate of blood pressure changes is also greater in hypertension, producing
a greater stress on arterial walls, is not known, however. Our study aimed at addressing this issue by computer analysis
of 24-hour ambulatory intra-arterial blood pressure recordings in 34 subjects (29 males), 13 normotensive subjects and
21 uncomplicated hypertensive subjects (mean age⫾SD, 40.4⫾11.8 years). The number, slope (mm Hg/s), and length
(beats) of systolic blood pressure ramps of 3 or more consecutive beats characterized by a progressive increase (⫹) or
reduction (⫺) in systolic blood pressure of at least 1 mm Hg per beat were computed for each hour and for the whole
24-hour period. Twenty-four-hour average systolic blood pressure was 112.9⫾2.1 and 159.4⫾5.7 mm Hg in
normotensive and hypertensive subjects, respectively. Over the 24 hours, the number and length of systolic blood
pressure ramps were similar in both groups, whereas the slope was markedly different (24-hour mean⫾SE slope,
4.80⫾0.30 in normotensives and 6.50⫾0.40 mm Hg/s in hypertensives, P⬍0.05). Ramp slope was not influenced by age
or reflex pulse interval changes, but it was greater for higher ramp initial systolic blood pressure values. Thus, in daily
life, hypertensive subjects are characterized by steeper blood pressure changes than normotensives, and this, regardless
of the mechanisms, may have clinical implications, because it may be associated with greater traumatic effect on the
vessel walls of hypertensive patients. (Hypertension. 2003;42:277-282.)
Key Words: blood pressure 䡲 hypertension, arterial 䡲 baroreflex 䡲 blood pressure monitoring
䡲 autonomic nervous system
E
pidemiological studies and antihypertensive drug trials
have shown that systolic and diastolic blood pressure
bear a clearcut relationship to the incidence of cardiovascular
morbidity and mortality,1,2 which, for this reason, is greater in
hypertensive then in normotensive individuals. Additionally, our
group and others have shown (1) that this relationship is closer
when 24-hour average blood pressures rather than office blood
pressures are considered3–9 and (2) that, for any given 24-hour
average blood pressure, the organ damage accompanying hypertension is more pronounced if the blood pressure variability that
occurs over the 24 hours is greater.3–5,10,11–17 This evidence may
suggest that a patient’s prognosis depends not only on average
blood pressure level but, to some extent, also on the degree of
daily life blood pressure fluctuation.
A third blood pressure phenomenon that may potentially
affect organ damage and prognosis is the rate at which the
changes in blood pressure over the 24 hours take place. This
is because faster blood pressure changes may produce a
greater stress on the arterial wall and thus more easily initiate
the cascade of events that ultimately result in permanent
cardiovascular lesions.18 –21 The prevailing rate of blood
pressure transient changes over the day and night in humans
has never been investigated, however. Nor has any investigation determined whether this rate is similar or different in
subjects with normal blood pressure compared with those
with high blood pressure. Our study set out to address these
2 issues.
Methods
Subjects
Our study included a total of 34 nonsmoking subjects (29 males),
whose body mass index ranged between 21 and 27 (mean⫾SE,
24.8⫾2.3). Occurrence of obstructive sleep apnea syndrome was
reasonably, although indirectly, excluded by interview of spouses on
subjects’ sleep features and by the evidence of a normal nocturnal
blood pressure and heart rate fall in all subjects.22,23 Fourteen
subjects (age 32.6⫾3.5 years, mean⫾SE) were normotensive volunteers in whom office blood pressure was persistently ⬍140/
90 mm Hg over 3 sets of office measurements performed at 1 month
intervals, and 20 subjects were essential hypertensive (office blood
pressure, measured as above, persistently ⱖ140/90 mm Hg; age
Received December 18, 2002; first decision January 8, 2003; revision accepted June 23, 2003.
From Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie Sanitarie, Università di Milano-Bicocca (G.M., G.P., E.T.); II Unità di
Riabilitazione Cardiologica e Malattie dell’Apparato Cardiovascolare, Ospedale S. Luca, IRCCS, Istituto Auxologico Italiano (G.M., G.P., E.T., F.G.),
Milan; and LaRC, Centro di Bioingegneria, Fondazione Don Gnocchi (P.C., R.T., M.D.R.), Milan, Italy.
Correspondence to Prof Giuseppe Mancia, Clinica Medica and Dipartimento di Medicina Clinica, Prevenzione e Tecnologie Sanitarie, Università di
Milano-Bicocca, Milano and Ospedale San Gerardo, Via Donizetti 106, 20052 Monza (MI). E-mail [email protected]
© 2003 American Heart Association, Inc.
Hypertension is available at http://www.hypertensionaha.org
DOI: 10.1161/01.HYP.0000084632.33942.5F
277
278
Hypertension
September 2003
50⫾2.8 years). The hypertensive patients were selected if they had
(1) no history or clinical evidence of hypertension-related complications (ie, coronary heart disease, heart failure, cerebrovascular
disease, renal insufficiency, or peripheral artery disease), (2) no
evidence of major subclinical organ damage (ie, electrocardiographic
or echocardiographic evidence of left ventricular hypertrophy, atherosclerotic plaques at an echo-Doppler evaluation of the carotid
arteries, retinal fundus of grade III or IV of the Keith-Wagener
classification, or proteinuria), and (3) antihypertensive treatment in
the past 2 months. Patients with diabetes mellitus and hypercholesterolemia (serum cholesterol ⬎240 mg/dL) were also excluded from
the study.
Blood Pressure Measurement
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In all subjects blood pressure was measured intra-arterially and in
ambulatory conditions over 24 hours (Oxford system),24,25 by means
of a catheter percutaneously inserted into the brachial or radial artery
of the nondominant arm, following performance of the Allen test to
establish preservation of the hand circulation by the ulnar artery. The
catheter (positioned in the artery after local anesthesia with 2%
lidocaine) was connected by a rigid-walled plastic tube to a plexiglas
box placed on the chest at the heart level. The box contained the
blood pressure transducer, a perfusion unit consisting of a 40 mL
heparinized saline solution, and a miniaturized battery-operated
peristaltic pump aimed at keeping the catheter patent throughout the
24 hours. The beat-to-beat blood pressure signal was stored on a
magnetic cassette recorder (Oxford Medilog, Oxford Instruments)
for subsequent analysis. During the recording the subjects were free
to move within the hospital area and to engage in the social activities
of hospital inpatients (TV watching, playing cards, walking in the
hospital garden, visits from relatives, etc). Further details on the
blood pressure monitoring technique used in this study are published.24 All subjects enrolled in the study after a detailed explanation of its nature and purpose. The protocol of the study was
approved by the ethical committees of our institutions.
Data Analysis
In each subject the blood pressure signal was converted from analog
to digital with a 12-bit resolution at 165 Hz. Systolic blood pressure
(SBP) values were derived from each heart beat. SBP time series
were scanned to identify SBP ramps of 3 or more consecutive beats
characterized, respectively, by a progressive increase or reduction in
SBP of 1 mm Hg per beat, which were termed SBP⫹ and SBP⫺,
respectively. The ramp slope was estimated by computing the slope
of the regression line between the SBP values included in the ramp
and time. The ramp length was estimated by the number of beats
included in the ramp. SBP⫹ and SBP⫺, accompanied and unaccompanied by reflex changes in pulse interval (lengthening and shortening, respectively), were separately analyzed. Pulse interval was
computed as the interval between consecutive systolic peaks, following parabolic interpolation of the pulse waveform peak. Previous
studies have shown this to correspond to RR interval values obtained
through an ECG in normal behavioral conditions.26 Further details
on the SBP ramp analysis have been published previously.27 Data
were averaged for each hour, for a 4-hour subperiod of the daytime
(from 8 AM to noon), for a 4-hour subperiod of the night (from
midnight to 4 AM), and for the whole 24 hours. The day and night
subperiods were selected based on the patients’ diaries indicating
that they were awake and asleep, respectively. The average ramp
slope was also calculated for each tertile of the distribution of the
SBP values occurring at the beginning of the ramps, separately in
normotensive and hypertensive subjects.
Data obtained in individual subjects were averaged separately for
the group of normotensive and hypertensive subjects. The unpaired
Student t test was used to assess the significance of the average
differences between groups, whereas the paired Student t test was
used to assess the significance of the differences between daytime
and nighttime subperiods in each group. When focusing on hourly
values, between-group differences were analyzed using ANOVA for
repeated measures. Differences between individual hours were also
assessed by post hoc analysis using a t test with a Bonferroni
Figure 1. Hourly systolic blood pressure (SBP) and heart rate
(HR) values in normotensive (N) and hypertensive (H) subjects.
Data are shown as mean⫾SE.
correction. The Pearson correlation coefficients were computed
between ramp parameters and 24-hour average blood pressure
values. Ramp parameters were also averaged over different tertiles of
SBP measured at the beginning of the ramp. Given the age difference
between groups, the potential influence of this factor in accounting
for the differences in ramp parameters between normotensive and
hypertensive subjects was addressed by linear correlation analysis
between ramp parameters and age. Statistical significance was
determined at P⬍0.05. Unless otherwise stated, the symbol ⫾ refers
to the standard error of the mean. Statistical analysis was carried out
by using SPSS software (SPSS Inc).
Results
The 24-hour average SBP was 112.9⫾2.1 mm Hg in the
normotensive and 159.4⫾5.7 mm Hg in the hypertensive
group, with a typical circadian blood pressure profile in both
groups (Figure 1).
As shown in Figure 2 (left panel), in both the normotensive
and the hypertensive groups, there were hundreds SBP⫹ and
SBP⫺ ramps over the day and night, for a total of several
thousand ramps of each type over the whole 24-hour recording
period, the number of both types of ramps being somewhat less
during the night than during the daytime. There was no significant difference in the number of the SBP⫹ and the SBP⫺
ramps between normotensive and hypertensive subjects during
the day, whereas either ramp type was significantly more
frequent in the latter than in the former group during the night
(Figure 2).
Mancia et al
Fast BP Changes in Hypertension
279
Figure 2. Average 24-hour, daytime and
nighttime values for the number, length,
and slope of SBP ramps (ramps⫹ and
ramps⫺ pooled). Data are separately
shown for normotensive (N) and hypertensive (H) subjects. Asterisks refer to
the level of statistical significance of the
between-group differences.
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As shown in Figure 2 (central panel), the length of the
SBP⫹ and SBP⫺ ramps was (1) usually about 41/2 beats, (2)
less during the night than during the day, and (3) superimposable over the 24 hours in normotensive and hypertensive
subjects. This was not the case for the ramp slope, however,
which throughout the 24 hours was invariably greater in
hypertensive than in normotensive subjects (Figure 2, right
panel, and Figure 3). For the whole 24-hour period, the
difference amounted to ⫹26.9% for SBP⫹ and ⫹37.0% for
Figure 3. Hourly slope of SBP ramps in normotensive (䢇) and
hypertensive (䡩) subjects. Data (mean⫾SE ) are shown separately for SBP⫹ and SBP⫺ and for the ramps of either type
pooled.
SBP⫺ ramps, in both instances reaching statistical significance. The difference in slope between the 2 groups showed
no correlation with age (Figure 4) and remained statistically
significant when the ramps unaccompanied by reflex changes
in pulse interval were separately considered (Figure 5). When
tertile SBP values at the beginning of the ramps were plotted
versus the corresponding ramp slope values (SBP⫹ and SBP⫺
pooled), there was a tendency for the ramp slope to be greater as
the initial SBP was greater. This was the case both for the
normotensive and for the hypertensive group (Figure 6).
Figure 4. Relationship of ramp slope (lower panel) and ramp
number (upper panel) with age in all the normotensive and the
hypertensive subjects of our study.
280
Hypertension
September 2003
Figure 5. Slope of SBP ramps accompanied (coupled, C) or
unaccompanied (uncoupled, NC) by reflex changes in RR interval. Data are shown as mean⫾SE for all the SBP⫹ and SBP⫺
ramps pooled over the 24 hours.
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Discussion
The novel finding of the present study is that the slope of the
rapid and short-duration changes in SBP, which were identified by computer analysis of the blood pressure signal during
a beat-to-beat 24-hour recording, was significantly and markedly greater in hypertensive subjects than in normotensive
individuals. The difference was (1) evident both during the
day and during the night and (2) equally clear when the SBP
rapid and short-duration changes consisted of a SBP increase
and when they consisted of a SBP reduction.
It is thus possible to conclude that, in daily life, hypertensive patients are characterized not only by a greater absolute
magnitude of overall blood pressure changes (as shown by
previous studies which quantified these changes as the
standard deviation of the 24-hour blood pressure values)24,28
but also by changes that occur more steeply than in normotensive subjects. This may have clinical implications because
the traumatic effect of intravascular pressure on the vessel
wall and the resulting alterations that may initiate and worsen
vascular remodeling and atherosclerosis may have a dynamic,
in addition to a static, component.19,20
Figure 6. Ramp slope versus each tertile of SBP values
observed at the beginning of ramps. The dashed line refers to
normotensive subjects (N), the continuous line to essential
hypertensives (H). For each group, white, gray, and black circles
refer to the lowest, the middle, and the highest SBP tertile,
respectively. Data are shown as average values ⫾SE for SBP⫹
and SBP⫺ ramps pooled.
The mechanisms responsible for the greater steepness of
the SBP changes seen in hypertensive patients are not
clarified by our study. It should be emphasized, however, that
in spite of the age difference between the 2 groups, this
phenomenon was not due to aging per se, because in the total
population of the study subjects, age did not bear any
relationship with ramp slope. It should also be emphasized
that the greater steepness of the SBP changes in hypertensive
patients did not depend on the reduced ability of these
subjects to oppose fast-occurring blood pressure alterations
through baroreflex changes in heart rate,29 because the
difference in ramp slope between the hypertensive and the
normotensive group persisted when only SBP ramps unaccompanied by reflex heart rate modifications were analyzed.
Thus, other possibilities should be considered. One, the
steeper changes in SBP observed in hypertensive subjects
could be due to the fact that the blood pressure effect of
environmental and psychological stimuli typical of daily life
were magnified at the vascular level by the increased wall
stiffness and/or the greater wall-to-lumen ratio30 that characterizes hypertension. An additional possibility is that the SBP
changes were steeper in hypertensive patients because, in
these patients, the blood pressure effects of environmental
and psychological stimuli are enhanced at a central level. This
would imply that, as described for animal models of hypertension,31–33 human essential hypertension is also characterized by a sympathetic hyper-reactivity to a variety of daily
life stimuli. A third possibility is that the steeper SBP changes
seen in hypertensive patients are accounted for by the inverse
relationship that exists between large artery distensibility and
blood pressure.34 –36 That is, as blood pressure increases, large
arteries become stiffer, causing a greater SBP change for any
given change in stroke volume. These possibilities are not
mutually exclusive, and all may contribute to the differences
we have found. The data reported in Figure 6, however, may
score in favor of a major contribution of the last mechanism
because, at a similar SBP (the highest tertile of the normotensive and the lowest tertile of the hypertensive group), the
ramp slopes were similar in normotensive and hypertensive
patients. This suggests that the higher slope of SBP ramps in
hypertensives patients than in normotensive subjects may
largely be due to their higher blood pressure levels per se.
Compared with the daytime, nighttime sleep is by and large
characterized by a lower blood pressure level and a smaller
blood pressure variability. Our study provides the first evidence that this condition is characterized also by blood
pressure changes that are less steep than during the day, this
being the case both in subjects with normal and in subjects
with an elevated blood pressure. This may offer an additional
explanation for the lower rate of cardiovascular morbid and
fatal events that have repeatedly been shown to occur during
the night.37 That is, this lower rate may depend, among other
nonmechanical factors,38 on a lower and more stable blood
pressure. It may additionally depend, however, on the fact
that blood pressure changes take place less steeply.
Finally, we would like to address a few potential limitations of
our study. First, our analysis is based on data collected in 34
subjects. This might appear as a relatively small number.
However, to maximize accuracy of slope estimations and make
Mancia et al
the data relevant to daily life conditions, we had to use 24-hour
intra-arterial blood pressure recordings, which prevented large
numbers of patients from being involved. Furthermore, the
amount of information obtained was not small if one considers
that a beat-by-beat recording carried out for 24 hours allows a
huge amount of data to be obtained for each individual subject
(more than 104 000 pulse waves for each recording). Second,
our study included mostly male subjects, which prevents us from
evaluating possible gender differences in the phenomenon we
have described. This issue will have to be addressed in future
studies.
Perspectives
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Our study adds novel information on the characteristics of BP
variability at normal and high blood pressure, by providing
for the first time data on the slope of beat-by-beat BP changes
in humans, assessed in daily life conditions. Data collected by
24-hour ambulatory intra-arterial BP recordings clearly show
that, in daily life, hypertensive patients are characterized by
fast and short-duration SBP increases and reductions that are
steeper than in normotensive subjects throughout the day and
night. These steeper BP changes may result from sympathetic
hyperreactivity to daily life stimuli, arteriolar remodeling,
and/or greater arterial stiffness. Regardless of the mechanisms, the increased ramp steepness may have clinical implications, because steeper rises and falls in intravascular pressure may be associated with greater traumatic effect on the
vessel walls and may facilitate vascular damage. This should
nevertheless be further addressed by future investigations,
possibly taking advantage of the present availability of
noninvasive techniques for continuous blood pressure
monitoring.39 – 41
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Daily Life Blood Pressure Changes Are Steeper in Hypertensive Than in Normotensive
Subjects
Giuseppe Mancia, Gianfranco Parati, Paolo Castiglioni, Roberto Tordi, Elena Tortorici, Fabio
Glavina and Marco Di Rienzo
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Hypertension. 2003;42:277-282; originally published online July 28, 2003;
doi: 10.1161/01.HYP.0000084632.33942.5F
Hypertension is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 2003 American Heart Association, Inc. All rights reserved.
Print ISSN: 0194-911X. Online ISSN: 1524-4563
The online version of this article, along with updated information and services, is located on the
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