(Hypertension. 1999;33:1123-1129.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Descriptive Epidemiology of Blood Pressure Response to Change in Body Position
The ARIC Study
From the Department of Epidemiology (C.J.N., W.D.R., G.H.) and the Collaborative Studies Coordinating Center (L.E.C.), School of Public Health, University of North Carolina, Chapel Hill; Department of Psychiatry (K.C.L.), School of Medicine, University of North Carolina, Chapel Hill; Division of Epidemiology and Clinical Applications, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md (A.R.S.); and Department of Public Health and Primary Health Care, University of Bergen, Bergen, Norway (G.S.T.).
Correspondence and reprint requests to Gerardo Heiss, MD, PhD, Department of Epidemiology, UNC-CH School of Public Health, Suite 306, NationsBank Plaza, 137 E Franklin St, Chapel Hill, NC 27514. E-mail gerardo_heiss{at}unc.edu
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Abstract—The epidemiology of a common measure of cardiovascular reactivity, the change in systolic blood pressure (
SBP) from the supine to the
standing position, is described in a cohort of 13 340 men and women
aged 45 to 65 years enrolled in the Atherosclerosis
Risk in Communities (ARIC) Study. The distribution of SBP was found
to be symmetrical and unimodal, with a mean value near zero
(-0.45 mm Hg). The range of SBP was from -63.2 to 54.3
mm Hg, and the standard deviation was 10.8. Stratification of SBP
by race and gender shows a slight shift in distribution toward higher
values for black men and women. SBP was categorized into deciles.
Participants in the top 30% and bottom 30% of the distribution were
compared with individuals in the middle 40% of the distribution, who
had little or no change in SBP on standing. Participants in the bottom
30% (ie, SBP decreased on standing) were significantly older, had a
greater prevalence of hypertension and peripheral vascular
disease, had higher values of SBP, and had more cigarette-years of
smoking. Among participants in the top 30% (ie, SBP increased on
standing), a significantly larger proportion were black, mean seated
SBP was higher, and the predicted risk of developing coronary
heart disease after 8 years was greater. The response of SBP to change
in posture showed considerable variability in a population sample of
middle-aged adults. Cardiovascular morbidity,
sociodemographic factors, and cigarette smoking were associated with
the magnitude and direction of the postural change.
Key Words: blood pressure • cardiovascular reactivity • epidemiology
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The response of blood pressure to change in body position has been used in epidemiological studies as a measure of cardiovascular reactivity. Sparrow et al1 reported that a 10-mm Hg or greater increase in diastolic blood pressure (DBP) from the supine to standing position significantly modified the effect of seated systolic blood pressure (SBP) and DBP on the incidence of myocardial infarction during 8.7 years of follow up in a cohort of middle-aged white men. On further investigation of this population, the investigators concluded that the difference between the supine and seated blood pressures is positively associated with subsequent development of systemic hypertension independent of supine blood pressure.
The response of blood pressure to change in body position is well suited as a measure of cardiovascular reactivity for epidemiological studies. Several experimental studies have suggested a differential response of blood pressure to standing due to ethnicity3 and gender.4 5 However, other studies found no gender differences.6 7 Little is known about the descriptive epidemiology of this measure of reactivity, especially among women and blacks. The purpose of this investigation was to focus on the descriptive epidemiology of the response of blood pressure to change in posture in a biracial, population-based sample, the Atherosclerosis Risk in Communities (ARIC) Study.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Study Population
The study population was drawn from the cohort component of the ARIC Study, which is sponsored by the National Heart, Lung, and Blood Institute. The ARIC cohort was selected as a probability sample of 15 792 men and women between 45 and 64 years of age from 4 US communities: Forsyth County, NC; Jackson, Miss; suburban Minneapolis, Minn; and Washington County, Md. The ARIC Study protocol was approved by the institutional review boards of participating institutions. All ARIC participants agreed voluntarily to participate in the study and gave written informed consent. Details of the sampling frames and methods and cohort examination procedures were described previously.8
Data from ARIC participants examined at the initial clinic visit were
used in these analyses (1987–1989). During the baseline
examination, cardiovascular conditions were determined
and risk factors were measured. Three measurements of blood pressure
were obtained with a random-zero sphygmomanometer while the participant
was seated. The mean of the second and third DBP and SBP measurements
were used for analysis. Height (cm), weight (kg), waist
circumference (measured at the umbilicus), and hip circumference
(measured at the widest point) were measured by trained technicians.
Blood was drawn for assays by the ARIC Central Lipid, Hemostasis, and
Chemistry Laboratories. Seated blood pressure measurement,
anthropometry, and venipuncture were performed while the
participant was fasting, and then a caffeine-free snack was provided.
Ankle and brachial blood pressures were measured by a Dinamap 1846 SX
automated blood pressure recorder. The ankle SBP was divided by the
brachial SBP to calculate the ankle-brachial index (ABI). Medical
history was recorded and years of smoking exposure were determined
during a home interview. Medications taken by each participant were
brought to the baseline examination and coded by a trained interviewer.
The presence of coronary heart disease (CHD) was determined by
reported physician diagnosis, evidence from the electrocardiographic
examination, or history of coronary
revascularization. Current hypertension was defined
as a seated SBP of 
140 mm Hg, a seated DBP of 90 mm Hg,
or the use of antihypertensive medications in the past 2 weeks.
Diabetes mellitus was defined as a fasting glucose level of >7.77
mmol/L, a nonfasting glucose level of >11.1 mmol/L, or use of
hypoglycemic medications in the 2 weeks before examination.
Participants were excluded from the sample if (1) they reported their race as other than black or white (n=48), (2) the postural change examination was not administered (n=1856), or (3) the postural change examination data were not fully recorded or missing (n=548). After exclusions, the sample size was 13 340. The postural change examination has been shown to be an accurate marker of autonomic dysfunction in diabetic individuals.9 Therefore, participants with diabetes (n=1410) were excluded from all postural change analyses to avoid confounding due to any potential relationship between autonomic dysfunction and diabetes.10
Measurement of Blood Pressure Response to Change in
Posture
The measurement of postural change in blood pressure was
conducted by a trained and certified technician. Supine and standing
blood pressures were measured by using a Dinamap 1846 SX oscillometric
device and a dedicated microcomputer. Details of the measurement of
blood pressure can be found in ARIC Manual 11: Sitting Blood
Pressure and Postural Changes in Blood Pressure and Heart
Rate.11 Supine measurements of blood
pressure and heart rate were taken after the participant had lain on
the examination table during the ultrasound examination for a minimum
of 25 minutes. Heart rate was measured on a beat-to-beat basis, and
blood pressure was determined approximately every 30 seconds. The
computer collected these data for 2 minutes. After the supine data were
collected, the participant immediately stood and additional blood
pressure measurements were taken for 2 minutes at 
30-second
intervals to assess the cardiovascular response to
change in posture. Participants were instructed to bend their elbows
and to hold their hands over the midriff in a comfortable position to
prevent the cuff from sliding, to distract the participant, and to
place him or her in a standard and comfortable position.
The ARIC investigators tested the validity of the Dinamap early in the study and found the device to be accurate and to provide highly repeatable blood pressure measurements (within-person SD, 2.5 mm; reliability coefficient, 0.96).12
Statistical Methods
The response variable, postural change in SBP (SBP), was
defined as the average of all available supine SBP readings minus the
average of SBP readings on standing (excluding the first blood pressure
reading after standing). Although all analyses were also
performed on postural change in DBP (DBP), only results for SBP
are presented here. The response of DBP was quite similar to
that of SBP, although it was 4 mm Hg greater on average.
Figure 1 shows a positive linear
association (
=-3.9, ß=1.2, and r=0.62) between SBP
and DBP.
|
Frequency histograms of SBP based on all participants (and on all
race and gender groups) were prepared, accompanied by descriptive
statistics. A categorical measure of SBP was created by stratifying
the variable into deciles. We then examined the distribution of
various demographic variables across deciles of SBP. These
results were obtained in a logistic regression model with probability
of demographic characteristics or positive prevalent disease status as
outcome variables and with indicators of deciles of SBP as
predictor variables, controlling for age and seated SBP. These
models were then expanded with the addition of race and gender as
predictors plus interaction terms of race and gender with the
indicators of deciles of SBP. We then created 3 SBP strata based
on the decile cutoffs: decrease in SBP on standing (deciles 1 through
3), little or no change in SBP on standing (deciles 4 through 7), and
increase in SBP on standing (deciles 8 through 10). The cutoffs for
these groups were <-4.83, -4.83 to 4.80, and >4.80 mm Hg,
respectively. The relative percentage difference in study
variables, such as serum lipids and disease prevalence, between the
value in the increase in SBP group (or decrease in SBP group) and the
value in the no change in SBP group was calculated (±95% confidence
interval), adjusting the difference for age and seated SBP. All
analyses were performed using SAS version 6.09 (SAS
Institute).
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Table 1 provides baseline characteristics of the ARIC Study sample for whom
SBP measurements
were available (n=13 340). This sample was not significantly different
in age, race, and gender distributions, anthropometric variables,
or seated SBP from participants who had missing SBP data. Figure 2 shows a frequency histogram of SBP
for the entire sample. A normal distribution curve was superimposed on
the histogram using the baseline mean and SD. Although the average
response of SBP was near zero (mean, -0.45; median, 0.08), the
range was large (-63.2 to 54.3 mm Hg; SD, 10.8). Table 2 lists related descriptive statistics
for the entire sample and each race/gender group. Although the shape of
the distribution was similar for each group, there was a slight
positive shift of the distribution for black participants; this shift
was more pronounced among men than women.
|
|
|
Estimates of the percentages of demographic characteristics and disease
prevalence by deciles of SBP after adjustments for age and seated
SBP are shown in Table 3. The race
interactions in the model for an ABI of <0.9 were statistically
significant (P<0.05). The gender interactions in the model
for age of >60 years were also significant (P<0.01).
Therefore, age- and SBP-adjusted estimates of the percentage of
participants with an ABI of <0.9 are presented separately for
blacks and whites, and age- and SBP-adjusted estimates of the
percentage of participants >60 years old are presented
separately for men and women. It is evident from Table 3 that
participants who had a decrease in SBP on standing (ie, those in the
lowest deciles of SBP) were older and had a greater age-adjusted
prevalence of disease. In contrast, a larger proportion of blacks had
an increase in SBP on standing (ie, were in the highest deciles of
SBP) compared with whites. Black participants also had a different
pattern of peripheral arterial disease
prevalence (estimated by the proportion with an ABI of <0.9) across
the deciles of SBP. The distribution curve for ABI of <0.9 across
SBP deciles was U- or J-shaped for blacks, whereas a generally
decreasing trend across deciles of SBP was observed for whites. The
distribution curve for prevalence of hypertension was U-shaped across
the deciles of SBP.
|
Figure 3 shows the relative percentage
difference (±95% confidence interval) in the prevalence or level of
selected cardiovascular risk factors between
nondiabetic participants who showed a change (increase or decrease) in
SBP on standing and those with little or no change in SBP on standing.
The relative percentage difference was adjusted for age and seated SBP
with 2 exceptions. The percentage difference in the probability of age
>60 years was not adjusted for age, and hypertension and 8-year risk
of developing CHD were not adjusted for seated SBP. The black bars
represent comparisons for the selected
cardiovascular risk factors between participants with a
SBP of <-4.83 (deciles 1 through 3) and those with a SBP
between -4.83 and 4.80 (deciles 4 through 7); white bars
represent comparisons for risk factors between participants
with a SBP of >4.80 (deciles 8 through 10) and those in deciles 4
through 7. Error bars represent 95% confidence intervals for
point estimates. For example, the decrease in SBP group had 10.1% more
mean cigarette-years of exposure than the no change group. The 95%
confidence interval for the point estimate was 4.4% to 15.7%. The
increase in SBP group had 5.9% fewer mean cigarette-years of exposure
than the no change group (point estimate, -5.9%; 95% confidence
interval, -12.10 to 0.19).
|
Results from Figure 3 are similar to those in Table 3. Study participants who exhibited a decrease in SBP on standing were older and had more age-adjusted concomitant disease than their counterparts who had a relatively small change in SBP on standing. There were 35% more individuals older than 60 years of age among the decrease in SBP group (21.9% versus 15.4%). Also, there were 15% more hypertensives (36.7% versus 29.2%), 47% more participants with an ABI of <0.9 (3.9% versus 2.4%), and a 22% difference in prevalence of CHD (5.0% versus 4.0%) in the decrease in SBP group. There were significantly more (21%) blacks among those who had an increase in SBP on standing (28.1% versus 22.7%). All of these differences were statistically significant. Gender differences between groups were small.
Differences in anthropometric variables between groups were virtually zero, except for the 2.6% difference in body mass index (BMI, 27.8 versus 27.1kg/m2) for the increase in SBP group, which was statistically significant. The percentage difference for serum lipids between change and no change groups was also quite small. Participants in the decrease in SBP group had a 1.9% greater mean total cholesterol level (5.59 versus 5.48 mmol/L), a 2.8% higher mean LDL cholesterol level (3.59 versus 3.49 mmol/L), and a 4.3% greater mean triglycerides level (3.33 versus 3.18 mmol/L). Participants in the increase in SBP group had a 0.8% greater mean total cholesterol level (5.53 versus 5.48 mmol/L) and a 1.3% higher mean LDL cholesterol level (3.54 versus 3.49 mmol/L). All of these differences were statistically significant. There was a near-zero difference in fasting serum glucose level and a small but statistically significant difference in mean serum insulin level (5.6%) within the increase in SBP group (11.3 versus 10.7 µU/mL) and a small but statistically significant difference (3.6%) within the decrease in SBP group (11.1 versus 10.7 µU/mL).
Although there was virtually no difference in seated DBP between the groups, there was a significant 4% greater seated SBP within both the increase (122 versus 117 mm Hg) and decrease (122 versus 117 mm Hg) in SBP groups. Smoking, measured in cigarette-years of exposure, was also significantly greater (10.1%) among the decrease in SBP group (351 versus 317 cigarette-years). Both the increase (4.9% versus 4.7%) and decrease (5.0% versus 4.7%) in SBP groups had a 5% greater predicted risk of developing CHD after 8 years, which was statistically significant. The 8-year CHD risk equation was based on an analysis of Framingham Study data.13
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The usual cardiovascular changes that follow postural change from the supine to standing position are well established. Blood begins to pool in the venous system on standing. This causes a decrease in venous return and a resultant drop in cardiac output. Systemic blood pressure falls with cardiac output, so the baroreceptors in the carotid arch relax and induce sympathetic stimulation. This promotes vasoconstriction and increases heart rate, which stabilizes cardiac output at a level lower than when supine. Mean blood pressure is maintained by an increase in total peripheral resistance. Overall, the response to standing is usually a very slight reduction of SBP (<4 mm Hg) and slight elevation of SBP (<10 mm Hg).14 Our results indicate that the response of SBP to standing is normally distributed around a mean near zero. However, the range of the distribution is quite wide (±60 mm Hg). Furthermore, it appears that an individual's
SBP value (ie, their position within the distribution)
is associated with a number of disease states and common
cardiovascular risk factors. Large fluctuations in heart rate and blood pressure occur in the first 20 to 30 seconds of standing upright.14 In the ARIC protocol, the first standing blood pressure is measured after 30 seconds in the upright position. Therefore, this early response was not included in the data analysis. Readings obtained after 1 minute indicated a very slight overall mean reduction in SBP (-0.45), yet we also saw that some participants had large (>20 mm Hg) decreases or increases in SBP on standing. Age, hypertension, CHD, smoking, systolic blood pressure, and an ABI of <0.9 were associated with a fall in SBP on standing.
ß-Blockade blunts the response of the cardiovascular
system to stress and therefore may lead to misclassification of SBP
if the sickest individuals have suppressed responses. However, Mills
and Dimsdale15 performed a thorough meta-analysis
of 59 studies examining the effects of ß-blockade on
cardiovascular reactivity to a variety of stressors,
including postural change. They found that even though ß-blockade
does diminish the response of heart rate to stress, response of blood
pressure is unaffected. A more strenuous stressor (ie, exercise) is
required before ß-blockade affects the response of blood pressure. As
a precautionary measure, we reran our models for Figure 3
excluding all participants on ß-blockers. These exclusions did not
materially change the point estimates or the width of confidence
intervals.
The association of postural hypotension with increasing age is well documented.16 17 18 19 The initial stroke volume and cardiac output reductions usually seen in response to postural change are more marked with increasing age, and the rise in total peripheral resistance is much less than seen in younger adults. Possible explanations for this response in older individuals include a decline in the sensitivity of cardiac ß-adrenergic responses,20 reduced baroreceptor sensitivity,21 22 and elevated circulating plasma noradrenaline levels that attempt to compensate for reduced receptor sensitivity but may blunt the normal response of an increase in noradrenaline release on standing.23
A fall in SBP on standing was associated with hypertension, smoking, SBP, and an ABI of <0.9. The prevalence of CHD was greater among those with a decrease in SBP as well and was statistically significant. Results of laboratory investigations by Abelmann and Fareeduddin24 and Zambrano and Spodick25 indicate that individuals with cardiovascular disease have a blunted heart rate and ejection time response to orthostatic stress. Structural changes in the circulatory system resulting in less compliant vessels would contribute to a decrease in their ability to vasoconstrict as well as a reduction in the sensitivity of the baroreflex mechanism. Both conditions would inhibit the return of blood pressure to normal levels on standing. However, the role of autonomic dysfunction, which was not measured in this study, cannot be ruled out.
The response to postural change was similar in men and women, as seen in a previous study.7 These findings are also supported by MacLennan et al,6 who found no significant difference in the prevalence of postural hypotension between men and women. However, other studies reported a gender difference in the blood pressure response to standing.4 5 Our results are the first reported from a large community-based, biracial sample of adults.
Although many variables were associated with a decrease in blood pressure on standing, only race, SBP, insulin level, BMI, and 8-year predicted risk of CHD were significantly associated with an increase in blood pressure in our study. The data indicate that individuals who had an increase in blood pressure on standing may be younger, smoke less, have less CHD, and have a greater prevalence of ABI <0.9 than their counterparts, but none of these differences were significant. It appears that different mechanisms should be postulated for an increase versus a decrease in SBP on standing.
That blacks had a greater SBP response to standing than whites is
consistent with findings from reactivity
studies.26 Light and Sherwood27 and more
recently Sherwood and Hinderliter28 investigated the
underlying causes of this association and proposed 3 possible
mechanisms. First, blacks may have greater -adrenergic activity or
-receptor sensitivity than whites. This would induce a larger
vasoconstrictor response in the vascular beds. Second, blacks may have
less ß-adrenergic activity or ß-receptor sensitivity than whites.
This would induce less vasodilation in skeletal muscle and other
tissues. Third, early structural changes in the vasculature may
potentiate vasoconstrictive responses without altered
-receptor activity or sensitivity. Fourth, these effects may occur
together and jointly contribute to enhanced vasoconstriction.
The U-shaped association of seated SBP with SBP, although small (4%
greater in both the SBP increase and SBP decrease group), is
interesting. It is probable that different mechanisms are responsible
for the association in the 2 groups. There is some indication in the
literature that postural hypotension and decreases in blood pressure on
standing may be greater in individuals with elevated average blood
pressure.6 29 The most plausible explanation for this is
that the SBP level contributes to decreased baroreflex
capacity.22 However, several recent studies report an
association between elevated blood pressure and increased blood
pressure reactivity.30 31 Although we have no information
on previous blood pressure for our study participants, it is possible
that individuals with a negative SBP may have had elevated blood
pressure for some time, resulting in decreases in baroreceptor
sensitivity. In contrast, individuals with a positive SBP may have
only recently had increases in blood pressure, possibly influenced by
their high stress reactivity.
Both decreases and increases in SBP in response to posture change were associated with similar, statistically significant increases in the 8-year predicted risk of CHD. Although this remains tentative until confirmed by incidence data, these results suggest that changes in SBP, regardless of direction, may be useful indices of cardiovascular risk in this age group.
Certain limitations apply to this study. First, the timing and number of blood pressure measurements deserve some discussion. The Dinamap blood pressure recorder was in an automatic recording mode that measured SBP and DBP as frequently as possible in a 2-minute period. Although this maximizes the number of available blood pressure measurements, it has the drawback of increasing the variability in timing and number of measurements. Therefore, individual blood pressures are not directly comparable with respect to length of time since standing. Because different mechanisms control blood pressure response at specific time points in the first several seconds after standing,14 the varied measurement times prevent us from examining the specific mechanisms involved in the blood pressure response to change in posture. Instead, a measure of reactivity integrated over nearly 2 minutes of standing was calculated as the difference of the mean supine and mean standing blood pressure measurements.
Although ARIC is a population-based study, the overall participation rate was 65% for the field center examination. As in most epidemiological studies, individuals who agree to participate in the study are likely to select themselves into the cohort according to a variety of attributes. Participants may be more likely to be healthier and have a higher socioeconomic status than individuals in the communities from which they were sampled. If that is the case, the estimates of disease prevalence may be conservative and not necessarily reflective of the true rates in these 4 communities. The magnitude of this possible bias is unknown. Because most of the black participants were inducted at the Jackson, Miss, field center, the ability to make generalizations on the basis of our findings in blacks is limited. Finally, these are cross-sectional data. Therefore, the associations reported neither suggest causality nor establish a temporal relationship between any of the variables studied and postural change in blood pressure.
However, this study is the first to examine blood pressure response to postural change in a large community-based sample of black and white adults. Previous studies have been conducted with smaller samples that have not been community based, or the study participants were adolescents,32 or the investigators chose to report the prevalence of orthostatic hypotension instead of absolute change in blood pressure.33 The quality control procedures established in the ARIC Study have been described previously.8 These rigorous measures are designed to ensure that data are collected uniformly at each center and over time and are also applied to the measurement of postural change in blood pressure. Examinations were performed by trained and certified technicians. Each participant had at least 20 minutes of comfortable rest before the start of the postural change examination. A clinic setting can be a stressor itself and may artificially increase blood pressure and blood pressure reactivity, but experiments have shown that catecholamines return to basal levels after 20 minutes of supine rest.34
Conclusion
Our findings indicate the practicality and usefulness of the
postural change in blood pressure examination in an epidemiological
study. The response of blood pressure to change in posture may serve as
a tool at the population level for measuring a variety of mechanisms
related to cardiovascular morbidity. Of particular
interest is the difference in SBP between black and white
participants. This may partially explain the high prevalence of
hypertension among US blacks, which is nearly twice that of
whites.35 Analysis of the association of this
pressor response with incident cardiovascular diseases
should be performed.
|
Acknowledgments |
|---|
The ARIC Study is carried out as a multicenter collaborative study supported by contracts N01-HC-55015, N01-HC-55016, N01-HC-55018, N01-HC-55019, N01-HC-55020, N01-HC-55021, and N01-HC-55022 from the National Heart, Lung, and Blood Institute. We thank the ARIC participants and the staff at the ARIC field centers, Ultrasound Reading Center, and Coordinating Center.
Received March 2, 1998; first decision May 19, 1998; accepted December 30, 1998.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Sparrow D, Tifft CP, Rosner B, Weiss ST. Postural changes in diastolic blood pressure and the risk of myocardial infarction: the Normative Aging Study. Circulation. 1984;70:533–537.
2. Sparrow D, Rosner B, Vokonas PS, Weiss ST. Relation of blood pressure measured in several positions to the subsequent development of systemic hypertension: the Normative Aging Study. Am J Cardiol. 1986;57:218–221.[Medline] [Order article via Infotrieve]
3. Ventner CP, Joubert PH. The relevance of ethnic differences in hemodynamic responses to the head-up tilt maneuver to clinical pharmacological investigations. J Cardiovasc Pharmacol. 1985;7:1009–1010.[Medline] [Order article via Infotrieve]
4. Gotshall RW, Tsai PF, Bassett Frey MA. Gender-based differences to the cardiovascular response to standing. Aviat Space Environ Med. 1991;62:855–859.[Medline] [Order article via Infotrieve]
5. Schondorf R, Low PA. Gender related differences in the cardiovascular responses to upright tilt in normal subjects. Clin Auton Res. 1992;2:183–187.[Medline] [Order article via Infotrieve]
6.
MacLennan WJ, Hall MRP, Timothy JI. Postural
hypotension in old age: is it a disorder of the nervous system or of
blood vessels? Age Ageing. 1980;9:25–31.
7. Moore KI, Newton K. Orthostatic heart rates and blood pressures in healthy young women and men. Heart Lung. 1986;15:611–617.[Medline] [Order article via Infotrieve]
8.
The ARIC Investigators. The
Atherosclerosis Risk in Communities (ARIC) study:
design and objectives. Am J Epidemiol. 1989;129:687–702.
9. Ewing DJ, Martyn CN, Young RJ, Clark BF. The value of cardiovascular autonomic function tests: 10 years experience in diabetes. Diabetes Care. 1985;8:491–498.[Abstract]
10. Krolewski AS, Warram JH, Cupples A, Gorman CK, Szabo AJ, Christlieb AR. Hypertension, orthostatic hypotension and the microvascular complication of diabetes. J Chronic Dis. 1985;38:319–326.[Medline] [Order article via Infotrieve]
11. The ARIC Investigators. ARIC Manual 11: Sitting Blood Pressure and Postural Changes in Blood Pressure and Heart Rate. ARIC Coordinating Center, Department of Biostatistics, University of North Carolina. Chapel Hill, NC, 1987.
12. Mundt KA, Chambless LE, Burnham CB, Heiss G. Measuring ankle systolic blood pressure: validation of the Dinamap 1846 SX. Angiology. 1992;43:555–566.
13. Anderson KM, Wilson PWF, Odell PM, Kannel WB. An updated coronary risk profile: a statement for health professionals. Circulation.. 1991;83:357–363.
14. Borst C, van Brederode JFM, Wieling W, van Montfrans GA, Dunning AJ. Mechanisms of initial blood pressure response to postural change. Clin Sci. 1984;67:321–327.[Medline] [Order article via Infotrieve]
15.
Mills PJ, Dimsdale JE. Cardiovascular
reactivity to psychosocial stressors: a review of the effects of
beta-blockade. Psychosomatics. 1991;32:209–220.
16. Rodstein M, Zeman FD. Postural blood pressure changes in the elderly. J Chronic Dis. 1957;6:581–588.
17. Lipsitz LA, Storch HA, Minaker KL, Rowe JW. Intra-individual variability in postural blood pressure in the elderly. Clin Sci. 1985;69:337–341.[Medline] [Order article via Infotrieve]
18.
Williams BO, Caird FI, Lennox IM. Haemodynamic response
to postural stress in the elderly with and without postural
hypotension. Age Ageing. 1985;14:193–201.
19. Goldstein IB, Shapiro D. Cardiovascular response during postural change in the elderly. J Gerontol. 1990;45:M20–M25.
20. Kendall MJ, Woods KL, Wilkins MR, Worthington DJ. Responsiveness to ß-adrenergic receptor stimulation: the effects of age are cardioselective. Br J Clin Pharmacol. 1982;14:821–826.[Medline] [Order article via Infotrieve]
21.
Gribbin B, Pickering TG, Sleight P, Peto R. Effect of
age and high blood pressure on baroreflex sensitivity. Circ
Res. 1971;29:424–431.
22. Shimada K, Kitazumi T, Ogura H, Sadakane N, Ozawa T. Differences in age-independent effects of blood pressure on baroreflex sensitivity between normal and hypertensive subjects. Clin Sci. 1986;70:489–494.[Medline] [Order article via Infotrieve]
23. Lake CR, Ziegler MG, Coleman MG, Kopin IJ. Age adjusted plasma norepinephrine levels are similar in normotensive and hypertensive subjects. N Engl J Med. 1977;296:208–209.[Medline] [Order article via Infotrieve]
24. Abelmann WH, Fareeduddin K. Increased tolerance of orthostatic stress in patients with heart disease. Am J Cardiol. 1969;23:354–362.[Medline] [Order article via Infotrieve]
25.
Zambrano SS, Spodick DH. Comparative responses to
orthostatic stress in normal and abnormal subjects:
evaluation by impedance cardiography. Chest. 1974;65:394–396.
26.
Light KC, Obrist PA, Sherwood A, James S, Strogatz D.
Effects of race and marginally elevated blood pressure on
cardiovascular responses to stress in young men.
Hypertension. 1987;10:555–563.
27. Light KC, Sherwood A. Race, borderline hypertension, and hemodynamic responses to behavioral stress before and after beta-adrenergic blockade. Health Psychol. 1989;8:577–596.[Medline] [Order article via Infotrieve]
28. Sherwood A, Hinderliter AL. Responsiveness to alpha- and beta-adrenergic receptor agonists: effects of race in borderline hypertensive compared to normotensive men. Am J Hypertens. 1993;6:630–635.[Medline] [Order article via Infotrieve]
29.
Mader SL, Josephson KR, Rubenstein LZ. Low prevalence
of postural hypotension among community-dwelling elderly.
JAMA. 1987;258:1511–1514.
30.
Menkes MS, Matthews KA, Krantz DS, Lundberg U, Mead LA,
Qaqish B, Liang KY, Thomas CB, Pearson TA.
Cardiovascular reactivity to the cold pressor test as a
predictor of hypertension. Hypertension. 1989;14:524–530.
31.
Matthews KA, Woodall KL, Allen MT.
Cardiovascular reactivity to stress predicts future
blood pressure status. Hypertension. 1993;22:479–485.
32.
Tell GS, Prineas RJ, Gomez-Marin O. Postural changes in
blood pressure and pulse rate among black adolescents and white
adolescents: The Minneapolis Children's Blood Pressure Study.
Am J Epidemiol. 1988;128:360–369.
33.
Rutan GH, Hermanson B, Bild DE, Kittner SJ, LaBaw F,
Tell GS. Orthostatic hypotension in older adults: the
Cardiovascular Health Study. Hypertension. 1992;19:508–519.
34.
McCrory WW, Klein AA, Rosenthal RA. Blood pressure,
heart rate, and plasma catecholamines in normal and
hypertensive children and their siblings at rest and after standing.
Hypertension. 1982;4:507–513.
35.
Joint National Committee on Prevention, Detection,
Evaluation, and Treatment of High Blood Pressure, National High Blood
Pressure Education Program Coordinating Committee. The sixth report of
the Joint National Committee on Prevention, Detection, Evaluation and
Treatment of High Blood Pressure and the National High Blood Pressure
Education Program Coordinating Committee. Arch Intern Med. 1997;157:2413–2446.
This article has been cited by other articles:
 |
|
 |
|
  K. M. Rose, M. L. Eigenbrodt, R. L. Biga, D. J. Couper, K. C. Light, A. R. Sharrett, and G. Heiss Orthostatic Hypotension Predicts Mortality in Middle-Aged Adults: The Atherosclerosis Risk in Communities (ARIC) Study Circulation, August 15, 2006; 114(7): 630 - 636. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. E. North, K. M. Rose, I. B. Borecki, A. Oberman, S. C. Hunt, M. B. Miller, J. Blangero, L. Almasy, and J. S. Pankow Evidence for a Gene on Chromosome 13 Influencing Postural Systolic Blood Pressure Change and Body Mass Index Hypertension, April 1, 2004; 43(4): 780 - 784. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. B. Harrap, J. S. Cui, Z. Y. H. Wong, and J. L. Hopper Familial and Genomic Analyses of Postural Changes in Systolic and Diastolic Blood Pressure Hypertension, March 1, 2004; 43(3): 586 - 591. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. J. Thomas, K. Liu, D. R. Jacobs Jr, D. E. Bild, C. I. Kiefe, and S. B. Hulley Positional Change in Blood Pressure and 8-Year Risk of Hypertension: The CARDIA Study Mayo Clin. Proc., August 1, 2003; 78(8): 951 - 958. [Abstract] [PDF]
|
|
|
|
 |
|
 K. Kario, K. Eguchi, S. Hoshide, Y. Hoshide, Y. Umeda, T. Mitsuhashi, and K. Shimada U-curve relationship between orthostatic blood pressure change and silent cerebrovascular disease in elderly hypertensives: Orthostatic hypertension as a new cardiovascular risk factor J. Am. Coll. Cardiol., July 3, 2002; 40(1): 133 - 141. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. L. Eigenbrodt, K. M. Rose, D. J. Couper, D. K. Arnett, R. Smith, and D. Jones Orthostatic Hypotension as a Risk Factor for Stroke : The Atherosclerosis Risk in Communities (ARIC) Study, 1987-1996 Stroke, October 1, 2000; 31(10): 2307 - 2313. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. S. Pankow, K. M. Rose, A. Oberman, S. C. Hunt, L. D. Atwood, L. Djousse, M. A. Province, and D. C. Rao Possible Locus on Chromosome 18q Influencing Postural Systolic Blood Pressure Changes Hypertension, October 1, 2000; 36(4): 471 - 476. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||