(Circulation. 1998;98:2290-2295.)
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports |
Orthostatic Hypotension Predicts Mortality in Elderly Men
The Honolulu Heart Program
From the Honolulu Heart Program, Kuakini Medical Center, Honolulu (K.H.M., I.J.S., D.C., J.D.C.); the John A. Burns School of Medicine, University of Hawaii, Divisions of Clinical Epidemiology and Geriatrics, Honolulu (K.H.M., I.J.S., J.D.C.); the Honolulu Epidemiology Research Unit, Division of Epidemiology and Clinical Applications, the National Heart, Lung, and Blood Institute, Honolulu, Hawaii (C.M.B., D.S.S.); and the Epidemiology, Demography, and Biometry Program, the National Institute on Aging, Bethesda, Md (D.F.).
Correspondence to Kamal H. Masaki, MD, 347 North Kuakini St, HPM-9, Honolulu, HI 96817. E-mail kamal{at}hhp2.hawaii-health.com
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Abstract |
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Background—Population-based data are unavailable concerning the predictive value of orthostatic hypotension on mortality in ambulatory elderly patients, particularly minority groups.
Methods and Results—With the use of data from the Honolulu Heart
Program's fourth examination (1991 to 1993), orthostatic
hypotension was assessed in relation to subsequent 4-year all-cause
mortality among a cohort of 3522 Japanese American men 71 to 93 years
old. Blood pressure was measured in the supine position and after 3
minutes of standing, with the use of standardized methods.
Orthostatic hypotension was defined as a drop in
systolic blood pressure (SBP) of 
20 mm Hg or in
diastolic blood pressure of 10 mm Hg. Overall
prevalence of orthostatic hypotension was 6.9% and
increased with age. There was a total of 473 deaths in the cohort over
4 years; of those who died, 52 had orthostatic hypotension.
Four-year age-adjusted mortality rates in those with and without
orthostatic hypotension were 56.6 and 38.6 per 1000
person-years, respectively. With the use of Cox proportional hazards
models, after adjustment for age, smoking, diabetes mellitus, body mass
index, physical activity, seated systolic blood pressure,
antihypertensive medications, hematocrit, alcohol intake, and prevalent
stroke, coronary heart disease and cancer,
orthostatic hypotension was a significant independent
predictor of 4-year all-cause mortality (relative risk 1.64, 95% CI
1.19 to 2.26). There was a significant linear association between
change in systolic blood pressure from supine position to
standing and 4-year mortality rates (test for linear trend,
P<0.001), suggesting a dose-response relation.
Conclusions—Orthostatic hypotension is relatively uncommon, may be a marker for physical frailty, and is a significant independent predictor of 4-year all-cause mortality in this cohort of elderly ambulatory men.
Key Words: mortality • aging • men • blood pressure
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Introduction |
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The prevalence of orthostatic hypotension varies substantially, depending on the methods used for detection and the groups being studied. Most studies have been in selected populations referred to a clinic for evaluation of syncope or dizziness,1 in which prevalence estimates are relatively high (>30%).
Epidemiological data indicate that orthostatic hypotension
has a prevalence of 4% to 33% in community-dwelling elderly
populations,1 2 3 but measurement protocols often
affect such estimates. Prevalence of orthostatic
hypotension was defined as a drop in systolic blood pressure
(SBP) of 20 mm Hg from the supine position to standing at
baseline in the Systolic Hypertension in the Elderly
Project (SHEP) and varied from 5.3% (decline in SBP at both 1 and
3 minutes) to 17.3% (drop in SBP at either 1 or 3
minutes).4 The Cardiovascular
Health Study (CHS) measured orthostatic hypotension in
those 65 years of age by use of a similar methodology to the
present study.5 Prevalence of
orthostatic hypotension in this group of predominantly
white elderly men and women was 16.2% and increased with age.
It has been suggested that orthostatic hypotension may be a normal consequence of aging, but this has been disputed.6 Normal aging is associated with a reduction in baroreceptor sensitivity and decreased cardiac responsiveness to sympathetic stimulation.7 8 The elderly are more likely to have inadequate homeostatic mechanisms for maintenance of blood pressure in the standing position and are more sensitive to the effects of medications.7 8 One study of elderly patients showed that orthostatic hypotension was significantly associated with lower supine systolic blood pressure and lower supine cardiac index, suggesting that underlying diseases rather than age are a better marker of orthostatic hypotension.9 Another study suggested that a blunted sympathetic response in elderly hypertensive Japanese patients predisposed those with hypertension to orthostatic hypotension.10
There is some controversy about racial differences in orthostatic hypotension. CHS and SHEP showed that no significant difference exists in prevalence of orthostatic hypotension between races; these 2 studies were composed predominantly of white subjects and black subjects.4 5 There may be similar abnormalities in autonomic and sympathetic nervous system function in white subjects and black subjects with hypertension.11 However, a study of 2 rural biracial townships showed that white subjects had twice the prevalence of orthostatic hypotension than black subjects, and this difference was statistically significant.12 Adequate data in people of Japanese ancestry are unavailable.
There are few published data on orthostatic hypotension as
a predictor of mortality in community-dwelling elderly subjects. We
hypothesize that orthostatic hypotension is a measure of
physical frailty and predicts mortality. The data collected in the
fourth examination of the Honolulu Heart Program in 1991 to 1993
provide an opportunity to explore the predictive value of
orthostatic hypotension for 4-year all-cause mortality in a
well-characterized, population-based cohort of elderly Japanese
American men. Orthostatic hypotension is now defined as a
drop in SBP 20 mm Hg or a drop in diastolic
blood pressure (DBP) 10 mm Hg from the supine position to
standing.13 Although there is great variability
in definitions of orthostatic hypotension in the
literature, we chose the above consensus definition in this study,
particularly because of relevance to clinical practice.
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Methods |
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Study Population
The Honolulu Heart Program is a prospective epidemiological study of cardiovascular disease. Participants are men of Japanese ancestry living on the island of Oahu, Hawaii, in 1965, born between 1900 and 1919 (age 45 to 68 years at the time of the first examination). Eight thousand six men participated in the first examination between 1965 and 1968. Details of the selection process for the cohort were published previously.14 The entire cohort has undergone 5 examinations.
This report is based on the fourth examination of the cohort conducted in 1991 to 1993 and the ascertainment of mortality that was conducted after the fourth examination until December, 1995. During the fourth examination, 3741 men aged 71 to 93 years were examined (80% of survivors). Some data, augmented by telephone interviews, were obtained for 98% of survivors. For this analysis, all variables of interest were available in 3522 participants. The study was approved by the institutional review committee of Kuakini Medical Center, procedures followed were in accordance with institutional guidelines, and informed consent was obtained from all participants.
Data Collection
The fourth examination included demographic information, medical
and psychological questionnaires, assessment of cognitive function,
fasting blood tests and a 2-hour glucose tolerance test, seated blood
pressure, anthropometry, spirometry, and an ECG collected in a
standardized manner consistent with previous examinations of
this cohort.15 16 In addition,
orthostatic blood pressures and pulse rate were measured
(supine and after 3 minutes of standing) in 3522 participants.
Morbidity and mortality surveillance by the monitoring of hospital discharge records and death certificates has been performed since the beginning of the study. For this report, mortality data were accumulated through December 1995. Data collection is believed to be essentially complete for all-cause mortality. Attrition in this cohort is known to be very small; at the fourth examination, only 5 men were lost to follow-up. Only all-cause mortality is used in this analysis because cause-specific mortality data are not yet available for this time period.
Measurement of Orthostatic Blood Pressures
Blood pressures were measured with a standard mercury
sphygmomanometer with a standardized protocol. Supine measurements were
taken after at least 15 minutes of rest. Standing measures were taken
after 3 minutes of standing. On standing, participants were asked
whether they were feeling any dizziness, faintness, or
light-headedness, and the examiner noted whether this was transient or
nontransient. The procedure was aborted for safety reasons if
necessary; this occurred very infrequently.
Definition of Orthostatic Hypotension
Orthostatic hypotension was defined as a drop in SBP
of 20 mm Hg from the supine to the standing position at 3
minutes or a drop in DBP of 10 mm Hg on standing, or
both.13
Measurement of Other Key Variables
Covariates were selected because of their potential relation
with either orthostatic hypotension or with mortality. We
used 2 categories of smoking status, current and past, compared with
never-smokers. Diabetes mellitus was defined by history (as told to the
participant by a physician), by taking medications (insulin or oral
hypoglycemics), or by fasting glucose 140 mg/dL, or by 2-hour
postload glucose 200 mg/dL.17 Body mass index
(BMI) was defined as weight in kilograms divided by height in meters
squared. Physical activity index was based on one used in
Framingham18 and the Honolulu Heart
Program,19 which consists of multiplying the
approximate oxygen consumption of five different levels of activity
with the reported usual numbers of hours a day engaged in that
activity. Use of antihypertensive medications was determined by direct
observation; participants were instructed to bring in all medications
taken in the previous 2 weeks. Serum lipids were not associated with
orthostatic hypotension and were not used in this
analysis.
Frailty Measures
Correlations of orthostatic hypotension with other
frailty measures were calculated. These included forced expiratory
volume in 1 second (FEV1), timed 10-foot walk,
and hand grip strength. Details about how these were measured have been
published previously.20 21
Data Analysis
Subjects were divided into those with and those without
orthostatic hypotension as defined above. Age-adjusted
4-year mortality rates, expressed per 1000 person-years of follow-up,
were calculated according to orthostatic hypotension
status. Three separate Cox proportional hazards models were considered
to assess the association between orthostatic hypotension
and mortality. The first adjusted for age alone. The second model
adjusted for age, current and past smoking, diabetes mellitus, body
mass index, physical activity index, SBP, antihypertensive medications,
hematocrit, and alcohol intake. A third model included the above
variables as well as prevalent coronary heart disease,
stroke, and cancer at the fourth examination.
The association between orthostatic hypotension and 4-year mortality rates in healthy men without chronic disease was also examined. Therefore the above analyses were repeated, excluding men with prevalent coronary heart disease, stroke, or cancer at the fourth examination. These chronic conditions are known to be the 3 most frequent causes of death in this cohort.22
The dose-response relations of mortality with orthostatic change in SBP and DBP were studied separately, by dividing participants into 6 groups on the basis of change in SBP from supine position to standing and 6 groups based on change in DBP from supine to standing. Tests for linear trend were performed, adjusting only for age. For DBP, because test for linear trend was not significant, the first 4 groups of change in DBP from supine position to standing were grouped together and compared with the last 2 groups.23
All statistical analyses were done with SAS software (SAS Institute).
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Results |
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The overall prevalence of orthostatic hypotension in this cohort was 6.9%. Prevalence of orthostatic hypotension increased with age, from 5.1% in those 71 to 74 years of age to 6.3% in those 75 to 79 years of age, to 9.2% in those 80 to 84 years of age, and 10.9% in those
85 years of
age (Figure 1
).
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The follow-up period was defined as the time between measurement of
orthostatic hypotension at the fourth examination (1991 to
1993) and December 1995. There was a total of 473 deaths in the entire
cohort over this time period; of those who died, 52 had
orthostatic hypotension at the fourth examination and 421
did not have orthostatic hypotension (Table 1). Those with
orthostatic hypotension survived a mean of 3.19 years after
examination 4 (range 0 to 4.75 years), whereas those without
orthostatic hypotension survived a mean of 3.37 years
(range 0 to 4.83 years). The unadjusted 4-year mortality rate was 1.8
times greater in men with orthostatic hypotension compared
with those without orthostatic hypotension (67.2 and 38.2
per 1000 person-years, respectively). After adjustment for age, 4-year
mortality rates were 56.6 per 1000 person-years in those with
orthostatic hypotension compared with 38.6 per 1000
person-years in those without orthostatic hypotension.
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Kaplan-Meier survival analysis according to
orthostatic hypotension status showed that those with
orthostatic hypotension had a significantly lower 4-year
survival compared with those without orthostatic
hypotension (P=0.0001) (Figure 2).
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Three separate Cox proportional hazards models were analyzed
with mortality as the end-point (Table 2). In the first model, the relative risk
(RR) for all-cause mortality associated with orthostatic
hypotension was 1.56 (95% CI=1.17 to 2.09) after adjustment for age
alone. Adjustment for other factors known to influence mortality (model
2) did not appreciably alter the relative risk (RR=1.61; 95% CI=1.17
to 2.22). Further adjustment for prevalent coronary heart
disease, stroke, and cancer also did not attenuate this association
(RR=1.64; 95% CI=1.19 to 2.26). Thus in all 3 models,
orthostatic hypotension was a significant independent
predictor of 4-year mortality.
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In addition, age, current and past smoking status, diabetes mellitus,
alcohol intake, prevalent coronary heart disease, and cancer
were also significantly positively associated with 4-year mortality,
whereas BMI, physical activity index, and hematocrit were significantly
negatively associated (Table 2
). There was no significant association
between 4-year mortality rate and seated SBP, use of antihypertensive
medications, and prevalent stroke.
On the basis of previous follow-up,22 the most common causes of death in the entire cohort are known to be cancer, coronary heart disease, and stroke. To avoid the potential influence of these prevalent diseases on the association of orthostatic hypotension with mortality, Cox proportional hazards models 1 and 2 were repeated, excluding men with prevalent cancer, coronary heart disease, or stroke at this examination. Adjusted for age (model 1), RR for mortality associated with orthostatic hypotension was 1.74 (95% CI=1.21 to 2.49); adjusting for age and risk factors (model 2), RR for mortality was 1.80 (95% CI=1.22 to 2.65). Thus even when subjects with the 3 most common prevalent diseases associated with mortality were excluded, orthostatic hypotension remained a significant independent predictor of 4-year mortality; this association was slightly stronger than without exclusions.
Because the definition of orthostatic hypotension is
somewhat arbitrary, we decided to examine the dose-response relation of
mortality with orthostatic change in SBP and DBP
separately. We divided participants into 6 groups on the basis of
change in SBP from the supine position to standing, starting with a
change 
-20 mm Hg, with increments of 10 mm Hg,
up to a change of >20 mm Hg. There was a significant
age-adjusted linear association between change in SBP from the supine
position to standing and 4-year mortality rate (test for linear trend,
P<0.001) (Figure 3).
Similarly, we divided participants into 6 groups on the basis of change
in DBP from the supine position to standing, starting with a change
-10 mm Hg, with increments of 5 mm Hg, up to a
change of >10 mm Hg. The age-adjusted test for linear trend
was not significant (P=0.075). However, when the first 4
groups of change in DBP from supine position to standing were grouped
together (-10 to 5 mm Hg), there was a significant
difference in 4-year mortality when compared with those in the last 2
groups of change, that is, change in DBP >5 mm Hg
(P=0.011) (Figure 3).
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We repeated Cox proportional hazards model 3 (adjusting for age, risk factors, and prevalent diseases) separately for those with only systolic orthostatic hypotension and those with only diastolic orthostatic hypotension. For systolic orthostatic hypotension, RR for mortality was 1.80 (95% CI=1.17 to 2.75), and for diastolic orthostatic hypotension, RR for mortality was 1.52 (95% CI=1.01 to 2.29), again demonstrating a stronger effect of systolic changes in blood pressure on mortality.
To examine the possibility that orthostatic hypotension is
associated with mortality because it is a marker of overall physical
frailty, we determined age-adjusted mean levels of several indicators
of frailty (timed 10-foot walk, hand grip strength, and
FEV1) by orthostatic status.
Orthostatic hypotension was significantly associated with
longer timed 10-foot walk (4.79 vs 4.31 seconds, P=0.005),
weaker hand grip strength (28.25 vs 30.03 kg, P=0.0001), and
lower FEV1 (1.95 vs 2.06 L/s, P=0.001)
after adjustment for age (Table 3). When
Cox proportional hazards model 3 was repeated including the 3 frailty
measures, the association between orthostatic hypotension
and mortality remained significant (RR 1.47, 95% CI=1.01 to 2.12),
although the strength of the association was somewhat weaker.
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Discussion |
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In this prospective study of elderly Japanese American men, we found a significant increase in the risk of 4-year all-cause mortality associated with orthostatic hypotension. This relation persisted at a highly significant level even after adjustment for a number of potential confounders and prevalent diseases such as cancer, coronary heart disease, and stroke. These data are consistent with those from a younger group of subjects with diastolic hypertension in the Hypertension Detection and Follow-Up Program (HDFP). The HDFP showed that systolic orthostatic hypotension was a significant predictor of 5-year mortality rates in young and middle-aged adults.24 For each mm Hg change in SBP, the odds ratio for mortality was 1.02 (P<0.05). However, when relative weight was added to the multiple logistic model, this association was no longer significant and there was an interaction between systolic orthostatic hypotension and diabetes in subjects in HDFP. In the HDFP, orthostatic change in DBP was not associated with mortality rates. In contrast, in the older Japanese men described here, even after adjustment for BMI, orthostatic hypotension continued to be a significant predictor of mortality. We did not observe an interaction between orthostatic hypotension and diabetes. In our study, the RR of all-cause mortality increases by 18% for every 10 mm Hg decrease in SBP from the supine position to standing.
To date, there has been only 1 small published study of the relation of orthostatic hypotension and mortality in elderly patients. A Finnish longitudinal analysis of 480 elderly subjects showed that neither change in SBP nor change in mean blood pressure were associated with mortality, but change in DBP was significantly associated with 10-year mortality.25
In the current study, the risk of death varies when using different definitions of orthostatic hypotension. We saw a significant linear dose-response relation between orthostatic change in SBP and mortality, whereas a threshold effect was seen with orthostatic change in DBP >5 mm Hg. With the use of the consensus definition of orthostatic hypotension that combines changes in SBP and DBP,13 some important information may be lost. It is possible that changes in SBP and DBP measure different aspects of blood pressure regulation and may be associated with different risk outcomes. In this population, there is an increase in mortality rate seen at lower levels of change in blood pressure than the consensus definition. On the basis of these findings, we suggest that a better definition of orthostatic hypotension in this cohort is a decrease in SBP of >10 mm Hg or a decrease in DBP of >5 mm Hg, from the supine position to standing in terms of its relation to subsequent mortality. Obviously, the consensus statement definition should continue to be used for the clinical diagnosis and management of orthostatic hypotension.
One of the limitations of this study is the lack of data on cause-specific mortality, although all-cause mortality may be a more reliable indicator in older populations in which cause of death is often multiple or unclear. The data reported here can only be generalized to an ambulatory male population because orthostatic hypotension was not measured in most subjects who were examined in the home or in nursing homes, and there were no women in the cohort. Thus the prevalence of orthostatic hypotension reported here is likely to be an underestimate. Future research should confirm these findings in other populations as well as assess other outcomes: cause-specific mortality, morbidity, independence, and physical functioning.
As in other epidemiological studies,4 5 prevalence of orthostatic hypotension in this population increased with age. However, the prevalence estimates of orthostatic hypotension in our subjects are lower than those reported in other epidemiological studies. This may be partly explained by a lower prevalence of many chronic diseases in this population.26 Another possible explanation is ethnic/genetic differences. Because there are no epidemiological data available from other Japanese populations, this question deserves further study. In addition, the intraindividual variability of blood pressure itself may affect prevalence data. An Italian study of elderly outpatients measured orthostatic hypotension at 2 visits 7 days apart, only one third of subjects had the same blood pressure at both visits.27 Another study of symptomatic elderly with documented orthostatic hypotension showed that in almost one third of patients orthostatic hypotension was not reproducible at a second visit, particularly if measurements were taken in the afternoon.28
There is debate concerning the causes of asymptomatic orthostatic hypotension in the elderly. Some believe that it is a normal accompaniment of aging reflecting baroreceptor dysfunction and decrease in responsiveness to sympathetic stimulation, whereas others claim that underlying disease or the use of medications may be more important7 8 9 or that it may be due to multiple rather than single causative factors.2
Some epidemiological studies have showed that orthostatic hypotension is a risk factor for falls5 and syncope,29 whereas others have not.30 31 One study suggested that assessment of dizziness on standing may be more important as a predictor of functional status, falls, and syncope than measuring postural change in blood pressure in elderly women.32 Others report a relation between use of antihypertensive medications and orthostatic hypotension8 33 ; this relation was not seen in our analyses.
We did find a statistically significant association between orthostatic hypotension and several frailty measures, including timed 10-foot walk, hand grip strength, and FEV1. When these 3 frailty measures were added to the Cox proportional hazards model 3 (adjusted for age, risk factors, and prevalent disease), orthostatic hypotension remained a significant predictor of mortality.
These results suggest that orthostatic hypotension may be a marker for a general lessening of physical strength in this cohort. It also suggests that physical frailty is a harbinger of death in these subjects. Frailty is considered to be the result of the effects of age, disease, and disuse, which cumulatively cause a reduction in physiological reserve.34 35 36 Orthostatic hypotension is easy to measure in clinical practice and can thus be a useful tool to screen for physical frailty in combination with other measures. It may be important to identify such frail elderly individuals to target interventions designed to prevent further decline. As life expectancy in the United States continues to increase, particularly for the "old-old" (those >85 years old), screening community living elderly patients with this simple, inexpensive test of physical frailty may have important public health implications.
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Acknowledgments |
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This research was supported by contract N01-HC-05102 from the National Heart, Lung, and Blood Institute, contract N01-AG-4-2149 from the National Institute on Aging, National Institutes of Health, Bethesda, Md, and grant HIGS-16-97 from the American Heart Association Hawaii Affiliate.
Received March 5, 1998; revision received July 24, 1998; accepted August 13, 1998.
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 G. Mancia and G. Grassi Orthostatic hypotension and cardiovascular risk: defining the epidemiological and prognostic relevance Eur. Heart J., September 3, 2009; (2009) ehp389v1. [Full Text] [PDF]
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 M. L. Mendu, G. McAvay, R. Lampert, J. Stoehr, and M. E. Tinetti Yield of Diagnostic Tests in Evaluating Syncopal Episodes in Older Patients Arch Intern Med, July 27, 2009; 169(14): 1299 - 1305. [Abstract] [Full Text] [PDF]
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 C. Mussi, A. Ungar, G. Salvioli, C. Menozzi, A. Bartoletti, F. Giada, A. Lagi, I. Ponassi, G. Re, R. Furlan, et al. Orthostatic Hypotension As Cause of Syncope in Patients Older Than 65 Years Admitted to Emergency Departments for Transient Loss of Consciousness J Gerontol A Biol Sci Med Sci, July 1, 2009; 64A(7): 801 - 806. [Abstract] [Full Text] [PDF]
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 A. Lipp, P. Sandroni, J. E. Ahlskog, R. D. Fealey, K. Kimpinski, V. Iodice, T. L. Gehrking, S. D. Weigand, D. M. Sletten, J. A. Gehrking, et al. Prospective Differentiation of Multiple System Atrophy From Parkinson Disease, With and Without Autonomic Failure Arch Neurol, June 1, 2009; 66(6): 742 - 750. [Abstract] [Full Text] [PDF]
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J. T. Groothuis, D. H. J. Thijssen, M. Kooijman, R. Paulus, and M. T. E. Hopman Attenuated peripheral vasoconstriction during an orthostatic challenge in older men Age Ageing, November 1, 2008; 37(6): 680 - 684. [Abstract] [Full Text] [PDF]
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 C. L. Sauder, E. E. Conboy, S. A. Chin-Sang, and C. A. Ray Otolithic activation on visceral circulation in humans: effect of aging Am J Physiol Renal Physiol, October 1, 2008; 295(4): F1166 - F1169. [Abstract] [Full Text] [PDF]
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 D Gupta and M D Nair Neurogenic orthostatic hypotension: chasing "the fall" Postgrad. Med. J., January 1, 2008; 84(987): 6 - 14. [Abstract] [Full Text] [PDF]
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 M. W. Ramsey, B. J. Behnke, R. D. Prisby, and M. D. Delp Effects of aging on adipose resistance artery vasoconstriction: possible implications for orthostatic blood pressure regulation J Appl Physiol, November 1, 2007; 103(5): 1636 - 1643. [Abstract] [Full Text] [PDF]
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J. E Naschitz and I. Rosner Orthostatic hypotension: framework of the syndrome Postgrad. Med. J., September 1, 2007; 83(983): 568 - 574. [Abstract] [Full Text] [PDF]
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 A. V. Chobanian Isolated Systolic Hypertension in the Elderly N. Engl. J. Med., August 23, 2007; 357(8): 789 - 796. [Full Text] [PDF]
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 K. D. Monahan Effect of aging on baroreflex function in humans Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2007; 293(1): R3 - R12. [Abstract] [Full Text] [PDF]
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 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]
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J E Naschitz, G Slobodin, N Elias, and I Rosner The patient with supine hypertension and orthostatic hypotension: a clinical dilemma. Postgrad. Med. J., April 1, 2006; 82(966): 246 - 253. [Abstract] [Full Text] [PDF]
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 L. C. M. Vloet, R. E. Pel-Little, P. A. F. Jansen, and R. W. M. M. Jansen High Prevalence of Postprandial and Orthostatic Hypotension Among Geriatric Patients Admitted to Dutch Hospitals J. Gerontol. A Biol. Sci. Med. Sci., October 1, 2005; 60(10): 1271 - 1277. [Abstract] [Full Text] [PDF]
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 O. Sasaki, H. Nakahama, S. Nakamura, F. Yoshihara, T. Inenaga, M. Yoshii, S. Kohno, and Y. Kawano Orthostatic hypotension at the introductory phase of haemodialysis predicts all-cause mortality Nephrol. Dial. Transplant., February 1, 2005; 20(2): 377 - 381. [Abstract] [Full Text] [PDF]
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 L M Allcock, K Ullyart, R A Kenny, and D J Burn Frequency of orthostatic hypotension in a community based cohort of patients with Parkinson's disease J. Neurol. Neurosurg. Psychiatry, October 1, 2004; 75(10): 1470 - 1471. [Abstract] [Full Text] [PDF]
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 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]
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A. V. Chobanian, G. L. Bakris, H. R. Black, W. C. Cushman, L. A. Green, J. L. Izzo Jr, D. W. Jones, B. J. Materson, S. Oparil, J. T. Wright Jr, et al. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure Hypertension, December 1, 2003; 42(6): 1206 - 1252. [Abstract] [Full Text] [PDF]
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 S. Castellani, R. Paniccia, C. Di Serio, G. La Cava, L. Poggesi, S. Fumagalli, G. F. Gensini, and G. G. Neri Serneri Thromboxane inhibition improves renal perfusion and excretory function in severe congestive heart failure J. Am. Coll. Cardiol., July 2, 2003; 42(1): 133 - 139. [Abstract] [Full Text] [PDF]
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K. D. Monahan and C. A. Ray Vestibulosympathetic reflex during orthostatic challenge in aging humans Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2002; 283(5): R1027 - R1032. [Abstract] [Full Text] [PDF]
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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]
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 R. J. Havlik, D. J. Foley, B. Sayer, K. Masaki, L. White, and L. J. Launer Variability in Midlife Systolic Blood Pressure Is Related to Late-Life Brain White Matter Lesions: The Honolulu-Asia Aging Study Stroke, January 1, 2002; 33(1): 26 - 30. [Abstract] [Full Text] [PDF]
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Task Force on Syncope, European Society of Cardiol, M Brignole, P Alboni, D Benditt, L Bergfeldt, J.J Blanc, P.E Bloch Thomsen, J.G van Dijk, A Fitzpatrick, S Hohnloser, et al. Guidelines on management (diagnosis and treatment) of syncope Eur. Heart J., August 1, 2001; 22(15): 1256 - 1306. [Abstract] [PDF]
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 C. A. Ray Interaction of the vestibular system and baroreflexes on sympathetic nerve activity in humans Am J Physiol Heart Circ Physiol, November 1, 2000; 279(5): H2399 - H2404. [Abstract] [Full Text] [PDF]
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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]
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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]
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 G. Dangas, J. R. Laird Jr, L. F. Satler, R. Mehran, G. S. Mintz, G. Larrain, A. J. Lansky, L. Gruberg, E. M. Parsons, R. Laureno, et al. Postprocedural Hypotension after Carotid Artery Stent Placement: Predictors and Short- and Long-term Clinical Outcomes Radiology, June 1, 2000; 215(3): 677 - 683. [Abstract] [Full Text]
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 Other Articles Noted Evid. Based Nurs., October 1, 1999; 2(4): 105 - 112. [Full Text]
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C. A. Ray and K. D. Monahan Aging Attenuates the Vestibulosympathetic Reflex in Humans Circulation, February 26, 2002; 105(8): 956 - 961. [Abstract] [Full Text] [PDF]
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