Postural hypertension is a condition in which the blood pressure rises abnormally during standing. The aim of this study is to determine the prevalence of postural hypertension and its association with morbidity and subsequent mortality. At the fourth examination (1991-1993) of the Honolulu Heart Program longitudinal cohort, 3741 Japanese-American men aged 71-93 were examined. Prevalence of postural hypertension in this cohort was 39%. Although there was a high prevalence of postural hypertension in this cohort, its clinical significance is questionable as there were no significant correlations with morbidity and subsequent mortality

Blanchette, Patricia L.

eVols at University of Hawaii at Manoa

Postural Hypertension in Elderly Men-The Honolulu Heart ProgramKannayiram Alagiakrishnan MD*, Kamel Masaki MD**, Irwin Schatz MD***,J. David Curb MD, MPH****, Patricia Blanchette MD, MPH*****AbstractPostural hypertension is a condition in which the blood pressurerises abnormally during standing. The aim of this study is todetermine the prevalence ofpostural hypertension and its association with morbidity and subsequent mortality.At the fourth examination (1991-1993) of the Honolulu Heart Program longitudinal cohort,3741 Japanese-American men aged 7 1-93 were examined. Prevalence of postural hypertension in this cohort was 39%. Althoughthere was a high prevalence of postural hypertension in this cohort,its clinical significance is questionable as there were no significantcorrelations with morbidity and subsequent mortality.IntroductionPostural hypertension or orthostatic hypertension is a condition inwhich the blood pressure rises during standing. There are only a fewcase reports and studies documenting this condition and it is not wellrecognized. The definition of orthostatic hypertension is not yetstandardized. One study defines it as an increase in diastolic bloodpressure from below 90 to above 90mm Hg on standing.’ Anotherstudy defines it as an increase in systolic blood pressure by 10 mmHg or more by the tilt test,2 and another by marked hypertension inthe upright position with normal pressure in the supine position.3Kozo et al define it as an elevation of systolic BP >20mm Hg at 2minutes after standing.4*FelIow in Geriatric Medicine, Geriatric Medicine Program, John A. Burns School ofMedicine, University of Hawaii, Honolulu, Hawaii 96817.**Assoc Professor of Medicine, Geriatric Medicine Program, John A. Burns School ofMedicine, University of Hawaii, Honolulu, Hawaii 96817.***Professor of Medicine, John A. Burns School of Medicine, University of Hawaii,Honolulu, Hawaii 96817.****Professor of Medicine and Epidemiology, Geriatric Medicine Program, John A. BurnsSchool of Medicine, University of Hawaii, Honolulu, Hawaii 96817.Professor of Medicine and Public Health, Division of Geriatric Medicine, John A.Burns School of Medicine, University of Hawaii, Honolulu, Hawaii 96817.Correspondence to:Kannayiram Alagiakrishnan MD347 N. Kuakini Street. HPM 9 Floor,Honolulu, Hawaii 96817Phone: 808-523-8461Fax: 808-528-1897e-mail: kannayir@hawaii.eduPostural hypertension was first reported by Schneider et al in1922, in 4.2% of 2000 apparently healthy airmen examined afterWorld War J5 The prevalence of postural hypertension varies. Inone study, orthostatic hypertension was found in 71% (15 of 21patients) of borderline hypertensives, while another study had aprevalence 8.7% (29 of 334)4 Streeten et a! showed that as manyas 10% of some hypertensive populations may have orthostatichypertension.’Various mechanisms for postural hypertension have been suggested. One study showed that decreased venous return causesdecreased cardiac output, increased sympathetic stimulation andexcessive arteriolar constriction.’ Other studies showed that patients have increased vascular adrenergic activity6 and excessiveincrease in peripheral vascular resistance during tilting.7 8 Therefore, the exact pathogenic mechanisms of postural hypertension arenot clear, even though abnormalities of autonomic nervous systemactivity may be etiologically related.Various studies have looked at the clinical significance ofpostural hypertension. One study demonstrated that neurobehavi oralfunctioning and activities of daily living were significantly loweredin people with postural hypertension. Additionally, moreperiventricular hyperintensities or advanced leukoaraiosis wereseen on MRI of the brain when compared with a normotensivegroup.3 In another study, an association with extreme dipping(marked fall in nocturnal blood pressure) and cerebrovasculardisease has been demonstrated.2’9The aim of this analysis is to determine the prevalence of posturalhypertension in elderly men of the Honolulu Heart Program longitudinal cohort and to study the association with morbidity andsubsequent mortality.MethodsStudy PopulationThe Honolulu Heart Program is a longitudinal cohort study ofcardiovascular disease which began in 1965. Participants were menof Japanese ancestry, living on the island of Oahu, Hawaii in 1965,and born between 1900 and 1919. The first examination wasperformed between 1965 —1968 and 8006 men were examined. Theentire cohort has undergone 6 examinations so far. At the fourthexamination (1991-1993), 3741 men aged 7 1-93 years were examined, representing 80% of the survivors. For this analysis. allvariables of interest were available in 3522 participants. The studywas approved by the institutional review board of Kuakini MedicalCenter, and procedures followed were in accordance with institutional guidelines.HAWAH MEOCAL JOURNAL, VOL 59, FEBRUARY 200048Data CollectionThe fourth examination included demographic questions, medicaland psychosocial interview assessment of cognitive function, fasting blood and 2hour GTT. EKG. anthropometry. blood pressures(seated, ankle-arm ratio, orthostatics). Diabetes mellitus was defined by history (as told to the participant by a physician).or byfasting glucose 140 mg/dl or by 2 hour post prandial glucose 200mg/dl. Body mass index (BMI ) was calculated as weight (kg)!height (square meter).Morbidity and mortality surveillance by the monitoring of hospital discharge records and death certificates has been performed sincethe beginning of the study. For this report, mortality data wereaccumulated through December 1997. Data collection is believed tobe essentially complete for all cause mortality. Attrition in thiscohort is known to be very small; at the fourth examination, only 5men were lost to follow-up.Seated blood pressure was measured twice with a mercury sphygmomanometer using a standardized protocol. Supine measurementstaken after at least 15 minutes of supine rest. Standing measurementswere taken 3 minutes after standing.Definition of Postural HypertensionNormally on standing , there is a fall in systolic BP of 10mm Hg anda rise in diastolic BP of 2-3 mm Hg)° Postural hypertension is asyndrome in which the blood pressure (systolic or diastolic) rises by10 mm Hg or more on standing.Statistical MethodsSubjects with postural hypotension were excluded. We comparedsubjects with and without postural hypertension. We studied crosssectional associations of postural hypertension with age , BMI,smoking status, seated hypertension. abnormal ankle brachial index,diabetes, prevalent CHD, CVA and cognitive impairment, andsubsequent 6 year mortality.Data are expressed as means ± standard deviation (SD) and aspercentages .Univariate and multivariate logistic regression modelswere used to calculate Odds Ratios(OR) and 95% confidenceinterval (CI) to study cross-sectional associations. Cox proportionalhazards models were used to study the association with subsequent6 —year mortality.ResultsPrevalence of postural hypertension in this cohort was 39%. Prevalence of postural hypertension was 38% between 71-74 years of age,38.9% between 75-79 years of age, 41.5% between 80-84 ofage, and37.5%in persons over 85 years of age.(Fig.1). There was no significant difference in prevalence rates between the 5 year age groups(chi square p= 0.522). The baseline characteristics of variables bypostural hypertension status are shown in Tablel. There was asignificant difference in prevalence of seated hypertension. 76.8%of those with postural hypertension had seated hypertension compared to 73% in those without postural hypertension. BMI is alsosignificantly associated with postural hypertension. There were nosignificant differences among those with and without posturalhypertension among variables like age, smoking status, abnormalankle- brachial index (ABI), prevalent diabetes, prevalent CHD,prevalent CVA, and cognitive impairment.Univariate logistic regression models showed that postural hypertension was significantly associated with seated hypertension (OR1.23, 95% CI 1.04-1.45) and BMI (OR 1.03. 95%C1 1.002-1.05).There were no significant associations with age, prevalent coronaryartery disease, stroke, cognitive impairment. diabetes, abnormalankle- brachial index and smoking status. (Table 2).We performed multivariate logistic regression analysis (Table 3)with postural hypertension as a dependent variable and age. BMIand seated hypertension as independent variables. Postural hypertension was significantly associated with BMI (OR 1.025,95% CI1.002-1050) and seated hypertension (OR 1.192, 95% CI 1.011-1.405), but not with age.Two separate Cox proportional hazards models were performedwith 6 year all cause mortality as the end point (Table 4). Posturalhypertension showed no significant association with 6 year all causeHAWAII MEDICAL JOURNAL, VOL 59, FEBRUARY 2000Figure 1.— Prevalence of postural hypertension by 5-year age groupsin the Honolulu Heart Program Cohort (n-3522). Chi square p-O.522.504085+ overallageTable 1.— Baseline characteristics of variables by Postural Hypertension StatusVariables Postural Htn Postural HtnPresent AbsentAge (years) 77.6 (+4.4) 77.5 (+4.5)BMI 23.4 (+3.1) 23.7 (+3.2)Smoking Status 7.41% 7.60%Seated Htn.* 76.84% 73%Abnormal ABI 11.89% 13.20%Prevalent Diab. 28.17% 28.10%Prevalent CHD 17.45% 15.90%Prevalent CVA 5.24% 4.50%Cognitive Imp. 12.28% 12.40%Continuous Variables- Means (± SD), t testsCategoncal Vaables-Percentages, chi square analysis*p <0.05Htn.= HypertensionDiab.= Diabetes49mortality. In the first model, the relative risk (RR) for all causemortality associated with orthostatic hypertension was 0.95 (95%CI0.82- 1.10) after adjustment for age alone. Adjustment for otherfactors like seated hypertension and BMI (model 2) also did notappreciably alter the results (RR0.97; 95%CI 0.83-1.12).DiscussionPhysiological mechanisms that ensure fairly small oscillations inblood pressure, with changes in posture are well known. Postural ororthostatic hypotension is commonly encountered and its physiology has been well characterised. The opposite, orthostatic or postural hypertension, has received scant attention and only few casereports and studies have been donei4Its clinical significance in theelderly population also remains unclear.Orthostatic hypertension has not been well defined. Sapru et aldefined orthostatic hypertension as marked hypertension in theupright position with normal pressures in the supine position.3Streeten et al defined orthostatic hypertension as an increase indiastolic BP from below 90 to above 90mm of Hg.’ Matsubayashiet al defined orthostatic hypertension as an elevation of SBP20 mmHg at 1 or 2 minutes after standing4and Kario et al defined it as anincrease in systolic BP by 10 mm Hg by tilt test.9 In our study wedefined postural hypertension as change in SBP or DBP 10mm Hgon standing after 3 minutes.Our cross-sectional data showed that the prevalence of posturalhypertension in this cohort is 39%. Postural hypertension is significantly associated with seated hypertension and BMI. There were nosignificant associations with other variables, prevalent diseases and6 year all-cause mortality.There are several strengths to this study. It is population- based,and the numbers are large. It is the only large study done in an elderlypopulation, with almost complete follow-up for morbidity andmortality outcomes.There are some limitations to this study. Seated blood pressurewas measured only twice and not multiple times. Orthostatic bloodpressure was measured once. Since blood pressure values are knownto vary with repeated measurements multiple measures would bepreferable. Secondly, morbidity associations that were studied werecross-sectional . Thirdly, there are no data on cause specific mortality in this analysis. Lastly data reported here can only be generalizedto an ambulatory male population, since there were no women in thecohort and orthostatics were not measured at home visits or nursinghome visits.In conclusion, even though there is a high prevalence of posturalhypertension in this population of elderly Japanese-American men,its clinical significance is questionable as there were no significantcorrelations with morbidity and subsequent mortality.AcknowledgementWe would like to thank Ms. Kim Siu for her assistance in preparing the manuscript.References1, Streeten DHP, Auchincloss Jr JH, Anderson OH, Richardson RL, Thomas FD, Miller JW. OrthostaticHypertension. Pathogenic Study. Hypertension, 1985; 7; 196.203.2. Kario K, Eguchi K, Nakagawa Y, Motai K, Shimada K. Relationships between extreme dippers andorthostatic hypertension in elderly hypertensive patients. Hypertension 1998 ;31(part 1); 77-82.3. Sarpu RP, Sleight P, Anand IS, Sambhi MP, Lopez R, Chuttani PN. Orthostatic Hypertension. Am. J. Med1979; 66; 177-182.4. Matsubayashi K, Okumiya K, Wada T, Osaki Y et al. Postural dysregulation in systolic blood pressurein associated with worsened scoring on neurobehavioral tunction tests and leukoaraiosis in the olderelderly living in a community. Stroke 1997; 28; 2169-2173.5. Schneider EC, Trusdell D. A statistical study ot the pulse rate and the arterial blood pressures inrecumbency, standing and after standard exercise. Am J. Physiol 1922; 61; 429-474.6. Hull DH, Woethuis RA, Cortese T, Longo MR Jr. Treibwasser JH. Borderline hypertension versusnormotension; Differential response to orthostatic stress. Am Heart J 1977; 94: 414-420.7. Benowitz ML, Zevin 5, Carlsen 5, Wright J, Schambela NM, Cheitlin M. Orthostatic Hypertension due tovascular adrenergic hypersensitivity. Hypertension 1996; 28; 42-46.8. Frolich ED, Tarazi RC, Ulrych M, Dustan HP, Page IH. Tilt test for investigating a neural component inHypertension: Its correlation with clinical characteristics. Circulation 1967: 36; 387-393.9. Kano K, Motai K, Mitsuhashi T et al. Autonomic nervous system dysfunction in elderly hypertensivepatients with abnormal diurnal blood pressure variation and relation to silent cerebrovascular disease.Hypertension 1997: 30; 1504 —1210. Lipsitz LA. Orthostatic Hypertension in the elderly. NEJM. Oct.5,1987,952.57HAWAII MEDICAL JOURNAL, VOL 59, FEBRUARY 2000Table 2.— Univariate Logistic Regression Analysis, with PosturalHypertension as the dependent variableVariables Odds Ratio (95% Cl)BMI 1.030 (1.0o2.1.o50)*Smoking 1.018 (0.911.1.159)Seated Hypertension 1.230 (1 .040-1 .45o)*Abnormal ABI 0.886 (0.716-1.048)Prevalent Diabetes 0.995 (0.878.1.038)Prevalent CHD 1.189 (0.859-1.646)Previous OVA 1.189 (0.859-1.646)cognitive Impairment 0.986 (0.797-1.220)‘p<0.05Table 3.— Multivariate Logistic Regression Analysis, with PosturalHypertension as the dependent variableVariables Odds RatioAge 1.009 (0.993-1.026)BMI 1.025 (1 .002-1 .050)’Seated Hypertension 1.192 (1.011-1.405)’‘p<005Table 4.— Cox Proportional Hazards models for association betweenPostural Hypertension and 6-year all-cause mortalityModels Relative Risk 95% ClModel 1 (Postural hypertension 0.95 0.82-1.10adjusted for age)Model 2 (Postural hypertension 0.97 0.83-1.12adjusted for age, seatedhypertension, and BMI)50

Postural hypertension in elderly men--the Honolulu Heart Program.

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Postural hypertension in elderly men--the Honolulu Heart Program.

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