0
We're unable to sign you in at this time. Please try again in a few minutes.
Retry
We were able to sign you in, but your subscription(s) could not be found. Please try again in a few minutes.
Retry
There may be a problem with your account. Please contact the AMA Service Center to resolve this issue.
Contact the AMA Service Center:
Telephone: 1 (800) 262-2350 or 1 (312) 670-7827  *   Email: subscriptions@jamanetwork.com
Error Message ......
Original Investigation |

Postural Hypotension and Postural Dizziness in Patients With Non–Insulin-Dependent Diabetes FREE

Jin-Shang Wu, MD; Feng-Hwa Lu, MD; Yi-Ching Yang, MD; Chih-Jen Chang, MD
[+] Author Affiliations

From The Department of Family Medicine, National Cheng Kung University Hospital, Tainan, Taiwan, Republic of China.


Arch Intern Med. 1999;159(12):1350-1356. doi:10.1001/archinte.159.12.1350.
Text Size: A A A
Published online

Background  Postural hypotension with a decline of 20 mm Hg or more in systolic blood pressure on standing is considered a potentially dangerous hypotensive response. Postural dizziness is often strongly associated with postural hypotension. However, there is conflicting evidence, and previous studies have been confined to the elderly, not specifically to patients with diabetes. Thus, we evaluated the association between postural hypotension and postural dizziness, and determined the factors most likely related to postural hypotension in patients with diabetes.

Methods  The subjects were 204 consecutive non–insulin-dependent patients with diabetes and 408 age- and sex-matched control subjects. Postural hypotension was defined as a decline of 20 mm Hg or more in systolic blood pressure 1 minute after standing. Postural dizziness was any feelings of dizziness, light-headedness, or faintness that occurred while standing during the examination.

Results  The prevalence of postural hypotension and postural dizziness in patients with diabetes was higher than in control subjects. Those patients with both diabetes and postural hypotension were older and had higher supine systolic blood pressures and higher plasma glycosylated hemoglobin and fasting glucose levels. They had higher prevalence of postural dizziness, hypertension, and cerebrovascular disease, and lower standing systolic blood pressures than those without postural hypotension. They also were more often being treated with antihypertensive agents. Only 32.8% of patients with diabetes with postural hypotension suffered from postural dizziness. Postural dizziness, hypertension, cerebrovascular disease, and plasma glycosylated hemoglobin levels were independently associated with postural hypotension in patients with diabetes.

Conclusions  Postural dizziness, glycemic control, hypertension, and cerebrovascular disease were important determinants of postural hypotension in patients with diabetes. Postural hypotension was associated with postural dizziness, but it cannot be determined clinically just from the presence of postural dizziness because the sensitivity for diagnosis of postural hypotension is low.

Figures in this Article

POSTURAL hypotension is considered the most dramatic clinical manifestation and hallmark of diabetic autonomic neuropathy.1,2 In patients with diabetes, autonomic neuropathy with abnormal cardiovascular reflex tests has been associated with increased mortality from unexpected sudden death and renal failure.3,4 However, there is no uniform criterion for postural hypotension that may be symptomatic or asymptomatic.5 Although postural hypotension is most commonly defined as a drop of 20 mm Hg or more in systolic blood pressure from the lying posture to the upright posture,611 the lack of symptoms associated with postural hypotension raises a question about the clinical value of this definition. It is reasonable to define postural hypotension as a particular decline in blood pressure that can predict a poor outcome.10 A study of the Hypertension Detection and Follow-up Program6 revealed that a decline of 20 mm Hg or more in systolic blood pressure after standing was associated with a high 5-year mortality rate, which indicated a poor prognosis for patients with diabetes complicated with hypertension. Epidemiological evidence also suggested that postural change with a decrease of 20 mm Hg or more in systolic blood pressure was a significant risk factor for fall and syncope.7,8 Furthermore, a drop of more than 20 mm Hg in postural systolic blood pressure was a risk factor for symptomatic occlusive cerebrovascular disease.9 Therefore, Lipsitz10 thought that postural hypotension with a decline of 20 mm Hg or more in systolic blood pressure on standing should be used to define a potentially dangerous hypotensive response.

Postural dizziness was believed to be due to reduced cerebral perfusion.8,12,13 However, Ohashi et al14 used single photon emission computed tomography to examine cerebral blood flow and showed that regional cerebral autoregulation was not associated with postural dizziness. Thus, the mechanism of postural dizziness may be heterogeneous.15 Clinically, postural dizziness is often strongly associated with postural hypotension, but the evidence is conflicted.11,1618 Some people with minor drops in systemic blood pressure develop clinical signs of cerebral ischemia and complain of dizziness or faintness on standing, whereas others with greater drops in blood pressure remain asymptomatic.12 Thus, some reports indicate that postural hypotension is related to postural dizziness,16,18 while others show that there is no association between postural hypotension and postural dizziness.11,17

Certain medications, normal aging, and some pathological changes such as diabetes mellitus, hypertension, and cerebrovascular disease are believed to be associated with postural hypotension.10,19,20 Similarly, postural dizziness is also associated with age, medication use, and comorbid diseases such as diabetes and stroke.16,21,22 Some of these associated factors are interrelated and interdependent, which may confound the relationship between postural hypotension and postural dizziness.

Studies on the factors most likely related to postural hypotension in subjects with diabetes have been few,23,24 and they did not examine postural hypotension as an outcome variable in multivariate analysis with adjustment for other confounding factors. One of the studies did not adjust for the use of medications, which was one of the important associated factors of postural hypotension.24 As for the association between postural hypotension and postural dizziness, some studies have examined their relationship,11,1618,25 but the subjects were limited to the elderly, not specifically to patients with diabetes. Therefore, we have conducted a case-controlled study to evaluate the association between postural hypotension and postural dizziness in patients with diabetes.

The subjects were 204 consecutive non–insulin-dependent patients with diabetes and 408 age- and sex-matched nondiabetic control subjects who underwent physical examinations for preventive reasons at the National Cheng Kung University Hospital between October 1992 and September 1994. Subjects were excluded from the study for sympathectomy, anemia, thyroid disorder, pregnancy, chronic alcohol use, and/or use of anti-Parkinson drugs, narcotics, sedatives, antipsychotic agents, or antidepressants within 2 weeks of the study. The subjects with diabetes included 114 men and 90 women with a mean age ± SD of 57.9 ± 10.5 years. The nondiabetic control subjects were 228 men and 180 women with a mean age ± SD of 57.1 ± 9.5 years.

Demographic characteristics, medical history, and use of medications were assessed using a standard structured questionnaire. All the subjects received a complete physical examination, measurement of seated blood pressure, body weight, height, and ophthalmic consultation. The laboratory tests included blood chemistry analysis, a 75-g oral glucose tolerance test after a 10-hour overnight fast, and standard 12-lead electrocardiography.

Blood pressure and heart rate were measured based on the American Heart Association recommendations26 with a vital sign monitor (DINAMAP TM, model 1846SX; Critikon Inc, Irvine, Calif). The participants were instructed to not consume alcohol, coffee, or tea, or to smoke cigarettes on the day of the examination. Measurements were obtained at least 3 hours after a meal in a quiet room. The appropriate-sized cuff was wrapped around the right upper arm and blood pressure and heart rate were recorded after the subject had rested in a supine position for at least 5 minutes. The subject was then asked to stand, with the entire forearm relaxed and supported at the heart level (fourth intercostal space) on an adjustable table; measurements of blood pressure and heart rate were repeated after 1, 2, and 3 minutes of standing.5,26 The subjects were asked about any feelings of dizziness, light-headedness, or faintness during the standing procedure and a positive or negative response was recorded.

Clinical diagnoses and definitions were determined as follows: (1) Diabetes mellitus was diagnosed with a fasting plasma glucose measurement of 7.8 mmol/L (140 mg/dL) or greater or 11.1 mmol/L (200 mg/dL) or greater 2 hours after a glucose load (75 g), when a history of diabetes was reported, or if the subject currently used insulin or an oral hypoglycemic agent.27 (2) Postural hypotension was defined as a drop in systolic blood pressure from the lying position to the upright position of 20 mm Hg or more after 1 minute of standing.11,16,25 (3) Postural dizziness was defined as any feelings of dizziness, light-headedness, or faintness while standing during the examination.11,16,25 (4) Body mass index (BMI or Quetelet index) was calculated as weight in kilograms divided by the square of the height in meters: weight (kg)/[height (m)]2. (5) Hypertension was defined as the average of 3 seated readings of systolic/diastolic blood pressure equal to or higher than 140/90 mm Hg or a positive response to a history of hypertension or current use of antihypertensive agents.28 (6) Cerebrovascular disease was defined as a previously documented stroke or transient ischemic attack, or presence of hemiparesis, asymmetric hyperreflexia, motor rigidity, or a positive Babinski reflex on physical examination.7 (7) Diabetic retinopathy included background and preproliferative and proliferative diabetic retinopathy.29 (8) Electrocardiography of left bundle-branch block or ischemic patterns were interpreted according to the Minnesota code.30 They included Q-QS abnormalities, various degrees of ST segment depression, T-wave changes, and left bundle-branch block (Minnesota code 1.1-3; 4.1-3; 5.1-3 and 7.1).30

Comparisons of categorical variables were analyzed using the χ2 test. Comparisons of continuous variables between the 2 groups were carried out using the Student t test or the Mann-Whitney U test, where appropriate. Analysis of variance was used for comparisons of blood pressure and levels of fasting plasma glucose, glycosylated hemoglobin, cholesterol, and triglycerides with covariance of age and BMI between the 2 groups. Stepwise multiple logistic regression analysis was used to assess the association of clinical variables with postural hypotension. P values of .05 or lower indicated statistical significance.

Table 1 shows the clinical characteristics of subjects with diabetes and nondiabetic control subjects. Subjects with diabetes had significantly higher BMI, seated blood pressure, and heart rate; they had significantly higher plasma creatinine, cholesterol, triglyceride, fasting glucose, and glycosylated hemoglobin levels, and a significantly higher prevalence of hypertension and use of antihypertensive agents than nondiabetic control subjects. However, there were no significant differences between subjects with diabetes and nondiabetic control subjects in age, sex, prevalence of cerebrovascular disease, or left bundle-branch block or ischemic patterns on electrocardiography.

Table Graphic Jump LocationTable 1. Comparison of Clinical Variables in Subjects With Diabetes and Nondiabetic Control Subjects*

Figure 1 reveals the prevalence of postural hypotension and postural dizziness in subjects with diabetes and nondiabetic control subjects. Subjects with diabetes had a significantly higher prevalence of postural hypotension and postural dizziness than nondiabetic control subjects (subjects with diabetes vs those without: postural hypotension, 28.4% vs 15.4%, P<.001; postural dizziness, 22.5% vs 15.4%, P=.03). If we used the criterion of decrease in systolic blood pressure of 20 mm Hg or greater within 3 minutes of standing as the diagnosis of postural hvpotension, subjects with diabetes also had significantly higher prevalence of postural hypotension and postural dizziness than nondiabetic control subjects (subjects with diabetes vs those without: postural hypotension, 36.3% vs 22.8%, P<.001; postural dizziness, 26.5% vs 19.1%, P=.04) (data not shown).

Place holder to copy figure label and caption
Figure 1.

Prevalence of postural hypotension and postural dizziness in subjects with diabetes and nondiabetic control subjects. P values are for the difference between the groups beneath the respective P value brackets.

Graphic Jump Location

Figure 2 illustrates the prevalence of postural dizziness in subjects with diabetes and nondiabetic control subjects with and without postural hypotension. Among subjects with diabetes, those with postural hypotension had a higher prevalence of postural dizziness than those without. However, only 19 (32.8%) of 58 subjects with both diabetes and postural hypotension suffered from postural dizziness. Among nondiabetic control subjects, there was no significant difference in the prevalence of postural dizziness between those with and those without postural hypotension.

Place holder to copy figure label and caption
Figure 2.

Prevalence of postural dizziness in subjects with diabetes and nondiabetic control subjects with and without postural hypotension. P values are for the difference between the groups beneath the respective P value brackets.

Graphic Jump Location

The prevalence of postural hypotension in subjects receiving different types of antihypertensive medications was as follows: calcium channel blockers, 18.8% (9/48); α-blockers, 26.3% (5/19); β-blockers, 13.6% (3/22); labetalol, 27.3% (3/11); angiotensin-converting enzyme inhibitors, 10.8% (4/37); diuretics, 30.0% (3/10); nitrates, 16.7% (2/12); and hydralazine, 33.3% (1/3). In univariate analysis, there was no association between postural hypotension and any of the above antihypertensive medications. Thus, we merged those subjects using the above antihypertensive medications into 1 group for analysis.

Table 2 presents the comparisons of clinical variables in the subjects with diabetes and nondiabetic control subjects with and without postural hypotension. Subjects with both diabetes and postural hypotension were older and had higher supine systolic blood pressures, higher plasma glycosylated hemoglobin and fasting glucose levels, and higher prevalences of hypertension and cerebrovascular disease, and use of antihypertensive agents; they had lower standing systolic blood pressure than subjects with diabetes without postural hypotension. There were no statistical differences between subjects with diabetes who had postural hypotension and those who did not in sex, BMI, supine resting heart rate, heart rate change (heart rate after 1 minute of standing vs supine resting heart rate), or duration of diabetes. There were no statistical differences in plasma albumin, cholesterol, triglyceride, or creatinine levels or in the prevalence of left bundle-branch block or ischemic patterns on electrocardiographic studies; and there were no statistical differences in diabetic retinopathy or the use of insulin and oral hypoglycemic agents. In nondiabetic control subjects, those with postural hypotension were older and had higher supine systolic blood pressure and prevalence of hypertension, and lower standing systolic blood pressure than those without postural hypotension.

Table Graphic Jump LocationTable 2. Comparison of Clinical Variables in Subject Groups Both With and Without Diabetes Mellitus and Postural Hypotension (PH)*

As compared with nondiabetic control subjects with postural hypotension, subjects with both diabetes and postural hypotension had higher plasma cholesterol, triglyceride, fasting glucose, and glycosylated hemoglobin levels, and higher prevalences of hypertension, cerebrovascular disease, and use of antihypertensive agents. Subjects with diabetes but without postural hypotension had higher BMI, higher supine and standing systolic blood pressure, higher plasma cholesterol, triglyceride, fasting glucose, and glycosylated hemoglobin levels, and higher prevalence of hypertension and use of antihypertensive agents than nondiabetic control subjects without postural hypotension.

To examine the relationship between postural hypotension and postural dizziness, the outcome variable was postural hypotension and the predictor variables included postural dizziness and other clinical variables in multiple logistic regression analysis (Table 3). For total study populations, the predictor variables included postural dizziness, age, BMI; plasma cholesterol, triglyceride, and creatinine levels; and diabetes mellitus, hypertension, cerebrovascular disease, and use of insulin or oral hypoglycemic and antihypertensive agents. The results show that an independently positive correlation existed between postural hypotension and the following variables: age (P=.005), diabetes mellitus (P=.005), and hypertension (P=.001). An increase in the number of these independently associated factors increased the likelihood of postural hypotension. In subjects with diabetes, the predictor variables of multiple logistic regression included postural dizziness, age, BMI; plasma cholesterol, triglyceride, creatinine, and glycosylated hemoglobin levels; and duration of diabetes, diabetic retinopathy, hypertension, cerebrovascular disease, and use of insulin or oral hypoglycemic and antihypertensive agents. The results demonstrated that postural dizziness (P=.02), glycosylated hemoglobin levels (P=.002), hypertension (P=.002), and cerebrovascular disease (P=.04) were independently associated with postural hypotension. In nondiabetic control subjects, the predictor variables included postural dizziness, age, and BMI; plasma cholesterol, triglyceride, creatinine, and glycosylated hemoglobin levels; and hypertension, cerebrovascular disease, and use of antihypertensive agents. The results indicated that age (P=.01) and hypertension (P=.01) were independently related to postural hypotension.

Table Graphic Jump LocationTable 3. Multiple Logistic Regression Analysis in the Relationship Between Clinical Variables and Postural Hypotension*

If we used the criterion of decrease in systolic blood pressure of 20 mm Hg or greater within 3 minutes of standing as the diagnosis of postural hypotension, the relationships between postural hypotension and postural dizziness were not changed in the diabetic, nondiabetic, and total groups. For total study populations, age (P=.002), diabetes mellitus (P=.03), hypertension (P=.002), and cerebrovascular disease (P=.04) were independently associated factors of postural hypotension. In subjects with diabetes, postural dizziness (P=.03), glycosylated hemoglobin levels (P=.008), hypertension (P=.005), and cerebrovascular disease (P=.01) were independently associated with postural hypotension. In nondiabetic control subjects, age (P=.004) and hypertension (P=.04) were independently related to postural hypotension (data not shown).

There are varying criteria for the diagnosis of postural hypotension19,20,31; the most recent consensus is a drop in blood pressure of at least 20 mm Hg systolic or 10 mm Hg diastolic within 3 minutes of either standing or head-up tilt of at least 60°.5 However, several important studies have examined the relationship between postural dizziness and postural hypotension with the test of 1 minute of standing.11,16,25 For comparison with the above studies, we used the criterion of 1 minute of standing in this study. The impact of changing the criterion from 1 minute to 3 minutes of quiet standing was only that the prevalence of postural hypotension and postural dizziness increased in subjects both with and without diabetes. However, there was no change in the relationship between postural hypotension and postural dizziness in the 2 groups.

Diabetes mellitus was an independently associated factor of postural hypotension in our study, which is consistent with the literature.1,3,19,32 Regarding the mechanism of postural hypotension in diabetes, there is more commonly a neurogenic cause usually associated with efferent involvement of the baroregulatory reflex arc with damaged sympathetic vasoconstrictor fibers in the splanchnic bed, muscle, and skin.5 In contrast, diminished cardiac acceleration may play a lesser role in the development of postural hypotension.33,34

Our patients with diabetes had a higher resting heart rate than nondiabetic control subjects, which is consistent with other reports.35,36 A higher resting heart rate is often observed in patients with diabetes, and this is due to cardiac vagal neuropathy.35,36 With progression of diabetic autonomic neuropathy, some patients experienced initial tachycardia that may be followed by a decreased heart rate and, ultimately, a fixed heart rate due to the progression of cardiac sympathetic nerve dysfunction.3739 The increase in heart rate on standing results from the dual effects of inhibition in cardiac vagal tone and increase in sympathetic tone.40 The heart rate change after standing in those subjects with postural hypotension was lower than in those without because sympathetic abnormalities in patients with diabetes are detectable almost exclusively after cardiac vagal neuropathy is impaired.4143 Although all of our subjects with postural hypotension, both with and without diabetes, had lower heart rate changes than those without postural hypotension, the difference was not significant. This may be due to the high fatality rate in subjects with postural hypotension3,4 and the minor role of diminished cardiac acceleration in the development of postural hypotension,33,34 thus causing an underestimate in the relationship between postural hypotension and heart rate change after standing.

Reported studies have revealed that poor glycemic control of diabetes mellitus, which is shown by increasing plasma glycosylated hemoglobin levels, was vulnerable to postural hypotension.23,24 In our patients with diabetes, plasma glycosylated hemoglobin was an independently positive factor correlated with postural hypotension. Therefore, good glycemic control is important in the prevention of postural hypotension in subjects with diabetes, which is also suggested in other reports.1,23,24

Duration of diabetes has often been perceived as an associated factor of postural hypotension, but the evidence was sparse. The prevalence of postural hypotension (the criteria of postural hypotension with a systolic blood pressure change of 30 mm Hg or more) increased with duration of diabetes in a young group (aged 18-34 years).24 However, our study and another report23 showed that duration was not independently associated with postural hypotension. Because postural hypotension was associated with increased mortality,3,4 the prevalence of postural hypotension in survivors would be diminished.24 This may be the partial explanation for the discrepancy between the prevalence of postural hypotension and duration of diabetes.

The prevalence of postural hypotension was 28.4% in our subjects with diabetes. Hilsted and Low1 reported 2 studies on diabetes mellitus complicated with postural hypotension in 19 (26%) of 73 patients and 7 (43%) of 16 patients. Tsutsu et al23 reported on 157 (18%) of 886 cases of patients with diabetes. The variation was considered to be due to the referral bias.1

The literature has revealed that cerebrovascular disease is a risk factor associated with postural hypotension,10,11,19 because it may interrupt the central nervous system pathways that control autonomic reflexes.32 Cerebrovascular disease was an independently associated factor of postural hypotension in our patients with diabetes. However, the Cardiovascular Health Study Collaborative Research Group did not find a positive association between postural hypotension and stroke,17 suggesting that a high fatality rate in strokes associated with postural hypotension (ie, the result of a survival effect) may explain the negative results in the association between stroke and postural hypotension.17

Our results suggest that hypertension is associated with postural hypotension in subjects with diabetes and in nondiabetic control and total subjects as well, which is consistent with the findings of other studies.11,16,18,25,44 Hypertension has been shown to be associated with impaired baroreflex sensitivity, which may be due to a decrease in vascular compliance and consequent diminution of baroreceptor stretch and relaxation during blood pressure changes.44,45 Moreover, an increase in blood pressure and the duration of hypertension may exacerbate the decline in baroreflex sensitivity, in part, causing postural hypotension.20,45

Although the literature has shown that antihypertensive medication was related to postural hypotension,10,19 our study and another report46 revealed that there was no significant association between postural hypotension and antihypertensive medication. Masuo et al47 showed that the incidence of postural hypotension decreased significantly followed by decreasing blood pressure and normalizing blood pressure with the use of antihypertensive drugs (especially calcium channel blockers, β-blockers, and angiotensin-converting enzyme inhibitors) in elderly patients with hypertension. This may be a partial explanation for the dissociation between postural hypotension and antihypertensive medication. Another factor could be due to an underestimation in a cross-sectional study if a past occurrence of a treatment adverse effect or related symptom led to an adjustment of the treatment regimen.46

The mechanism of postural dizziness remains obscure and may be heterogeneous.12 Some reports have suggested postural hypotension or cerebral ischemia may be involved in postural dizziness,12,13 and others have suggested vestibular dysfunction, vision impairment, and disorders in the proprioceptive system may be also involved.15,48 Thus, postural hypotension is just 1 of the causes of postural dizziness, and it is not surprising that only 19 (32.8%) of 58 subjects with diabetes and postural hypotension suffer from postural dizziness. This is consistent with other reports suggesting that postural hypotension may be a cause of postural dizziness, but most subjects with postural hypotension in the studies of the elderly16,18 did not suffer from postural dizziness. Thus, the sensitivity was low for the diagnosis of postural hypotension based solely on the presence of postural dizziness relative to the diagnosis based on the postural blood pressure changes. Therefore, postural hypotension cannot be clinically determined just from the presence of postural dizziness.

In conclusion, the prevalence of postural hypotension and postural dizziness in patients with diabetes was higher than in nondiabetic control subjects. Only 32.8% of subjects with both diabetes and postural hypotension suffered from postural dizziness. Age, diabetes mellitus, and hypertension were independently associated with postural hypotension. Plasma glycosylated hemoglobin levels, postural dizziness, hypertension, and cerebrovascular disease are independent determinants of postural hypotension in subjects with diabetes. Clinically, older adults and patients with diabetes mellitus or hypertension should receive regular monitoring of supine and upright blood pressure changes. Good glycemic control is important in preventing postural hypotension in patients with diabetes. Postural hypotension was associated with postural dizziness in subjects with diabetes, but it cannot be diagnosed clinically just from the postural dizziness because of the low sensitivity in the diagnosis of postural hypotension based only on postural dizziness relative to the diagnosis based on postural systolic blood pressure changes.

Accepted for publication October 15, 1998.

This study was supported by grant NCKUH-R-85-50 from the Intramural Research Fund of the National Cheng Kung University Hospital, Tainan, Taiwan, Republic of China.

Reprints: Chih-Jen Chang, MD, Department of Family Medicine, National Cheng Kung University Hospital, 138 Sheng Li Rd, Tainan, 70428, Taiwan, Republic of China (e-mail: Jins@mail.ncku.edu.tw).

Hilsted  JLow  PA Diabetic autonomic neuropathy. Low  PAed.Clinical Autonomic Disorders Evaluation and Management. 2nd ed. Philadelphia, Pa Lippincott-Raven1997;487- 507
Ewing  DJ Cardiac autonomic neuropathy. Jarrett  RJed.Diabetes and Heart Disease. Amsterdam, the Netherlands Elsevier Science Publishers1984;99- 132
Ewing  DJCampbell  IWClarke  BF The natural history of diabetic autonomic neuropathy. QJM. 1980;4995- 108
Watkins  PJMackay  YD Cardiac denervation in diabetic neuropathy. Ann Intern Med. 1980;92304- 307
Link to Article
The Consensus Committee of the American Autonomic Society and the American Academy of Neurology, Consensus statement on the definition of orthostatic hypotension, pure autonomic failure, and multiple system atrophy. Neurology. 1996;461470
Link to Article
Davis  BRLangford  HGBlaufox  MDCurb  YDPolk  BFShulman  NB The association of postural changes in systolic blood pressure and mortality in persons with hypertension: the Hypertension Detection and Follow-up Program experience. Circulation. 1987;75340- 346
Link to Article
Lipsitz  LAPluchino  FCWei  JYRowe  JW Syncope in institutionalized elderly: the impact of multiple pathological conditions and situational stress. J Chronic Dis. 1986;39619- 630
Link to Article
Lipsitz  LA Abnormalities in blood homeostasis that contribute to falls in the elderly. Clin Geriatr Med. 1985;1637- 648
Dobkin  BH Orthostatic hypotension as a risk factor for symptomatic occlusive cerebrovascular disease. Neurology. 1989;3930- 34
Link to Article
Lipsitz  LA Orthostatic hypotension in the elderly. N Engl J Med. 1989;321952- 957
Link to Article
Mader  SLJosephson  KRRubenstein  LZ Low prevalence of postural hypotension among community-dwelling elderly. JAMA. 1987;2581511- 1514
Link to Article
Wollner  LMcCarthy  STSoper  NDMacy  DJ Failure of cerebral autoregulation as a cause of brain dysfunction in the elderly. BMJ. 1979;11117- 1118
Link to Article
Stark  RJWodak  J Primary orthostatic cerebral ischemia. J Neurol Neurosurg Psychiatry. 1983;46883- 891
Link to Article
Ohashi  NYasumura  SShojaku  HNakagawa  HMizukoshi  K Cerebral autoregulation in patients with orthostatic hypotension. Ann Otol Rhinol Laryngol. 1991;100841- 844
Sloane  PDBaloh  RW Persistent dizziness in geriatric patients. J Am Geriatr Soc. 1989;371031- 1038
Ensrud  KENevitt  MCYunis  CHulley  SBGrimm  RHCummings  SRStudy of Osteoporotic Fractures Research Group, Postural hypotension and postural dizziness in elderly women: the study of osteoporotic fractures. Arch Intern Med. 1992;1521058- 1064
Link to Article
Rutan  GHHermanson  BBild  DEKittner  SJLaBaw  FTell  GSThe Cardiovascular Health Study Collaborative Research Group, Orthostatic hypotension in older adults. Hypertension. 1992;19508- 519
Link to Article
Susman  J Postural hypotension in elderly family practice patients. J Am Board Fam Pract. 1989;2234- 237
Mader  SL Orthostatic hypotension. Med Clin North Am. 1989;731337- 1349
Mader  SL Aging and postural hypotension: an update. J Am Geriatr Soc. 1989;37129- 137
Sloane  PBlazer  DGeorge  LK Dizziness in a community elderly population. J Am Geriatr Soc. 1989;37101- 108
Katsarkas  A Dizziness in aging: a retrospective study of 1194 cases. Otolaryngol Head Neck Surg. 1994;110296- 301
Link to Article
Tsutsu  NNunoi  KYokomizo  YKikuchi  MFujishima  M Relationship between glycemic control and orthostatic hypotension in type 2 diabetes mellitus: a survey by the Fukuoka Diabetes Clinic Group. Diabetes Res Clin Pract. 1990;8115- 123
Link to Article
Krolewski  ASWarram  JHCupples  AGorman  CKSzabo  AJChrislieb  AR Hypertension, orthostatic hypotension and the microvascular complications of diabetes. J Chronic Dis. 1985;38319- 326
Link to Article
Tilvis  RSHakala  SMValvanne  JErkinjuntti  T Postural hypotension and dizziness in a general aged population: a four-year follow-up of the Helsinki Aging Study. J Am Geriatr Soc. 1996;44809- 814
Frohlich  EDGrim  CLabarthe  DRMaxwell  MHPerloff  DWeidman  WH Recommendations for human blood pressure determination by sphygmomanometers. Hypertension. 1988;11209A- 222A
Link to Article
World Health Organization Expert Committee on Diabetes Mellitus, Second Report: WHO Technical Report Series No. 727.  Geneva, Switzerland World Health Organization1985;9- 12
The Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure, The Fifth Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (JNC V). Arch Intern Med. 1993;153154- 183
Link to Article
Nathan  DM Long-term complications of diabetes mellitus. N Engl J Med. 1993;3281676- 1685
Link to Article
Blackburn  HKeys  A The electrocardiogram in population studies: a classification system. Circulation. 1960;211160- 1175
Link to Article
Schatz  IJ Orthostatic hypotension, II: clinical diagnosis, testing, and treatment. Arch Intern Med. 1984;1441037- 1041
Link to Article
Ziegler  MGRuiz-Ramon  PShapiro  MH Abnormal stress responses in patients with disease affecting the sympathetic nervous system. Psychosom Med. 1993;55339- 346
Link to Article
Hilsted  JGalbo  HChristensen  NJ Impaired cardiovascular responses to graded exercise in diabetic autonomic neuropathy. Diabetes. 1979;28313- 319
Link to Article
Hilsted  JParring  HHChristensen  NJBenn  JGalbo  H Hemodynamics in diabetic orthostatic hypotension. J Clin Invest. 1981;681427- 1434
Link to Article
Wheeler  TWatkins  PJ Cardiac denervation in diabetes. BMJ. 1973;4584- 586
Link to Article
Sundkvist  GAlmer  LLilja  B Respiratory influence on heart rate in diabetes mellitus. BMJ. 1979;1924- 925
Link to Article
Lloyd-Mostyn  RHWatkins  PJ Defective innervation of heart in diabetic autonomic neuropathy. BMJ. 1975;315- 17
Link to Article
Bennett  THosking  DJHampton  JR Cardiovascular control in diabetes mellitus. BMJ. 1975;2585- 587
Link to Article
Ewing  DJCampbell  IWClarke  BF Heart rate changes in diabetes mellitus. Lancet. 1981;1183- 186
Link to Article
Wieling  WVan Lieshout  JJ Maintenance of postural normotension in humans. Low  PAed.Clinical Autonomic Disorders Evaluation and Management. 2nd ed. Philadelphia, Pa Lippincott-Raven1997;77- 81
Ewing  DJMartyn  CNYoung  RJClarke  BF The value of cardiovascular autonomic function tests: 10 years experience in diabetes. Diabetes Care. 1985;8491- 498
Link to Article
Wieling  WBorst  Cvan Dongen Torman  MAvan der Hofstede  JWvan Brederode  JFEndert  EDunning  AJ Relationship between impaired parasympathetic and sympathetic cardiovascular control in diabetes mellitus. Diabetologia. 1983;24422- 427
Link to Article
Sundkvist  G Autonomic nervous function in asymtomatic diabetic patients with signs of peripheral neuropathy. Diabetes Care. 1981;4529- 534
Link to Article
Lipsitz  LAStorch  HAMinaker  KLRowe  JW Intra-individual variability in postural blood pressure in the elderly. Clin Sci. 1985;69337- 341
Gribbin  BPickering  TGSleight  PPeto  R Effect of age and high blood pressure on baroreflex sensitivity in man. Circ Res. 1971;29424- 431
Link to Article
Strogatz  DSKeenan  NLBarnett  EMWagner  EH Correlates of postural hypotension in a community sample of elderly blacks and whites. J Am Geriatr Soc. 1991;39562- 566
Masuo  KMikami  HOgihara  TTuck  ML Changes in frequency of orthostatic hypotension in elderly hypertensive patients under medications. Am J Hypertens. 1996;9263- 268
Link to Article
Belal  A  JrGlorig  A Dysequilibrium of aging (presbyastasis). J Laryngol Otol. 1986;1001037- 1041
Link to Article

Figures

Place holder to copy figure label and caption
Figure 1.

Prevalence of postural hypotension and postural dizziness in subjects with diabetes and nondiabetic control subjects. P values are for the difference between the groups beneath the respective P value brackets.

Graphic Jump Location
Place holder to copy figure label and caption
Figure 2.

Prevalence of postural dizziness in subjects with diabetes and nondiabetic control subjects with and without postural hypotension. P values are for the difference between the groups beneath the respective P value brackets.

Graphic Jump Location

Tables

Table Graphic Jump LocationTable 1. Comparison of Clinical Variables in Subjects With Diabetes and Nondiabetic Control Subjects*
Table Graphic Jump LocationTable 2. Comparison of Clinical Variables in Subject Groups Both With and Without Diabetes Mellitus and Postural Hypotension (PH)*
Table Graphic Jump LocationTable 3. Multiple Logistic Regression Analysis in the Relationship Between Clinical Variables and Postural Hypotension*

References

Hilsted  JLow  PA Diabetic autonomic neuropathy. Low  PAed.Clinical Autonomic Disorders Evaluation and Management. 2nd ed. Philadelphia, Pa Lippincott-Raven1997;487- 507
Ewing  DJ Cardiac autonomic neuropathy. Jarrett  RJed.Diabetes and Heart Disease. Amsterdam, the Netherlands Elsevier Science Publishers1984;99- 132
Ewing  DJCampbell  IWClarke  BF The natural history of diabetic autonomic neuropathy. QJM. 1980;4995- 108
Watkins  PJMackay  YD Cardiac denervation in diabetic neuropathy. Ann Intern Med. 1980;92304- 307
Link to Article
The Consensus Committee of the American Autonomic Society and the American Academy of Neurology, Consensus statement on the definition of orthostatic hypotension, pure autonomic failure, and multiple system atrophy. Neurology. 1996;461470
Link to Article
Davis  BRLangford  HGBlaufox  MDCurb  YDPolk  BFShulman  NB The association of postural changes in systolic blood pressure and mortality in persons with hypertension: the Hypertension Detection and Follow-up Program experience. Circulation. 1987;75340- 346
Link to Article
Lipsitz  LAPluchino  FCWei  JYRowe  JW Syncope in institutionalized elderly: the impact of multiple pathological conditions and situational stress. J Chronic Dis. 1986;39619- 630
Link to Article
Lipsitz  LA Abnormalities in blood homeostasis that contribute to falls in the elderly. Clin Geriatr Med. 1985;1637- 648
Dobkin  BH Orthostatic hypotension as a risk factor for symptomatic occlusive cerebrovascular disease. Neurology. 1989;3930- 34
Link to Article
Lipsitz  LA Orthostatic hypotension in the elderly. N Engl J Med. 1989;321952- 957
Link to Article
Mader  SLJosephson  KRRubenstein  LZ Low prevalence of postural hypotension among community-dwelling elderly. JAMA. 1987;2581511- 1514
Link to Article
Wollner  LMcCarthy  STSoper  NDMacy  DJ Failure of cerebral autoregulation as a cause of brain dysfunction in the elderly. BMJ. 1979;11117- 1118
Link to Article
Stark  RJWodak  J Primary orthostatic cerebral ischemia. J Neurol Neurosurg Psychiatry. 1983;46883- 891
Link to Article
Ohashi  NYasumura  SShojaku  HNakagawa  HMizukoshi  K Cerebral autoregulation in patients with orthostatic hypotension. Ann Otol Rhinol Laryngol. 1991;100841- 844
Sloane  PDBaloh  RW Persistent dizziness in geriatric patients. J Am Geriatr Soc. 1989;371031- 1038
Ensrud  KENevitt  MCYunis  CHulley  SBGrimm  RHCummings  SRStudy of Osteoporotic Fractures Research Group, Postural hypotension and postural dizziness in elderly women: the study of osteoporotic fractures. Arch Intern Med. 1992;1521058- 1064
Link to Article
Rutan  GHHermanson  BBild  DEKittner  SJLaBaw  FTell  GSThe Cardiovascular Health Study Collaborative Research Group, Orthostatic hypotension in older adults. Hypertension. 1992;19508- 519
Link to Article
Susman  J Postural hypotension in elderly family practice patients. J Am Board Fam Pract. 1989;2234- 237
Mader  SL Orthostatic hypotension. Med Clin North Am. 1989;731337- 1349
Mader  SL Aging and postural hypotension: an update. J Am Geriatr Soc. 1989;37129- 137
Sloane  PBlazer  DGeorge  LK Dizziness in a community elderly population. J Am Geriatr Soc. 1989;37101- 108
Katsarkas  A Dizziness in aging: a retrospective study of 1194 cases. Otolaryngol Head Neck Surg. 1994;110296- 301
Link to Article
Tsutsu  NNunoi  KYokomizo  YKikuchi  MFujishima  M Relationship between glycemic control and orthostatic hypotension in type 2 diabetes mellitus: a survey by the Fukuoka Diabetes Clinic Group. Diabetes Res Clin Pract. 1990;8115- 123
Link to Article
Krolewski  ASWarram  JHCupples  AGorman  CKSzabo  AJChrislieb  AR Hypertension, orthostatic hypotension and the microvascular complications of diabetes. J Chronic Dis. 1985;38319- 326
Link to Article
Tilvis  RSHakala  SMValvanne  JErkinjuntti  T Postural hypotension and dizziness in a general aged population: a four-year follow-up of the Helsinki Aging Study. J Am Geriatr Soc. 1996;44809- 814
Frohlich  EDGrim  CLabarthe  DRMaxwell  MHPerloff  DWeidman  WH Recommendations for human blood pressure determination by sphygmomanometers. Hypertension. 1988;11209A- 222A
Link to Article
World Health Organization Expert Committee on Diabetes Mellitus, Second Report: WHO Technical Report Series No. 727.  Geneva, Switzerland World Health Organization1985;9- 12
The Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure, The Fifth Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (JNC V). Arch Intern Med. 1993;153154- 183
Link to Article
Nathan  DM Long-term complications of diabetes mellitus. N Engl J Med. 1993;3281676- 1685
Link to Article
Blackburn  HKeys  A The electrocardiogram in population studies: a classification system. Circulation. 1960;211160- 1175
Link to Article
Schatz  IJ Orthostatic hypotension, II: clinical diagnosis, testing, and treatment. Arch Intern Med. 1984;1441037- 1041
Link to Article
Ziegler  MGRuiz-Ramon  PShapiro  MH Abnormal stress responses in patients with disease affecting the sympathetic nervous system. Psychosom Med. 1993;55339- 346
Link to Article
Hilsted  JGalbo  HChristensen  NJ Impaired cardiovascular responses to graded exercise in diabetic autonomic neuropathy. Diabetes. 1979;28313- 319
Link to Article
Hilsted  JParring  HHChristensen  NJBenn  JGalbo  H Hemodynamics in diabetic orthostatic hypotension. J Clin Invest. 1981;681427- 1434
Link to Article
Wheeler  TWatkins  PJ Cardiac denervation in diabetes. BMJ. 1973;4584- 586
Link to Article
Sundkvist  GAlmer  LLilja  B Respiratory influence on heart rate in diabetes mellitus. BMJ. 1979;1924- 925
Link to Article
Lloyd-Mostyn  RHWatkins  PJ Defective innervation of heart in diabetic autonomic neuropathy. BMJ. 1975;315- 17
Link to Article
Bennett  THosking  DJHampton  JR Cardiovascular control in diabetes mellitus. BMJ. 1975;2585- 587
Link to Article
Ewing  DJCampbell  IWClarke  BF Heart rate changes in diabetes mellitus. Lancet. 1981;1183- 186
Link to Article
Wieling  WVan Lieshout  JJ Maintenance of postural normotension in humans. Low  PAed.Clinical Autonomic Disorders Evaluation and Management. 2nd ed. Philadelphia, Pa Lippincott-Raven1997;77- 81
Ewing  DJMartyn  CNYoung  RJClarke  BF The value of cardiovascular autonomic function tests: 10 years experience in diabetes. Diabetes Care. 1985;8491- 498
Link to Article
Wieling  WBorst  Cvan Dongen Torman  MAvan der Hofstede  JWvan Brederode  JFEndert  EDunning  AJ Relationship between impaired parasympathetic and sympathetic cardiovascular control in diabetes mellitus. Diabetologia. 1983;24422- 427
Link to Article
Sundkvist  G Autonomic nervous function in asymtomatic diabetic patients with signs of peripheral neuropathy. Diabetes Care. 1981;4529- 534
Link to Article
Lipsitz  LAStorch  HAMinaker  KLRowe  JW Intra-individual variability in postural blood pressure in the elderly. Clin Sci. 1985;69337- 341
Gribbin  BPickering  TGSleight  PPeto  R Effect of age and high blood pressure on baroreflex sensitivity in man. Circ Res. 1971;29424- 431
Link to Article
Strogatz  DSKeenan  NLBarnett  EMWagner  EH Correlates of postural hypotension in a community sample of elderly blacks and whites. J Am Geriatr Soc. 1991;39562- 566
Masuo  KMikami  HOgihara  TTuck  ML Changes in frequency of orthostatic hypotension in elderly hypertensive patients under medications. Am J Hypertens. 1996;9263- 268
Link to Article
Belal  A  JrGlorig  A Dysequilibrium of aging (presbyastasis). J Laryngol Otol. 1986;1001037- 1041
Link to Article

Correspondence

CME
Meets CME requirements for:
Browse CME for all U.S. States
Accreditation Information
The American Medical Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The AMA designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM per course. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Physicians who complete the CME course and score at least 80% correct on the quiz are eligible for AMA PRA Category 1 CreditTM.
Note: You must get at least of the answers correct to pass this quiz.
You have not filled in all the answers to complete this quiz
The following questions were not answered:
Sorry, you have unsuccessfully completed this CME quiz with a score of
The following questions were not answered correctly:
Commitment to Change (optional):
Indicate what change(s) you will implement in your practice, if any, based on this CME course.
Your quiz results:
The filled radio buttons indicate your responses. The preferred responses are highlighted
For CME Course: A Proposed Model for Initial Assessment and Management of Acute Heart Failure Syndromes
Indicate what changes(s) you will implement in your practice, if any, based on this CME course.
Submit a Comment

Multimedia

Some tools below are only available to our subscribers or users with an online account.

Web of Science® Times Cited: 15

Related Content

Customize your page view by dragging & repositioning the boxes below.

Articles Related By Topic
Related Collections
PubMed Articles
JAMAevidence.com

Users' Guides to the Medical Literature
Clinical Resolution

Users' Guides to the Medical Literature
Clinical Scenario