Postural Blood Pressure Response Research Articles

Age-related normative changes in phasic orthostatic blood pressure in a large population study: findings from The Irish Longitudinal Study on Ageing (TILDA).

In this report, we provide the first normative reference data and prevalence estimates of impaired orthostatic blood pressure (BP) stabilization, initial orthostatic hypotension, and orthostatic hypotension based on beat-to-beat blood pressure methods in a population-representative sample. Participants were recruited from a nationally representative cohort study (≥50 years). Beat-to-beat systolic BP, diastolic BP, and heart rate records were analyzed among those who underwent an active stand test (n=4475). Normograms were estimated by use of generalized additive models for location, shape, and scale with Box-Cox power exponential distribution. Prevalence estimates of impaired BP stabilization, initial orthostatic hypotension, and orthostatic hypotension are reported. Orthostatic BP responses in adults aged 50 to 59 years stabilized within 30 seconds of standing, with older groups taking 30 seconds or longer. The total prevalence of impaired BP stabilization was 15.6% (95% confidence interval [CI], 14.1%-17.1%), increasing with age to 41.2% (95% CI, 30.0%-52.4%) in people ≥80 years old. Initial orthostatic hypotension occurred in 32.9% (95% CI, 31.2%-34.6%) of the population aged ≥50 years, with no age gradient evident. The prevalence of orthostatic hypotension was 6.9% (95% CI, 5.9%-7.8%) in the total population, increasing to 18.5% (95% CI, 9.0%-28.0%) in those aged ≥80 years old. Significant age-related differences exist in the time course of postural BP responses, with abnormal responses taking longer than 30 seconds to stabilize. Impaired BP stabilization is more common as we age, affecting more than two-fifths of the population aged ≥80 years, and may play a future role in the management of falls and syncope.

Circulation : Clinical Summaries

<i>Circulation</i> : Clinical Summaries

Early postural blood pressure response and cause-specific mortality among middle-aged adults: what is the role of diastolic blood pressure?

Dear Editor, With interest we have read the article by Fedorowski et al. [1], which provides valuable information about cause-specific mortality in middle-aged subjects with orthostatic hypotension. In their study orthostatic hypotension (defined as a decrease in systolic blood pressure ≥20 mmHg and/or decrease in diastolic blood pressure ≥10 mmHg within 3 min of standing) was associated with mortality through injuries and neurologic diseases. Our major comment is that the article lacks data on the postural diastolic pressure response, both in describing the whole group with orthostatic hypotension, and the analyses of all cause and cause-specific mortality. Surprisingly, orthostatic hypotension and postural systolic blood pressure decline was not associated with cardiovascular mortality, although there was such an association in a smaller rescreened subsample. In other studies orthostatic hypotension was associated with myocardial infarction in middle-aged adults [2] and home dwelling elderly [3]. Unfortunately Fedorowski et al. [1] did not study the influence of postural diastolic blood pressure decline on cause-specific mortality. There might be a crucial role of diastolic blood flow on myocardial perfusion and subsequently myocardial infarction and cardiovascular mortality [3]. Postural diastolic, but not systolic blood pressure decline, seems to be associated with an increased risk of myocardial infarction [3]. Moreover in the same study population of the Malmo Preventive Project already the association was found that postural diastolic, but not systolic blood pressure decline predicts coronary events [4]. In conclusion, Fedorowski et al. [1] added very valuable information to the current knowledge of orthostatic hypotension through information on cause-specific mortality. However we miss in their study specific data on cause-specific mortality in relation to postural diastolic blood pressure decline and especially regarding cardiovascular mortality. References Fedorowski A, Hedblad B, Melander O. Early postural blood pressure response and cause-specific mortality among middle-aged adults. Eur J Epidemiol 2011. Rose KM, Tyroler HA, Nardo CJ, Arnett DK, Light KC, Rosamond W et al. Orthostatic hypotension and the incidence of coronary heart disease: the Atherosclerosis Risk in Communities study. Am J Hypertens 2000; 13(6 Pt 1): 571–8. Luukinen H, Koski K, Laippala P, Airaksinen KE. Orthostatic hypotension and the risk of myocardial infarction in the home-dwelling elderly. J Intern Med 2004; 255(4): 486–93. Fedorowski A, Stavenow L, Hedblad B, Berglund G, Nilsson PM, Melander O. Orthostatic hypotension predicts all-cause mortality and coronary events in middle-aged individuals (The Malmo Preventive Project). Eur Heart J 2010; 31(1): 85–91.

Early postural blood pressure response and cause-specific mortality among middle-aged adults

Orthostatic hypotension (OH) is associated with increased total mortality but contribution of specific death causes has not been thoroughly explored. In this prospective study, authors followed up 32,068 individuals without baseline history of cancer or cardiovascular disease (69% men; mean age, 46 years; range, 26–61 years) over a period of 24 years. Hazard ratios (HRs) for total and cause-specific mortality associated with presence of OH and by quartiles of postural systolic blood pressure response (∆SBP) were assessed using multivariate adjusted Cox regression model. A total of 7,145 deaths (22.3%, 9.4 deaths/1,000 person-years) occurred during follow-up. Those with OH (n = 1,943) had higher risk of death due to injury (HR, 1.88; 1.37–2.57) and neurological disease (HR, 2.21; 1.39–3.51). Analogically, risk of death caused by injury and neurological disease increased across the quartiles of ∆SBP from hyper- (Q1SBP, +8.5 ± 4.7 mmHg) to hypotensive response (Q4SBP, −13.7 ± 5.7 mmHg; HR, 1.32; 1.00–1.72, and 1.84; 1.20–2.82, respectively) as did also risk of death due to respiratory disease (Q4SBP vs. Q1SBP: HR, 1.53; 1.14–2.04). In contrast, risk curve for cerebrovascular death was U-shaped with nadir in the mildly hypotensive 3rd quartile of ∆SBP (−5.0 ± 0.1 mmHg, Q3SBP vs. Q1SBP: HR, 0.75; 0.54–1.03; P for linear trend = 0.021). Additionally, cardiovascular mortality was increased among 5,805 rescreened participants (mean age, 53 years; 9.8% OH positive: HR, 1.54; 1.24–1.89, and Q4SBP vs. Q1SBP: 1.27; 1.02–1.57, respectively). In summary, increased mortality predicted by blood pressure fall on standing is associated with injuries, neurodegenerative, and respiratory diseases, as well as with cardiovascular disease in older adults. Moreover, both increase and pronounced decrease of SBP during early orthostasis indicate higher risk of cerebrovascular death.

Clinical phenotype of subjects with Parkinson's disease and orthostatic hypotension: Autonomic symptom and demographic comparison

The objective of this study was to characterize the phenotypic associations of orthostatic hypotension (OH) in Parkinson's disease (PD). One hundred fifty-nine subjects with PD underwent assessment including autonomic symptom severity scoring, disease-specific rating scales, and measurement of postural blood pressure response. Symptoms of autonomic impairment weakly correlated with disease duration and severity. A posture and gait instability (PIGD) motor phenotype was associated with greater severity of autonomic symptoms. Eighty subjects (50.3%) had OH. These subjects were older, more likely to be male, and taking larger doses of dopaminergic medications than those without OH. There was no difference in disease severity or duration between those with and those without OH. Symptomatic dizziness did not distinguish between groups, although subjects with OH had more symptoms of generalized autonomic impairment than those without. Progressive autonomic involvement may be linked to disease progression in PD, particularly in patients with a PIGD phenotype, but dichotomization into groups with and without OH is a relatively insensitive method for demonstrating this. Longitudinal studies of changes in autonomic reflex abnormalities, autonomic symptom profiles, and motor severity might clarify these associations.

Syncope and orthostatic hypotension

purpose: The purpose of this study was to determine the postural blood pressure response over time, the prevalence of orthostatic hypotension in patients with syncope, and the relationship of orthostatic hypotension to recurrence of symptoms. patients and methods: We prospectively evaluated 223 patients with syncope in a standardized manner. Orthostatic responses were measured in a standardized fashion at 0, 1, 2, 3, 5, and 10 minutes or until symptoms occurred. Follow-up was obtained at 3-month intervals. Causes of syncope were assigned by predetermined criteria. results: Orthostatic hypotension (20 mm Hg or greater systolic blood pressure decline) was found in 69 patients (31%). The median time to reach minimal standing systolic blood pressure was 1 minute for all subjects. In patients with orthostatic hypotension (20 mm Hg or greater), mean time to reach minimum blood pressure was 2.4 minutes. The vast majority of patients with significant orthostatic hypotension had this finding within 2 minutes of standing. Orthostatic hypotension was common in patients for whom other probable causes of syncope were assigned. The recurrence of syncope was not related to the degree of orthostatic hypotension; however, the recurrence of dizziness and syncope as endpoints was lower in patients with 20 mm Hg or greater systolic blood pressure reductions as compared with patients with lesser degrees of orthostatic blood pressure declines. conclusion: Orthostatic hypotension is common in patients with syncope and is detected in the vast majority of patients by 2 minutes. Although symptom recurrence on follow-up was lower in patients with more severe orthostatic hypotension, the clinical significance of this finding needs to be further defined by future studies.

Effects of Meals and Time of Day on Postural Blood Pressure Responses in Young and Elderly Subjects

Previous data suggest that postural and postprandial hypotension are common in elderly subjects. This study evaluated the effect of age, meals, and time of day on supine and standing blood pressure (BP) and heart rate in healthy young and elderly subjects. A postural BP protocol was performed on 10 young and 16 elderly subjects during an overnight stay. The protocol included first morning and postprandial readings. The systolic and diastolic BP responses to standing were not significantly different between the two groups and were not affected by time of day. Postprandial recumbent BPs declined significantly only in the older subjects. There was no effect of meals on the BP response to standing. We conclude that healthy elderly subjects have a postprandial decline in BP even when supine. However, the BP response to standing is similar in young and elderly subjects and is not impaired by overnight rest or meals. This suggests that the regulation of BP after meals and with standing may be different.

Effects of meals and time of day on postural blood pressure responses in young and elderly subjects

• Previous data suggest that postural and postprandial hypotension are common in elderly subjects. This study evaluated the effect of age, meals, and time of day on supine and standing blood pressure (BP) and heart rate in healthy young and elderly subjects. A postural BP protocol was performed on 10 young and 16 elderly subjects during an overnight stay. The protocol included first morning and postprandial readings. The systolic and diastolic BP responses to standing were not significantly different between the two groups and were not affected by time of day. Postprandial recumbent BPs declined significantly only in the older subjects. There was no effect of meals on the BP response to standing. We conclude that healthy elderly subjects have a postprandial decline in BP even when supine. However, the BP response to standing is similar in young and elderly subjects and is not impaired by overnight rest or meals. This suggests that the regulation of BP after meals and with standing may be different. (<i>Arch Intern Med</i>. 1989;149:2757-2760)

Effect of Timing and Number of Baseline Blood Pressure Determinations on Postural Blood Pressure Response

We hypothesized that the blood pressure response to standing may depend on the method of establishing baseline blood pressure. Three hundred elderly subjects previously completed a postural blood pressure protocol with three supine baseline blood pressure readings obtained two minutes apart prior to standing. Comparison of the readings showed a significant drop between the first and the second (P less than .001) but not between the second and third supine systolic blood pressures. The difference between the first supine systolic blood pressure and the one minute standing blood pressure was significantly greater than that between the third supine systolic blood pressure and the one minute standing blood pressure (P less than .001). A second group was prospectively studied to determine whether the change in blood pressure after standing was greater if only a single baseline reading was taken rather than multiple readings, and whether the decline in blood pressure over three readings was related to duration supine or to the number of blood pressures taken. This group also demonstrated a decline in systolic blood pressure with three serial readings. We conclude that supine blood pressure declines significantly between the first and second readings taken two minutes apart and is secondary to the repetition of readings and not the duration supine. However, this change in supine blood pressure does not significantly alter the blood pressure response to standing. Thus, it appears that a single baseline supine blood pressure measurement is adequate for determining the postural blood pressure response, and that pooling of multiple baseline readings may not be appropriate.

MEXILETINE FOR TREATMENT OF CHRONIC PAINFUL DIABETIC NEUROPATHY

Sixteen of nineteen patients completed a randomised double-blind crossover trial to assess the effect of oral mexiletine (10 mg/kg bodyweight daily) on the symptoms and signs of chronic painful diabetic neuropathy. The median age of the sixteen patients was 50 years (range 30-64). Assessment with a five-item clinical symptom scale showed significant improvement during the mexiletine phase compared with the placebo phase. Pain was reduced during mexiletine but not during placebo, as assessed by a visual analogue rating scale. Mexiletine treatment had no effect on tendon reflexes, vibration threshold levels, beat-to-beat variation in heart rate during deep breathing, and postural blood pressure response. Mild side-effects were seen in three of the sixteen patients during mexiletine treatment.

The Effect of Naproxen on Acute Mountain Sickness and Vascular Responses to Hypoxia

The role of prostaglandins in the pathogenesis of acute mountain sickness and two hypoxia-induced vascular responses was evaluated using the cyclooxygenase inhibitor naproxen. Eleven men spent 24 hours at sea level, followed by 34 hours of decompression to 428 mm Hg while receiving naproxen (N), 250 mg twice daily or placebo (P) in a double-blind crossover trial. Serum naproxen levels measured by high pressure liquid chromatography were not changed by hypoxia. The severity of acute mountain sickness (AMS) by the Environmental Symptom Questionnaire scores and observer assessment were unaffected by drug treatment. Retinal artery diameter measured from projected fundus photographs was increased after 27 hours at altitude (11.4 +/- .5 mm) vs. sea level (9.4 +/- .5 mm, p less than 0.05) during both trials. Upright mean arterial pressure fell after 6 hours at altitude (79 +/- 3 mm Hg during N and P vs. 92 +/- 3 at sea level, p less than 0.01). Minute ventilation, end expiratory alveolar PO2 and PCO2 did not differ between drug trials. This study suggests vasodilating prostaglandins do not have a major role in the genesis of AMS, hypoxia-induced retinal vasodilatation, or postural blood pressure responses in man.

Redevelopment of essential hypertension after cessation of long term therapy; preliminary findings.

We have previously found that the vascular hypertrophy that accounts for the maintenance of a substantial fraction of the elevation of the total peripheral resistance index (TPRI) in essential hypertension can be almost completely reversed by one years antihypertensive treatment (1). On ceasing treatment, blood pressure returns rapidly to pretreatment values suggesting that the original cause of the hypertension is still present. In the present study, 7 patients stopped a standard regimen for 10 weeks after at least 2 years of normotension. In the first week, standing and lying blood pressure increased related to rise in supine cardiac index and TPRI. Thereafter standing pressures, supine systolic blood pressure and cardiac index (CI) increased further, but supine diastolic blood pressure and TPRI did not alter. Changes in measurements of resting sympathetic activity, plasma volume or renin-angiotensin did not account for these observations. The return of hypertension after stopping effective therapy has some features previously described in borderline hypertension, particularly increasing systolic blood pressure, CI and postural blood pressure responses. Some of the changes may reflect the relative preponderance of cardiac and vascular amplifiers.