Postprandial Hypotension In Patients Research Articles

Asymptomatic postprandial hypotension in patients with diabetes: The KAMOGAWA-HBP study.

Aims/IntroductionPostprandial hypotension (PPH) refers to a decrease in systolic blood pressure by ≥20 or to <90 mmHg from baseline ≥100 mmHg within 2 h of a meal. Previous studies have reported an association between diabetes and PPH; however, the characteristics of PPH in patients with diabetes remain unclear.Materials and MethodsWe recruited patients with diabetes who regularly attended the diabetes outpatient clinic. Participants were instructed to carry out three sets of blood pressure measurements at six time points: just before and right after, and 30, 60, 90 and 120 min after their main meal of the day. Data on PPH symptoms were collected during an interview. To investigate the relationships between explanatory variables, PPH and associated symptoms, we carried out multiple logistic regression analyses.ResultsWe analyzed data from 300 participants. There were 150 (50.0%) participants with PPH. Systolic blood pressure before a meal was significantly associated with PPH (odds ratio [OR] 1.56, 95% confidence interval [CI] 1.30–1.86, P < 0.001), after adjusting for covariates. Furthermore, age (OR 1.08, 95% CI 1.01–1.16, P = 0.027), hemoglobin A1c level (OR 2.39, 95% CI 1.01–5.64, P = 0.030) and coefficients of variation of R‐R intervals (OR 0.79, 95% CI 0.65–0.97, P = 0.032) were significantly associated with asymptomatic PPH.ConclusionsHalf of the present study outpatients with diabetes had PPH. High systolic blood pressure before a meal was significantly associated with the risk of PPH. Older adults and patients with higher levels of hemoglobin A1c or an autonomic dysfunction might have difficulties recognizing symptoms of PPH.

Clinical observation of postprandial hypotension in patients with hypertensive and coronary heart disease

Objective: To explore the prevalence and clinical characteristics of postprandial hypotension(PPH) in patients with essential hypertension and coronary heart disease. Methods: A total of 197 patients with essential hypertension and coronary heart disease, who had been treated in the First Department of Cardiology of the Second Hospital of Hebei Medical University from December, 2013 to December, 2014 were included. The patients' blood pressure before breakfast, lunch and dinner and 30, 60, 90, 120 minutes after the meal were monitored. Subjects were classified into PPH group (n=37) and non-PPH group (NPPH, n=160) according to postprandial decrease in systolic blood pressure, to explore the clinical characteristics and related factors and the major adverse cardiac and cerebral vascular events of PPH. Results: Among 197 patients, 37 cases (18.8%) showed at least once postprandial decline in systolic blood pressure greater than and equal to 20 mmHg. The incidence of PPH after breakfast and dinner were higher than lunch (P<0.05). There was no significant difference in the incidence of PPH among different age groups, among patients accompanied with different diseases, and among patients with different dining position (all P>0.05). According to the baseline systolic blood pressure, patients can be divided into 4 groups(<120 mmHg, 120-129 mmHg, 130-139 mmHg, >140 mmHg), the higher the level of the baseline systolic blood pressure was, the higher the incidence of PPH was. And the incidence of major adverse cardiac and cerebral vascular events in patients during hospitalization were increased by PPH. Conclusions: The prevalence of PPH in the patients with essential hypertension and coronary heart disease is 18.8%. The incidence of PPH after breakfast and dinner is higher than lunch. The baseline systolic blood pressure is considered to be the risk factor of PPH. And PPH could lead to an increase of the incidence of major adverse cardiac and cerebral vascular events.

Postprandial hypotension in patients with advanced neurological intractable diseases

Background: Postprandial hypotension (PPH) is widely known to occur in patents with various neurological diseases as well as diabetes patients, and also in elderly individuals, while it is often overlooked in bedridden patients.

O162 Postprandial hypotension in neurological diseases: A systematic review and meta-analysis

Objectives To perform a systematic review with meta-analysis of available scientific evidence regarding the frequency of postprandial hypotension (PPH) in neurological diseases. Methods A systematic review of the literature (up to January 2017) identified 323 studies, of which 10 reported frequency of PPH in neurological diseases compared to healthy controls. Of these, 5 were performed in Parkinson’s disease (PD), 2 in multiple system atrophy (MSA), 1 in Alzheimer’s disease (AD) and 2 in diabetic neuropathy (DN). Results Meta-analysis showed significantly higher frequency of PPH in patients with neurological diseases compared to healthy controls (143/279 patients and 40/207 controls; OR 5.43, 95%CI 2.85–10.32; p 0.00001 ). In all four diseases, patients had significantly higher frequency of PPH compared to healthy controls (103/191 patients and 31/126 controls; OR 3.65, 95%CI 2.00–6.64, p 0.0001 ; 19/27 patients and 0/24 controls; OR 89.55, 95%CI 2.65–3030.33; p = 0.01; 7/10 patients and 6/23 controls; OR 6.61, 95%CI 1.28–34.14; p = 0.02; 14/51 patients and 3/34 controls; OR 4.83, 95%CI 1.20 ± 19.41; p = 0.03 for PD, MSA, AD and DN respectively). Discussion PPH has been associated with increases in the risk of syncope, falls, stroke angina and mortality. As the majority of patients with PPH are asymptomatic, the diagnosis is often overlooked. Conclusion PPH is more frequent in patients with neurological diseases compared to healthy controls. Significance These findings should prompt further research focusing on the epidemiology and pathophysiology of PPH in different neurological diseases.

Postprandial hypotension in neurological disorders: systematic review and meta-analysis.

Postprandial hypotension (PPH) has been associated with increased risk of syncope, falls, stroke, angina and mortality. As the majority of patients with PPH are asymptomatic, the diagnosis is often overlooked. The aim of this study was to perform a systematic review and meta-analysis of available scientific evidence on the likelihood of PPH in neurological diseases. A systematic review of the literature (PubMed library, Cochrane Database for Systematic Reviews and Cochrane Central Register of Controlled Trials for results up to January 2017) identified 327 studies, of which 11 reported the frequency of PPH in patients with neurological diseases compared to healthy controls. These 11 studies were on patients with Parkinson's disease (PD; n = 6 studies), multiple system atrophy (MSA; n = 1), Alzheimer's disease (AD; n = 1) and diabetic neuropathy (DN; n = 2). The meta-analysis revealed that patients with neurological diseases had a significantly higher frequency of PPH than healthy controls [147/289 patients vs. 41/217 controls; odd ratio (OR) 5.23, 95% confidence interval (CI) 2.90-9.45, p<0.00001]. For each of the four diseases, the respective patients had a significantly higher frequency of PPH than healthy controls (PD: 107/201 patients vs. 32/136 controls; OR 3.49, 95% CI 2.09-5.83, p<0.0001; MSA: 19/27 patients vs. 0/24 controls; OR 89.55, 95% CI 2.65-3030.33, p=0.01; AD: 7/10 patients vs. 6/23 controls; OR 6.61, 95% CI 1.28-34.14, p=0.02; DN: 14/51 patients vs. 3/34 controls; OR 4.83, 95%CI 1.20-19.41, p=0.03). The likelihood of having PPH is higher in patients with neurological diseases than in healthy controls. These findings should prompt further research focusing on the epidemiology and pathophysiology of PPH in different neurological diseases.

Recommending Small, Frequent Meals in the Clinical Care of Adults: A Review of the Evidence and Important Considerations.

Small, frequent meals (SFMs) are a dietary regimen characterized by multiple small eating episodes throughout the day. Clinical nutrition guidelines recommend SFMs (eg, 6-10 meals) to patients experiencing common symptoms (eg, early satiety) and gastrointestinal-related symptoms. However, whether the provision of SFMs palliatively improves morbidity of nutritionally at-risk individuals has yet to be elucidated. This narrative review summarizes current clinical guidelines recommending SFMs for the management of diseases in adult patients (≥18 years), with supporting experimental and epidemiologic evidence, and it provides suggestions pertaining to this recommendation by drawing on potential considerations from investigations in healthy adults. Limited studies suggest that SFMs may promote higher energy and fluid intakes, reduce gastrointestinal-related symptoms (including vomiting, bloating, and fullness), and prevent postprandial hypotension in patients with primary autonomic failure. Potential health complications related to SFMs include unwarranted weight gain, suboptimal nutrition quality, later meal times, sleep disturbances, limited intermittent fasting, and disordered eating that may exacerbate the underlying disease or related symptoms. Thus, it is prudent for health professionals to supplement SFM recommendations with additional guidance on meal size, frequency, and timing, with a strong emphasis on healthy meal quality. Future research should recognize a standardized definition for SFMs and utilize better methods to obtain reliable data on meal patterns.

GW26-e1329 The prevalence and risk factors of postprandial hypotension in patients with coronary heart disease

GW26-e1329 The prevalence and risk factors of postprandial hypotension in patients with coronary heart disease

Association and dissociation of orthostatic hypotension and postprandial hypotension in patients with Parkinson's disease. A clinical study of the background

Association and dissociation of orthostatic hypotension and postprandial hypotension in patients with Parkinson's disease. A clinical study of the background

Role of intestinal peptides and the autonomic nervous system in postprandial hypotension in patients with multiple system atrophy

Postprandial hypotension (PPH) is a major clinical problem in patients with autonomic failure such as that observed in multiple system atrophy (MSA). The pathophysiology of PPH remains unclear, although autonomic dysfunction and gastrointestinal vasoactive peptides have been suspected to participate in its pathogenesis. We measured blood pressure and plasma levels of glucose, insulin, noradrenaline, neurotensin, glucagon-like peptide (GLP)-1 and GLP-2 before and after meal ingestion in 24 patients with MSA to reveal the roles of the autonomic nervous system and gastrointestinal vasoactive peptides in PPH. We performed a second meal-ingestion test by administering acarbose to evaluate the effects of acarbose (an α-glucosidase inhibitor) on PPH and vasoactive peptides in 14 patients with MSA and PPH. We also evaluated blood pressure responses to the head-up tilt test and heart rate variability in all the patients. Severities of PPH and orthostatic hypotension were significantly correlated. Patients with PPH had significantly worse orthostatic hypotension and lower heart rate variability than those without PPH. Postprandial GLP-1 secretion was higher in patients with PPH than in those without PPH. No significant differences were observed in the postprandial increases in plasma levels of glucose, insulin, noradrenaline, neurotensin or GLP-2. Acarbose significantly attenuated postprandial hypotension and tended to decrease GLP-2 secretion. Our results indicate that autonomic failure is involved in the pathogenesis of PPH and confirm that acarbose has a preventive effect against PPH in patients with MSA. Decreased postprandial secretion of GLP-2, which increases intestinal blood pooling, may attenuate PPH in patients with MSA.

The osmopressor response to water drinking

Water drinking elicits profound pressor responses in patients with impaired baroreflex function and in sinoaortic-denervated mice. Healthy subjects show more subtle changes in heart rate and blood pressure with water drinking. The water-induced pressor response appears to be mediated through sympathetic nervous system activation at the spinal level. Indeed, water drinking raises resting energy expenditure in normal weight and obese subjects. The stimulus setting off the response is hypoosmolarity rather than water temperature or gastrointestinal stretch. Studies in mice suggest that this osmopressor response may involve transient receptor potential vanniloid 4 (Trpv4) receptors. However, the (nerve) cell population serving as peripheral osmosensors and the exact transduction mechanisms are still unknown. The osmopressor response can be exploited in the treatment of orthostatic and postprandial hypotension in patients with severe autonomic failure. Furthermore, the osmopressor response acutely improves orthostatic tolerance in healthy subjects and in patients with neurally mediated syncope. The phenomenon should be recognized as an important confounder in cardiovascular and metabolic studies.

Postprandial hypotension in patients with multiple system atrophy or pure autonomic failure

Postprandial hypotension in patients with multiple system atrophy or pure autonomic failure

Acarbose, an α-Glucosidase Inhibitor, Attenuates Postprandial Hypotension in Autonomic Failure

Postprandial hypotension is an important clinical condition that predisposes to syncope, falls, angina, and cerebrovascular events. The magnitude of the fall in blood pressure after meals depends on enteric glucose availability. We hypothesized that acarbose, an alpha-glucosidase inhibitor that decreases glucose absorption in the small intestine, would attenuate postprandial hypotension. Acarbose or placebo was given 20 minutes before a standardized meal in 13 patients with postprandial hypotension in the setting of autonomic failure (age: 65+/-2.64 years; body mass index: 25+/-1.08 kg/m(2); supine plasma norepinephrine: 110+/-26.6 pg/mL). Four patients were studied in a single-blind protocol and 9 patients in a double-blind, randomized, crossover fashion. Patients were studied supine, and blood pressure, heart rate, and neuroendocrine parameters were obtained at baseline and for 90 minutes after meal intake. After adjusting for potential confounders, acarbose significantly attenuated the postprandial fall in systolic and diastolic blood pressures by 17 mm Hg (95% CI: 7 to 28; P=0.003) and 9 mm Hg (95% CI: 5 to 14; P=0.001), respectively. Furthermore, acarbose effectively reduced plasma levels of insulin, a known vasodilator, by 11 microU/mL (95% CI: 5 to 18; P=0.001) compared with placebo. After adjusting for insulin levels, the attenuation of postprandial hypotension by acarbose remained significant, indicating that additional mechanisms contribute to this effect. In conclusion, 100 mg of acarbose successfully improved postprandial hypotension in patients with severe autonomic failure. This effect is not explained solely by a reduction in insulin levels.

Effects of daily water drinking on orthostatic and postprandial hypotension in patients with multiple system atrophy

It has been demonstrated that the increased blood pressure (BP) caused by a single dose of water alleviates orthostatic hypotension (OH) and postprandial hypotension (PPH) in patients with autonomic failure (AF). The aim of this study was to evaluate the practical effect of daily water drinking on OH and PPH in the morning when patients with AF are usually most affected. In five patients with multiple system atrophy (MSA) characterized by intractable OH and PPH, we measured seated, standing and postprandial BP in the morning without and with ingestion of 350 ml tap water at 07.30 hours for seven successive days. The changes from the basal BP level at 07.30 hours (DeltaBP) were assessed as an index of the effect of water drinking. Water drinking elicited a rapid pressor response in all patients. The DeltaBP during sitting, standing and after a meal following water drinking (day 1 and day 7) was significantly higher than without water drinking (day 0). The effects of reducing OH and PPH on day 7 were equivalent to those on day 1. No adverse effects associated with daily water drinking were observed, except later diuresis, which occurred in one patient. Daily water drinking demonstrated constant pressor effects in the morning with no severe adverse effects in MSA patients. This finding suggests that water drinking should be tried as a practical measure to prevent or reduce OH and PPH.

Voglibose inhibits postprandial hypotension in patients with neurological disorders as well as in elderly people,

Voglibose inhibits postprandial hypotension in patients with neurological disorders as well as in elderly people,

Pathophysiology of postprandial hypotension in patients with progressive autonomic failure. Difference of cerebral blood flow during post-prandial hypotension between pure autonomic failure and multiple system atrophy

Pathophysiology of postprandial hypotension in patients with progressive autonomic failure. Difference of cerebral blood flow during post-prandial hypotension between pure autonomic failure and multiple system atrophy

Pathophysiology of post-prandial hypotension in patients with progressive autonomic failure. Hemodynamic changes in common carotid blood flow

Pathophysiology of post-prandial hypotension in patients with progressive autonomic failure. Hemodynamic changes in common carotid blood flow

Pathophysiology of post-prandial hypotension in patients with progressive autonomic failure. VI. Comparison of gut peptide responses to oral intake of glucose and protein

Pathophysiology of post-prandial hypotension in patients with progressive autonomic failure. VI. Comparison of gut peptide responses to oral intake of glucose and protein

Pathophysiology of post-prandial hypotension in patients with progressive autonomic failure. V. Comparative study of hemodynamic responses to protein and glucose loadings

Pathophysiology of post-prandial hypotension in patients with progressive autonomic failure. V. Comparative study of hemodynamic responses to protein and glucose loadings

Pathophysiology of post-prandial hypotension in patients with progressive autonomic failure. IV. Cerebral blood flow during post-prandial hypotension

Pathophysiology of post-prandial hypotension in patients with progressive autonomic failure. IV. Cerebral blood flow during post-prandial hypotension

The pathophysiology of postprandial hypotension in patients with progressive autonomic failure. II. Comparison with orthostatic hypotension

The pathophysiology of postprandial hypotension in patients with progressive autonomic failure. II. Comparison with orthostatic hypotension