(Stroke. 1995;26:1811-1816.)
© 1995 American Heart Association, Inc.
Articles |
Postprandial and Orthostatic Cardiovascular Changes After Acute Stroke
From the University Division of Medicine for the Elderly, The Glenfield Hospital, Leicester, UK.
Correspondence to Dr T.G. Robinson, University Division of Medicine for the Elderly, The Glenfield Hospital, Groby Rd, Leicester LE3 9QP, UK.
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Abstract |
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Background and Purpose Large falls in blood pressure after meals have been demonstrated in fit and frail elderly subjects; these changes may be associated with an increased incidence of stroke. Postprandial falls in BP may be particularly deleterious after acute stroke, when normal baroreflex mechanisms and cerebral autoregulation are already impaired, resulting in stroke progression. Therefore, the postprandial hemodynamic responses to orthostasis were examined in nine acute stroke subjects and eight age-, sex-, and blood pressure–matched control subjects after an oral energy load.
Methods All subjects were studied on two occasions in a randomized, double-blind, crossover trial after administration of either oral glucose (1 g/kg body wt) or equivalent isovolumic, isosmotic xylose (0.83 g/kg). Measurements of blood pressure, pulse rate, and forearm blood flow were recorded for 30 minutes preprandially and 90 minutes postprandially. Hemodynamic responses to 60° tilt, along with plasma glucose and insulin changes, were measured at baseline and at 30-minute intervals postprandially.
Results Supine mean arterial and diastolic blood pressures fell significantly after glucose but not xylose ingestion in control subjects (P<.03) but not stroke subjects, whereas supine pulse rate increased in stroke subjects (P<.04) only. No significant changes in forearm vascular resistance were recorded in either control or stroke subjects. After tilt, stroke subjects showed a fall in mean arterial pressure compared with control subjects preprandially (P=.03) and at 30 (P<.005) and 90 (P<.03) minutes postprandially, although no differences were observed between the xylose and glucose phases. Orthostatic tolerance was maintained in control subjects throughout both phases of the study. Pulse rate increased significantly to tilt at all time intervals in both groups, although there were no significant changes in forearm vascular resistance.
Conclusions Acute stroke subjects are not at significantly greater risk of blood pressure falls in response to an oral energy load than age-, sex-, and blood pressure–matched control subjects. Unlike control subjects, the stroke group had an increased pulse rate postprandially, which could result in a compensatory rise in cardiac output as a result of increased sympathetic nervous system activity in the poststroke period. Although orthostatic blood pressure control is impaired after acute stroke, these changes are unaffected by meals.
Key Words: aged • blood pressure • cerebrovascular disorders • hypotension
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Falls in BP after meals have now been convincingly demonstrated in both fit normotensive and hypertensive elderly subjects1 2 3 and institutionalized elderly.4 However, no such BP changes have been demonstrated in healthy young subjects when similar protocols are used.2 3 PPH probably results from age-related alterations in cardiovascular homeostatic mechanisms, including impairment of baroreceptor sensitivity5 and a decrease in insulin-induced sympathetic nervous system activation.6 Carbohydrate type and content of the meal also appear to be important contributing factors,7 8 as do higher BP levels3 9 10 and coexisting autonomic failure.11 12
Krajewski and colleagues13 have recently found an increase in calculated cerebrovascular resistance postprandially. This could be an important etiologic factor in the genesis of acute stroke, particularly in those with a compromised cerebrovascular circulation, as well as result in stroke progression after the acute event. Kamata and colleagues14 recently described a patient with evidence of severe middle cerebral artery disease and impaired cerebral vasodilatory responses to acetazolamide, who had repetitive, stereotyped transient ischemic attacks after food ingestion. Although studies of the diurnal variability in stroke occurrence have found an increased incidence associated with lower BP levels,15 16 a specific postprandial effect has not been assessed. Postprandial BP changes may also explain the increased prevalence of syncopal episodes in elderly institutionalized subjects4 as well as the reduced postprandial exercise tolerance in those with angina pectoris.17
Cerebral infarction has been reported to be associated with an impairment of orthostatic BP control, which Appenzeller and Descarries18 attributed to a blunting of baroreflex sensitivity after stroke. In another study of "chronic" stroke subjects, they demonstrated that baroreceptor function was further impaired by the oral administration of 75 g glucose.19 Johnson and colleagues20 have also described a series of patients with evidence of cerebrovascular disease who demonstrated marked orthostatic hypotension and evidence of impaired BP responses to the Valsalva maneuver.
Under normal conditions, cerebrovascular autoregulation ensures that cerebral blood flow is maintained over a wide range of systemic BP.21 However, abnormalities of cerebrovascular autoregulation and regional cerebral blood flow are well documented in response to an ischemic insult such as acute stroke.22 23 24 After the acute event, cerebral blood flow is dependent on systemic BP, and thus abnormal postprandial and orthostatic BP responses may have important implications in the clinical management of acute stroke patients. However, to our knowledge there have been no controlled trials of the changes in postprandial BP in acute stroke subjects.
We therefore proposed to study the BP responses to an oral energy load and orthostasis in acute stroke patients to assess whether such patients have a greater risk of BP fall in response to food and/or postural change than matched control subjects and to study possible mechanisms for any BP change including PR, FBF, and insulin and glucose responses.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Subjects
Nine subjects (6 men, 3 women; mean±SEM age, 67.2±2.1 years; age range, 54 to 74 years) were recruited after admission to the medical wards of the Leicester Teaching Hospitals for first-time acute anterior circulation stroke (three dominant hemispheres). All subjects had neurological signs lasting longer than 24 hours and were neurologically stable at the time of the study. Subjects were hemodynamically stable, did not require intravenous fluid administration, and were not biochemically dehydrated. They were dependent in activities of daily living (as assessed by a modified Rankin score
3) as a result of
their stroke; had no history of ischemic heart disease,
diabetes mellitus, atrial fibrillation, or conditions associated with
autonomic dysfunction; and were not receiving antihypertensive therapy
or medication known to affect cardiovascular or
autonomic responses. All subjects had cerebral infarction diagnosed by
head CT scan (5 cortical [1 with hemorrhagic transformation], 2
subcortical, and 2 lacunar). None had significant clinical carotid
artery stenosis, although carotid Duplex ultrasound scanning
was not routinely performed. In addition, 8 control subjects (4 men, 4
women; mean±SEM age, 66.1±1.9 years; age range, 60 to 74 years) were
recruited from among respondents to a local newspaper advertisement.
Control subjects with known diagnoses of ischemic heart
disease, diabetes mellitus, atrial fibrillation, cerebrovascular
disease, or conditions associated with autonomic dysfunction were
excluded. No subject received antihypertensive therapy or medication
known to affect cardiovascular or autonomic responses,
and all subjects were within 15% of ideal body weight (mean, 70.5±2.6
kg; range, 49.7 to 85.7 kg; body mass index, 24.4±0.7
kg/m2). Subjects gave their informed consent, and the study
was approved by the Leicestershire Hospitals Ethics Committee.
Protocol
Each subject was studied on two occasions at least 3 days apart
in a randomized, double-blind, crossover trial. Stroke subjects
were studied between 7 and 21 days after stroke onset to allow the
acute BP changes following acute stroke to stabilize.25
All studies were performed in the morning after an overnight fast,
including abstaining from smoking, alcohol, and all caffeinated
products. The investigations took place in a quiet room (ambient
temperature, 20°C to 24°C), and the subjects were asked to
micturate before the start of the study. On arrival, height and weight
were recorded, and supine BP was measured on three occasions in
both arms with a standard mercury sphygmomanometer
(diastolic phase V). There were no interarm differences in
BP in control or stroke subjects. All subjects were then familiarized
with the protocol, including the tilt procedure. An
intravenous cannula was inserted into an antecubital fossa
vein, patency was maintained with a heparinized saline flush (Pump-Hep,
Leo Laboratories Ltd), and the monitoring equipment was applied.
BP and PR were measured with the use of the Finapres (Ohmeda 2300 Finapres NIBP, Ohmeda). This is a fully automated instrument that allows continuous noninvasive measurement of finger arterial pressure. It uses the arterial clamp technique of Penaz26 and is well validated against intra-arterial BP measurements.27 28 In control subjects, the cuff was attached to the middle finger of the nondominant hand and in stroke subjects to the middle finger of the hemiparetic hand. Mean BP values for each time point were calculated for the preceding 8 beats, and the Finapres readings were updated every 4 beats. Readings were downloaded to a printer throughout the study period.
FBF was measured by venous occlusion plethysmography29 with mercury-in-silicone elastomer strain gauges.30 Venous return was occluded at a subdiastolic pressure of 40 mm Hg for 8 seconds at a rate of 4 cycles per minute by a cuff placed around the upper arm. Simultaneous occlusion of the arterial circulation to the hand was achieved by inflating a cuff at the wrist to 40 mm Hg above systolic BP. FBF was then calculated as milliliters per minute per 100 mL of forearm, and resting FVR was derived by dividing mean arterial BP by FBF. This well-established method is acceptable to subjects and correlates strongly with Doppler flowmetry.31 FBF was assessed in the nonhemiparetic arm of stroke subjects because of the potential for vasomotor changes in the hemiparetic arm.
After 30 minutes of supine rest on a tilt table, a blood sample was drawn for the measurement of preprandial blood glucose and plasma insulin. During the next 30 minutes, preprandial measurements of BP and PR were recorded for 2 minutes before and for 3 minutes during 60° tilt with the use of a foot plate and restraining support straps. FBF was also measured; during tilt both arms were kept at heart level by specially designed supports fitted to the tilt table to avoid hydrostatic artifacts. The tilt procedure was repeated, and mean preprandial supine and tilt BP and PR values were calculated.
The subjects then consumed either a control xylose drink (0.83 g/kg body wt) or a glucose drink (1 g/kg body wt) at room temperatures during a period of 5 minutes while semirecumbent. Xylose was chosen as an isosmotic, isovolumic monosaccharide drink, which is nonabsorbed and nonmetabolized compared with glucose. Subjects then returned to the supine position, and continuous measurements of BP and PR were recorded for the next 90 minutes. Recordings of BP, PR, and FBF were taken at 30, 60, and 90 minutes during tilt, as previously described. Additional blood samples for the measurement of blood glucose and plasma insulin were drawn immediately before tilt on each occasion.
Assay Methods
Blood glucose was measured by the glucose oxidase method (Astra
Reagent Kit, Beckman Instruments Inc). Plasma insulin was assayed with
the use of a radioimmunoassay kit (Coat-A-Count Insulin,
Diagnostic Products Corp). Sensitivity for this assay
was 1.2 µIU/mL, with an interassay coefficient of 7.3%.
Statistical Analysis
Data are presented as mean±SEM. Statistical comparisons
between baseline paired and unpaired normally distributed data were
made by Student's paired and unpaired t tests,
respectively. To reduce the overall probability of a type I error,
Bonferroni's correction factor was used as indicated in the text for
multiple comparisons.
BP and PR readings were analyzed from the printed Finapres
output to provide 5-minute supine and 15-second tilt mean values. Mean
BP and PR values for the last 5 minutes of every 15 minutes for supine
readings and the last 15 seconds of every minute for tilt readings were
used for subsequent analysis. Comparison of differences in the
changes in BP, PR, and FVR over time after xylose and glucose ingestion
between control and stroke groups was made with the use of
repeated-measures ANOVA with the GLM program of the
SAS statistical package. Group, time, treatment, and
interaction terms were studied, and a value of P
.05 was
considered statistically significant.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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All subjects consumed the entire drink on both occasions, and none reported any symptoms during the study period. Clinic BP was 145±8/79±5 mm Hg and 154±10/88±5 mm Hg in control subjects and stroke patients, respectively.
Supine Hemodynamic Responses
There were no significant differences in preprandial supine
Finapres BP and FVR between the two phases for control or stroke
groups. Although supine PR tended to be higher in the stroke group,
this difference did not reach statistical significance
(Table
). The changes in MAP and PR during the 90 minutes
after xylose and glucose ingestion are shown in Fig 1
for both groups.
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,
) or glucose (
, 
) in control and stroke subjects,
respectively. Values are expressed as mean±SEM. Occasionally SE bars
are omitted for clarity. *P<.02 (control glucose compared
with control xylose and stroke glucose), **P<.04 (time
effect in stroke group only).
In control subjects, there was a greater fall in supine
diastolic BP and MAP (Fig 1
) after glucose compared with
xylose ingestion, which was reflected by significant
treatment-by-time interactions (P=.05 and
P<.02, respectively, corrected for multiple comparisons),
although the difference for supine systolic BP changes did not reach
statistical significance. However, there were no significant
differences in BP responses between phases in stroke subjects.
When we compare the BP responses, there was a greater fall in supine
MAP (Fig 1) and diastolic BP after glucose in control than
in stroke subjects, which was reflected by significant
group-by-time interactions (P<.02 and
P<.03, respectively), although there was no significant
group difference for supine systolic BP changes. There was no
associated significant change in PR in control subjects. However, PR
increased in the stroke group, which was reflected by a significant
time effect (P<.04, Fig 1), but no treatment effect was
observed. A maximum rise of 7 beats per minute was observed 30 minutes
after glucose loading. There were no associated significant changes in
FVR in either stroke or control groups (data not shown).
Hemodynamic Responses to Tilt
Preprandial hemodynamic variables between the
two phases for control or stroke groups were similar (Table), although
preprandial tilt PR was significantly higher in both groups. The
changes in MAP and PR during the 3 minutes after 60° tilt are shown
in the top and bottom panels of Fig 2, respectively,
with changes from supine values expressed at minute intervals up to 3
minutes after tilt preprandially and 30, 60, and 90 minutes
postprandially.
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In control subjects, there were no significant changes in MAP after
tilt in both phases. However, when we compared the MAP responses to
tilt between groups, there was a significant fall in stroke patients
compared with control subjects after xylose ingestion (Fig 2, top
panel), reflected by significant group-by-time effects
(preprandial, P=.03; 30 minutes, P<.005), and
after glucose ingestion (preprandial, P<.02; 30 minutes,
P=.002; 90 minutes, P<.03). No treatment effect
was observed in the stroke group. PR increased significantly after tilt
at all time intervals in control subjects and stroke patients, although
there were no significant treatment-by-time or
group-by-time interactions (Fig 2, bottom panel). There were no
significant changes in FVR in either stroke or control groups.
Changes in Plasma Insulin and Blood Glucose Levels
Plasma insulin levels between the two phases for both control and
stroke subjects were not significantly different preprandially (Fig 3). The rise in plasma insulin after glucose ingestion
was greater compared with xylose for control and stroke subjects
(P=.0001). Peak plasma insulin levels occurred 60 minutes
after glucose ingestion, with a mean increase of 60.6 µIU/mL (95% CI
of the increase, 31.2 to 90.0 µIU/mL).
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Preprandial blood glucose levels were 4.4±0.1 and 5.7±0.5 mmol/L in control and stroke subjects, respectively, and were not significantly different. As expected, the increase in plasma glucose levels after glucose loading was greater than after xylose loading in both control and stroke subjects (P=.0001), but there was no significant overall difference in the changes between the two groups. Peak blood glucose levels occurred 60 minutes after glucose ingestion and were not significantly different, with a mean increase of 2.5 mmol/L (95% CI of the increase, 2.0 to 4.8 mmol/L) in the control group and 4.3 mmol/L (95% CI of the increase, 1.6 to 7.1 mmol/L) in the stroke group.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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It has been suggested that after stroke, glucose ingestion may significantly impair baroreceptor sensitivity.18 19 This may result in large postprandial falls in BP, and such rapid reductions in BP in the acute stroke period are best avoided. A recent case report has highlighted the possible relationship between PPH and stroke.15 The aim of the present study was to address whether postprandial falls in BP occurred after acute stroke and to compare the results with a matched control group. Perhaps surprisingly, the study failed to show that oral glucose resulted in a decrease in BP in the acute stroke period, although a significant postprandial fall in BP was demonstrated in the control group. No postprandial BP changes were seen after xylose ingestion in either group. The findings in the control group are in keeping with the results of other studies using a similar number of subjects and glucose load.3 32 33 However, the acute stroke group did show impairment of orthostatic tolerance compared with control subjects with a reduction in MAP on tilting preprandially and postprandially, although no difference was observed between the xylose and glucose phases. These changes occurred despite an increase in PR, although there was no change in peripheral vascular resistance as measured by FBF.
BP Changes in the Acute Stroke Group
No significant postprandial BP changes were observed in the acute
stroke group in the present study, despite changes that might
have been expected in view of the reported impairment of baroreceptor
sensitivity with cerebrovascular disease,18 the
further worsening of baroreceptor sensitivity in stroke subjects by
glucose loading,19 and the greater preprandial fall with
tilt. A previous study of elderly chronic ambulant stroke patients also
reported no differences in postprandial BP control after a 2.6-MJ (50%
carbohydrate) meal compared with a sham meal (water
only).34 A link between PPH and stroke has been
suggested,18 19 although only one case has been
reported.15 However, the present controlled study has
not found acute stroke subjects to be at greater risk of PPH. This may
have important clinical implications because it suggests that PPH need
not be taken into account in the management of stroke subjects.
Any tendency toward a postprandial BP fall after acute stroke may be compensated for by the increase in sympathetic nervous system activity after acute stroke,35 36 resulting in an increase in PR and cardiac output. Baseline PRs were higher in stroke patients than in control subjects, although this difference did not reach formal statistical significance, and there was a significant postprandial increase in PR not seen in control subjects. However, we did not make quantitative measurements of cardiac output or sympathetic nervous system activity to support or refute this hypothesis.
Orthostatic BP control in the acute stroke subjects was impaired, with significant falls in MAP compared with control subjects preprandially and postprandially, but no difference in effect was observed between the xylose and glucose phases. This has important implications in the clinical management of stroke patients because such orthostatic BP changes may be a risk factor for stroke extension in the acute period when cerebral blood flow is sensitive to sudden alterations in systemic BP. Previous studies reporting abnormalities of orthostatic BP control have been of chronic stroke patients. Farnsworth and Heseltine34 reported a significant mean reduction in systolic BP of 11 mm Hg after postural change, as have others.20
Impaired orthostatic control in stroke subjects may reflect blunted baroreflex function,18 although an appropriate compensatory increase in PR was observed that was not significantly different from control subjects. Age may also be an important factor in determining cardiovascular responses to orthostatic stress in stroke subjects. Korpelainen and colleagues37 studied subjects within 10 days of stroke and found no differences from control subjects in orthostatic BP responses. However, their subjects had a mean age of only 51.4 years (compared with 67.2 years in the present study), and the oldest subject studied was 67 years. Gross38 reported impaired circulatory reflex function to the Valsalva maneuver in a group of subjects with chronic cerebrovascular disease and found that age was a more important factor than cerebrovascular disease in producing the deterioration. Finally, cerebrovascular disease has been implicated in the deterioration of cardiovascular reflexes by producing ischemic brain stem changes that interfere with the baroreceptor reflex arc,18 20 although the subjects in the present study had no evidence of brain stem ischemic damage. However, abnormalities of circulatory reflex function are not significantly different between stroke subjects with carotid or vertebrobasilar disease,38 although the precise mechanism underlying autonomic dysfunction after cerebral hemisphere stroke is unclear.
BP Changes in the Control Group
The postprandial falls seen in MAP and diastolic BP
are in keeping with previous work in elderly normal subjects using a
75-g glucose load, and the following mean reductions have been reported
for systolic BP, MAP, and diastolic BP, respectively: 5, 6, and 6 mm
Hg3; 5, 7, and 9 mm Hg32; and 1, 8, and 7 mm
Hg.33 However, Lipsitz and colleagues39
observed no significant BP effects with an energy load similar to that
in the present study. Despite the fall in BP after glucose
ingestion in control subjects, there was no significant rise in PR, a
finding in keeping with that of other reports1 7 8 but not
all.3 This may reflect blunted baroreceptor responses
secondary to increasing age5 or elevated blood glucose or
insulin levels.19 40 The failure to increase heart rate
may also be due to the insulin-mediated antagonism of the
noradrenaline-induced positive chronotropic
effect.41 However, it seems unlikely that glucose and
insulin are primarily responsible for these changes because there were
similar responses in both control and stroke groups, and other
investigators have reported that insulin and glucose have no effect on
baroreceptor sensitivity.33 It is also unlikely that there
was marked baroreceptor impairment in control subjects in the
present study because there were significant increases in PR and BP
after tilt, findings similar to that in other postprandial BP studies
in the elderly.7
There was also no compensatory increase in FVR (as assessed by changes in FBF) in control subjects, which may have contributed to the fall in BP. Sidery and colleagues10 similarly reported a lack of peripheral vasoconstriction, although in the calf, in healthy elderly subjects after a 2.5-MJ meal. However, Lipsitz and colleagues42 have demonstrated intact forearm vasoconstrictor responses in healthy elderly subjects in response to a 1.6-MJ meal.
Insulin may also produce PPH independent of its effects on baroreceptor function by direct vasodilatation,43 44 impaired vasoconstrictor responses to catecholamines,45 or antagonism of noradrenaline-induced chronotropic effects.41 However, there were no differences in insulin responses to glucose between control and stroke groups. Increasing age may also impair myocardial chronotropic and inotropic responses to catecholamines46 and cardiac and peripheral vascular responsiveness to ß-adrenergic stimulation.47 The roles of other proposed mechanisms such as vasoactive gut peptides,48 adenosine,49 and possible changes in plasma volume were not investigated in the present study.
Conclusions
We found no evidence of a postprandial fall in BP in acute stroke
subjects, unlike the control group, and an increase in PR was only
noted in the stroke group postprandially. This increase in PR could
result from the increased sympathetic nervous system activity after
stroke and could lead to a greater postprandial increase in cardiac
output than in control subjects. However, orthostatic BP
control was impaired after acute stroke but was unaffected by glucose
or xylose loading. The exact mechanisms underlying these
hemodynamic changes after acute cerebral hemisphere
stroke remain unclear. Orthostatic but not postprandial BP
changes may be a risk factor for stroke extension in the acute period
and therefore may be important considerations in the clinical
management of patients.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported by a grant from the Stroke Association of the United Kingdom (Dr Robinson).
Received April 6, 1995; revision received June 19, 1995; accepted July 7, 1995.
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