(Hypertension. 1999;33:565-568.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Postprandial Hypotension Is Associated With Asymptomatic Cerebrovascular Damage in Essential Hypertensive Patients
From the Department of Geriatric Medicine (K.K.), Second Department of Internal Medicine, Ehime University School of Medicine, Onsen-gun, Ehime, Japan.
Correspondence to Katsuhiko Kohara, MD, Department of Geriatric Medicine, Ehime University School of Medicine, Onsen-gun, Ehime 791-0295, Japan. E-mail koharak{at}m.ehime-u.ac.jp
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Abstract |
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Abstract—To elucidate the relationship between postprandial hypotension (PPH) and asymptomatic cerebrovascular damage, we evaluated changes in blood pressure after a meal by 24-hour blood pressure monitoring in 70 hospitalized essential hypertensive patients aged
50 years. They
received a diet containing standard nutritional ingredients with
120 mmol (7 g) NaCl and were free from medication for at least 1
week. PPH was defined as the mean reduction of systolic blood
pressure during 2 hours after a meal. Patients were divided into three
groups according to mean values of PPH after 3 meals: PPH-1 (n=16,
5 mm Hg
PPH<10 mm Hg), PPH-2 (n=18, PPH10 mm Hg),
and normal (n=36, PPH<5 mm Hg). As asymptomatic
cerebrovascular damage, lacunae and leukoaraiosis were evaluated
by magnetic resonance imaging. PPH did not correlate with daytime or
nighttime blood pressure or the nondipper phenomenon; however, PPH was
significantly related to asymptomatic cerebrovascular
damage. The prevalence of lacunae in the normal, PPH-1, and PPH-2
groups was 44%, 69%, and 83%, respectively (
2=8.22,
P<0.05). The number of lacunae in the normal, PPH-1,
and PPH-2 groups was 1.0±1.3, 1.3±1.2, and 1.9±1.4,
respectively (F[2,67]=3.2, P<0.05). The prevalence of
advanced leukoaraiosis in the normal, PPH-1, and PPH-2 groups was 44%,
50%, and 83%, respectively (2=7.63,
P<0.05). Severity score of leukoaraiosis in the normal,
PPH-1, and PPH-2 groups was 1.5±0.7, 1.7±0.8, and 2.1±0.7,
respectively (F[2,67]=4.3, P<0.05). These findings
indicate that elderly hypertensive patients with marked PPH should be
considered to have advanced cerebrovascular damage even in the absence
of abnormal neurological findings.
Key Words: blood pressure monitoring • elderly • hypotension, postprandial • lacuna • leukoaraiosis • blood pressure variability
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Introduction |
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Alteration of the diurnal change in blood pressure (BP) has been shown to be related to several clinical abnormalities, including advanced end-organ damage,1 2 3 secondary hypertension,4 and autonomic nervous system dysfunction.5 Several studies have demonstrated a linkage between asymptomatic brain damage and alteration of the diurnal change in BP.2 6 7 8 Recently, it has also been shown that dysregulation of postural change in BP is associated with advanced silent cerebrovascular damage in hypertension in the elderly.9
Asymptomatic cerebrovascular damage, often found in elderly hypertensive individuals, is associated with cognitive dysfunction,9 depression of mood,10 and reduced capacity of the cerebral circulation.11 12 It has also been shown that patients with asymptomatic lacunae have a significantly higher incidence of future stroke than normal subjects.13
Postprandial hypotension (PPH) is a relatively common phenomenon frequently observed in elderly hypertensive patients.14 However, only a few studies have investigated the effect of PPH on the diurnal change in BP in hypertensive patients.15 16 In our previous study,16 we evaluated PPH with ambulatory BP monitoring (ABPM) and showed that PPH contributed to the variability of BP in the daytime and the morning surge of BP, independent of the dipper and nondipper phenomena. Clinically, PPH can cause light-headedness, fainting, falls, or even transient ischemic attack.14 Recently, it has also been shown that PPH is an independent risk factor for future mortality, coronary events, and stroke.17 These findings suggest the relevance of PPH to cerebrovascular damage.
The objective of the present study was to elucidate whether PPH is associated with asymptomatic cerebral damage. Since daily activity, including the awake and sleeping times, as well as the contents of meals could significantly influence diurnal change in BP, the present study was performed on hospitalized essential hypertensive patients with standardized daily activities and meals.
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Methods |
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Seventy hospitalized essential hypertensive patients aged
50
years participated in the study. They were recruited from consecutive
cases admitted to the Second Department of Internal Medicine, Ehime
University Hospital, for the evaluation of hypertension and agreed to
undergo brain magnetic resonance imaging (MRI). All of the participants
were free from any abnormal neurological findings. Patients with
autonomic nervous dysfunction, congestive heart failure, previous
myocardial infarction, or history of symptomatic
cerebrovascular accident including transient ischemic attack
were excluded from the study. The contents of meals, times of meals,
and daily activities were standardized. Total caloric intake for the
patients was 126 kJ/kg (30 kcal/kg) ideal body wt per day. The dietary
composition was 66% carbohydrate, 16% protein, and 18% fat for each
patient. Meal times were 8 to 8:30 AM for breakfast, noon
to 12:30 PM for lunch, and 6 to 6:30 PM for
dinner. Snacks and drinks, including coffee after meals, were
prohibited.16 All procedures were approved by the ethics
committee of Ehime University Hospital. Informed consent to the
procedure was obtained from each patient.
Twenty-Four–Hour BP Determination
Twenty-four–hour BP was measured by a cuff-oscillometric method
(TM-2421, A/D Ltd). BP was measured every 30 minutes from 6
AM to 10 PM and every 60 minutes from 10
PM to 6 AM on the following
day.5 16 Daytime and nighttime BPs were obtained as the
average values during the awake period between 6 AM and 10
PM and during the sleep period between 10 PM
and 6 AM, respectively.5 16 Patients were
allowed to move freely but asked to sit quietly on a bed or chair
during BP measurement. The waking time, time needed to fall asleep, and
quality of sleep were assessed by interview with each patient.
Postprandial change in BP was defined as the difference between mean
systolic BP (SBP) during 1 hour before and during 2 hours after
a meal.16 BP values during the meal were excluded to avoid
the influence of postural or eating-related change in BP. Patients were
divided into the following three groups according to the mean
postprandial change in SBP for three meals: PPH-1 (n=16, 5
mm HgPPH<10 mm Hg), PPH-2 (n=18, PPH10 mm Hg), and
normal (n=36, PPH<5 mm Hg).
Magnetic Resonance Imaging
MRI was performed using a superconducting magnet with a main
field strength of 1.5 T. As asymptomatic cerebrovascular
damage, the presence of lacunae was evaluated in all patients. A lacuna
was defined as a low-signal-intensity area (>0.3 cm and <1.5 cm) on
T1-weighted images that was also visible as a hyperintense lesion on
T2-weighted images. The number of lacunae per patient was counted.
Leukoaraiosis, deep white matter lesions, depicted on T2-weighted
images was classified into four grades: grade I, no abnormality or
minimal periventricular signal hyperintensities in the form
of caps confined exclusively to the anterior horns or rims lining the
ventricles; grade II, hyperintensities in both the anterior and
posterior horns of the lateral ventricles or
periventricular unifocal patches; grade III, multiple
periventricular hyperintense punctate lesions and their
early confluence; and grade IV, multiple areas of high signal intensity
reaching confluence in the periventricular
region.9 White matter lesions were scored from 1 to 4
according to the grade. One author who was blinded to the clinical
status of the subjects interpreted all MRI scans.
Statistical Analysis
All values are expressed as mean±SD if not specified otherwise.
Differences among groups were evaluated by analysis of variance
followed by Duncan's multiple range test. Difference in prevalence was
analyzed by 2 test. A probability less
than 0.05 was defined as significant.
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Results |
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Postprandial Change in SBP
Figure 1
summarizes daytime changes
in SBP in the normal, PPH-1, and PPH-2 groups. A decline in SBP was
observed after each meal. It was also notable that PPH contributed to
the fluctuation of SBP.
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Table 1 summarizes demographic and
hemodynamic parameters in the three groups.
Among the three groups, there were no difference in sex, body mass
index, duration of hypertension, and other risk factors, including
smoking, hyperlipidemia, and diabetes mellitus. The
prevalence of previous antihypertensive treatment also did not differ
among the three groups (81% for normal, 75% for PPH-1, and 72% for
PPH-2). However, patients in the PPH-2 group were significantly older
than those in the normal and PPH-1 groups. Daytime and nighttime BPs as
well as nocturnal change in SBP also did not differ among the three
groups.
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Asymptomatic Brain Damage and PPH
Table 2 summarizes
asymptomatic cerebrovascular damage in each group of
patients. There was a significant difference in the prevalence of
lacunae (2=8.22, P<0.05), number
of lacunae (F[2,67]=3.2, P<0.05), prevalence of advanced
leukoaraiosis (gradeII) (2=7.63,
P<0.05), and the severity score of leukoaraiosis
(F[2,67]=4.3, P<0.05) among the three groups. The
prevalence and severity of asymptomatic cerebrovascular
damage were significantly greater in the PPH-2 group.
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To further clarify the relationship between PPH and
asymptomatic brain damage, mean postprandial change in SBP
was evaluated according to the number of lacunae and the grade of
leukoaraiosis (Figure 2). There was a
severity-dependent augmentation of mean PPH according to the severity
of both lacunae and leukoaraiosis.
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Discussion |
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The circadian alteration of BP has been shown to be closely related to asymptomatic cerebrovascular damage in elderly hypertensive patients. The nondipper phenomenon2 and the extreme dipper phenomenon6 have been reported to be related to asymptomatic cerebrovascular damage. Recently, Matsubayashi et al9 reported that postural dysregulation of BP was associated with asymptomatic cerebrovascular damage in elderly subjects. Elderly subjects who showed orthostatic hypotension as well as orthostatic hypertension had advanced asymptomatic brain lesions.9 They speculated that long-standing excessively altered changes in BP may impair cerebral perfusion and bring about changes, such as lacunae and leukoaraiosis, in the elderly.
In the present study, we observed a significant correlation between PPH and asymptomatic brain damage. Although PPH has been reported to be more common than orthostatic hypotension,18 a close relationship between the two conditions has also been reported.19 Since we did not evaluate orthostatic hypotension in the present study, we could not exclude the possibility that our finding was a mere reflection of the higher prevalence of orthostatic hypotension in patients with advanced PPH.
The preprandial BP level was significantly higher in the PPH-2 group
for all meals than in the normal group (Table 1
). It is possible
that the daytime BP would be higher in patients with PPH if they did
not eat a meal. If the preprandial BP level was assumed as the daytime
BP (ie, elimination of the effect of PPH), patients with marked PPH
might have a profound decrease in nighttime BP. These findings may
indicate that patients with PPH had an excessive change in BP not
only after meals but also at night, and this change might contribute to
the impairment of cerebral perfusion. Krajewski et al20
measured blood flow velocity of the middle cerebral artery in elderly
patients with PPH by the transcranial Doppler method
after a test meal. Although the meal did not change mean blood flow
velocity, the pulsatility index was significantly increased after the
meal, suggesting vasoconstriction of cerebral arteries after
meals.20 They speculated that postprandial
vasoconstriction led to cerebral ischemia. Several lines of
evidence suggest that leukoaraiosis reflects the decrease in cerebral
circulation. These findings, together with the finding of the
present study that patients with PPH had a higher prevalence of
organic brain damage, further support the impairment of cerebral
circulation in patients with PPH.
The definition of PPH in the present study was rather arbitrary.14 Although we defined PPH as the difference in SBP before and after a meal,16 there is no definition of PPH when BP is evaluated by ABPM. Accordingly, we also evaluated the relationship between the degree of asymptomatic cerebrovascular damage and PPH. We observed a severity-dependent augmentation of PPH according to the severity of both lacunae and leukoaraiosis.
BP assessment by ABPM provides more useful information than assessment of 24-hour mean BP. ABPM can also assess diurnal change of BP, including the dipper and nondipper phenomena, white coat hypertension, and BP variability. Recently, Aronow and Ahn17 reported the prognosis of elderly patients with PPH in their prospective study. They found that PPH was an independent risk factor for future mortality, coronary events, and stroke. The present study further suggests the usefulness of evaluating PPH by ABPM, since PPH could also indicate the presence of asymptomatic cerebrovascular damage in addition to the prognosis of future cardiovascular events.
In summary, we showed that PPH was significantly related to asymptomatic cerebrovascular damage in essential hypertension in the elderly, even in the absence of abnormal neurological findings. It may be worthwhile to evaluate postprandial change in BP measured by ABPM for further information about asymptomatic brain damage in elderly hypertensive patients.
Received September 16, 1998; first decision October 22, 1998; accepted November 2, 1998.
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