From the Department of Neurology, Kyoto Second Red Cross Hospital (Y.Y.,
K.O., M.H.), and the Department of Neurology, Kyoto University (Japan) (I.A.,
J.K.).
Correspondence to Yasumasa Yamamoto, MD, Department of Neurology, Kyoto Second Red Cross Hospital, 355–5 Haruobicho Kamigyoku, Kyoto 602, Japan.
Methods—We studied 105 patients with symptomatic
lacunar infarcts who underwent repeated MRI and 24-hour BP monitoring
in the period between the two MRI examinations. The patients were
divided into five groups according to their outcome as follows: group
1, those who showed neither symptomatic episodes nor the
development of new silent lesions detected by repeated MRI; group 2,
those who only showed the development of silent lacunae; group 3, those
who showed development of diffuse white matter lesions only; group 4,
those who showed the development of both silent lacunae and diffuse
white matter lesions; and group 5, those who showed
symptomatic cerebrovascular disease. Groups 2 through 5
were then compared with group 1 with respect to the ambulatory BP
values.
Results—The average follow-up period was 3.2±2.6 years
(mean±SD). In all patients in group 4 and group 5, nighttime
systolic BPs were significantly higher than in group 1 (both
P<.01), and the magnitude of the nocturnal
systolic BP dip and diastolic BP dip in group 4 and
group 5 were significantly smaller than in group 1 (all
P<.01). In patients who took antihypertensive agents,
the 24-hour systolic and diastolic BPs and
nighttime systolic and diastolic BPs in group 4
were significantly higher than in group 1 (P<.01,
P<.01, P<.001, P<.01,
respectively). The magnitude of the nocturnal systolic and
diastolic BP dip in group 5 was significantly smaller than
in group 1 (both P<.01).
Conclusions—A high average ambulatory BP, especially nighttime
BP, and a reduced nocturnal BP dip may have an adverse effect on the
development of silent ischemic lesions and
symptomatic stroke attack in patients with lacunar
infarcts.
The studies mentioned above were conducted with casual BP values. Since
the introduction of ABPM devices, many reports have demonstrated that
hypertensive target organ damage can be more accurately demonstrated by
the 24-hour monitored BP than by the casual
BP.21 22 23 Most authors have reported that
nondippers, patients with an absent or decreased nocturnal dip in their
BP, tended to have more severe target organ damage, including
cerebrovascular disease,21 24 25 than dippers
with a normal nocturnal dip in BP. Verdecchia et
al26 conducted a prospective study and reported
that cardiovascular morbidity was higher in nondippers
than in dippers among women. Conversely, recent reports have suggested
that excessive falls in the nighttime BP27 28 or
a lowering of nighttime BP by antihypertensive
agents29 could produce cerebral ischemic
lesions. Therefore, the issue as to what degree the nighttime BP should
be controlled also remains unresolved.
Since 1990, we have been pursuing a prospective study to clarify the
appropriate BP for the prevention of silent and symptomatic
infarctions and to test whether the J-curve phenomenon exists for the
daytime BP or nighttime BP.
Because both lacunar infarcts and diffuse white mater lesions are
related to small artery disease (in which hypertension may play a major
role), we restricted the subjects to lacunar infarct patients. We then
followed them by tracking the progression of silent lesions, which
consisted of lacunar infarcts and diffuse white mater lesions, as well
as the recurrence of cerebrovascular disease by using MRI and
ABPM.
Twenty-Four-Hour Blood Pressure Monitoring
Magnetic Resonance Imaging
Patient Follow-up
Statistical Analysis
There were no significant differences among the five groups in age,
sex, complications from diabetes mellitus,
hypercholesterolemia, smokers, and the degree
of lacune, although the percentages of diabetes mellitus and
hypercholesterolemia tended to be higher in
groups 4 and 5. There were significant differences among the five
groups in the degree of diffuse white matter lesions
(P=.0015) (ANOVA). However, when groups 2 though 5 were each
compared with group 1, there were no significant differences.
Casual and ABP Values Between Groups
Sex Differences
Antihypertensive Treatment
Patients Without Antihypertensive Treatment
Patients With Antihypertensive Treatment
Over the past few decades, a considerable number of longitudinal
studies have been performed on the relationship between BP and stroke,
and most have demonstrated that a high BP is strongly related to stroke
occurrence.4 5 6 7 8 9 Most of these studies, however,
were based on the casual BP and symptomatic cerebrovascular
disease. The introduction of the ABPM and MRI have now made it possible
for us to study the relation of BP to the development of
cerebrovascular lesions more precisely, including silent
cerebrovascular lesions. This study is the first that was performed
prospectively with ABPM and MRI. We restricted the subjects to patients
with lacunar infarcts, which are believed to be directly related to
hypertension, and excluded those patients with atherothrombotic
occlusion and stenosis, so that we could explore the relation
between BP and ischemic cerebrovascular lesions more precisely
by studying a homogeneous patient group.
A high average ambulatory BP, especially at night, had a high
correlation with the development of both lacunar and white matter
lesions in the group that did not take antihypertensive agents [group
D(-)] and in the group that took antihypertensive agents [group
D(+)]. This correlation was demonstrated more clearly in group D(+)
than in group D(-). These results have much in common with the
previous cross-sectional studies that suggested that the nocturnal BP
had a higher correlation with target organ damage than the casual or
daytime BP. It has been assumed that persistent pressure overload would
increase the progression of hypertensive organ
damage.21 22 23 26 34 35 We conclude that the
findings in this longitudinal study have directly supported these
assumptions.
Both lacunar and white matter lesions have been believed to be strongly
associated with hypertension.36 37 38 39 In this
study, lacunae were identified only when they were located in the basal
ganglia, subcortical white matter, and pons. This appears to be
compatible with Fisher's definition,36 in which
lacunae are infarcts caused by the occlusion of branches of perforating
arteries. Lesions that measured less than 3 mm were not counted as
lacunae, so as to exclude état criblé. We identified
diffuse white matter lesions when they were located in the deep
subcortical white matter, which might correspond to characteristic
pathological findings, including a focal area with the prominent loss
of myelin and axons, small ischemic, microcystic infarcts, and
associated gliosis. These kinds of lesions are considered to reflect
ischemic tissue damages.33 We excluded
periventricular caps and smooth halos, which consist of
decreased myelin content, the loss of the ependymal cell layer, and
reactive gliosis,40 from diffuse white matter
lesions.
In group D(+)2 and D(+)3, lacunar and diffuse white matter lesions
developed, respectively. The nighttime BP tended to be higher in these
two groups, although not significantly when compared with group D(+)1.
It seems possible that a high nighttime BP might produce either lacunar
or diffuse white matter lesions. Moreover, it is clear that a higher
nighttime BP causes both lacunar and diffuse white matter lesions to
occur at the same time. In patients in whom both lacunar and diffuse
white matter lesions have developed, a progression to Binswanger's
disease41 42 is likely. In actual fact, the
severity of diffuse white matter lesions on the first MRI tended to be
greater in group 4 than in the other groups. Some of the patients in
these groups could have been classified as having Binswanger's disease
from the beginning, and the other patients in these groups are likely
to develop Binswanger's disease. Thus a sustained high BP overnight
may accelerate the development of Binswanger's disease.
The reduced nocturnal BP dip also tended to be smaller in groups 4 and
5 (Table 2
Over the last several years, two questions have been the subject of
controversy: whether a diminished nocturnal BP dip is the cause or the
consequence of hypertensive organ damage and whether this condition has
a beneficial or a harmful effect on organ damage. Traditionally, there
have been two different views: one was that sustained high BP overnight
might have adverse effects on end-organ
damage21 22 23 26 34 35 and the other was that a
diminished nocturnal BP dip might protect against end-organ damage
caused by a decrease in the blood flow during
sleep.43 This study demonstrated that nondippers
tended to have a worse prognosis than dippers in longitudinal studies.
As Table 2
There are reports attributing nondipper mechanisms to autonomic
disturbance. We showed that autonomic disturbances play
a role as one of the mechanisms associated with a diminished nocturnal
BP decline.25 Kohara et
al44 showed that the nondipper phenomenon was due
to the failure of withdrawal of sympathetic tone at night, and Ebata et
al45 pointed out that increased
In this study, it appears that there were no patients in whom an
excessively low BP, in either their daytime or nighttime BP, might have
accelerated ischemic lesions (Fig 2
It should be noted that if dippers and nondippers were equated
according to their daytime BP, the average 24-hour BP or nighttime BP
would be higher in the nondippers. Because BP is usually monitored on
the basis of the casual BP, which is measured during the daytime, one
ought to consider this fact when determining suitable BP levels
throughout a 24-hour period.
A high average ABP and a reduced nocturnal BP dip may have adverse
effects on the prognosis of patients with lacunar infarcts. Although
multiple factors contribute to the development of new lesions, we can
expect to attenuate the development of silent cerebrovascular lesions
and the recurrence of stroke by controlling BP more carefully.
The mechanisms by which new lesions develop might go beyond these
results. Further investigation is necessary to clarify these
issues.
Received September 3, 1997;
revision received December 18, 1997;
accepted December 18, 1997.
© 1998 American Heart Association, Inc.
Original Contributions
Adverse Effect of Nighttime Blood Pressure on the Outcome of Lacunar Infarct Patients
Abstract
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Background and
Purpose—Antihypertensive therapy has dramatically reduced the
incidence of stroke recurrence; however, recent studies have
suggested that the excessive lowering of blood pressure (BP) could
cause ischemic cerebral lesions. We conducted a prospective
study using MRI and ambulatory blood pressure monitoring to elucidate
the appropriate BP control level for the prevention of silent and
symptomatic cerebral infarction.
Key Words: Binswanger's disease • blood pressure, nocturnal • lacunar infarction • white matter
Introduction
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
The issue of the
control of blood pressure levels in stroke prevention remains
unresolved. Uncontrolled hypertension has been shown to produce
arteriosclerosis in small vessels and
atherosclerosis in medium-sized vessels in the brains
of experimental animals with hypertension.1 2
Antihypertensive medications can prevent these pathological changes in
medium-sized vessels.3 Antihypertensive therapy
reduces cerebrovascular and cardiovascular morbidity
and mortality in humans with chronic
hypertension.4 5 6 7 8 9 Nevertheless, several studies
have suggested that an excessive lowering of BP can cause
ischemic stroke10 11 12 13 14 and a decline in
cognitive function.15 These studies also suggest
that decreased BP might reduce cerebral blood flow, especially in
chronic stroke patients in whom an upward shift of the autoregulatory
range was recognized after the acute period had
passed,16 even though it is widely thought that a
high sustained BP may accelerate pathological changes in the cerebral
vessels of the brain.17 18 19 Irie and his
colleagues14 reported that the J-curve
phenomenon, in which there is a point beyond which BP reduction in
hypertensive subjects is no longer beneficial and possibly even
deleterious, which has been recognized in cardiac
events,20 was also found in ischemic
stroke recurrences.
Subjects and Methods
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Subjects
We studied 105 patients with symptomatic lacunar
infarcts that were located in the supratentorial
region; those patients were followed up with MRI and 24-hour BP
monitoring. The patients were selected in the following manner. Two
hundred eighty-five patients with symptomatic lacunar
infarcts for the first time were treated in our clinic at Kyoto Second
Red Cross Hospital between January 1991 and December 1996. Of these 285
patients, 182 who had undergone 24-hour BP monitoring for over 4 weeks
after ictus were registered in this study and were informed that
follow-up MRI scans would be conducted in the future. All of the
patients consented to participate in this study. Excluded were 28
patients in whom the dosage and kinds of antihypertensive agents had
been changed after 24-hour BP monitoring, 22 patients who had not
undergone a repeat MRI during the follow-up period, 23 patients who had
dropped out, and 4 patients who had died. Thus a total of 105 patients
who underwent repeat MRI as well as 24-hour BP monitoring in the period
between the two MRI examinations were enrolled in this study. Patients
who had embologenic cardiac disease and obvious
atheromatous stenotic lesions as detected by
MRA were excluded. Antiplatelet drugs were administrated to all of
the patients.
We monitored the 24-hour BP by using a portable automatic
recorder (ABPM-630, Nippon Corin Co) after the patients had
undergone their first MRI examination. The accuracy of the equipment
had been established30 and the pattern of
circadian BP change were thought to be reproduced well in same
person.31 The 24-hour BP monitoring was carried
out in an outpatient office and was managed by the authors of this
study during a period in which each patient's BP appeared to be
appropriately controlled as detected by the casual BP, with and without
antihypertensive drugs. The goals of the casual BP control were
determined as follows: SBPs were controlled below the level of 160
mm Hg in patients who were 69 years old or younger; 170 mm Hg in
patients who were 70 to 79 years old; and 180 mm Hg in patients
who were 80 to 89 years old; DBPs were controlled below the level of
95 mm Hg in all age groups. Blood pressure was recorded at
30-minute intervals over 24 hours from 1 PM to 1
PM next day. ABP values, including the average 24-hour BP,
daytime BP, and nighttime BP, were calculated as follows. SBP and DBP
were averaged over successive 30-minute periods throughout the 24-hour
period. The mean daytime (6 AM to 10 PM) and
nighttime (10:30 PM to 5:30 AM) BP values were
also calculated. The magnitude of the nocturnal BP dip was calculated
as [(mean daytime BP-mean nighttime BP)/average BP for the entire 24
hours]x100.
MRI scans were performed with 1.0-T superconducting magnets
(Impact, Siemence) at least twice during the follow-up period. The
first MRI was performed during the period from 14 days to 42 days after
ictus of lacunar stroke. A diagnosis of lacunar stroke was made when
both lacunar syndrome and lacunar infarcts were confirmed in the MRI
scan. Basically, patients underwent MRI once a year, and several
patients who seemed to be less well controlled, every 6 months.
Transverse T1-weighted scans (TR: 525 ms/TE: 14 ms), T2-weighted scans
(TR: 3500 ms/TE: 16 ms), and proton density images (TR: 3500 ms/TE: 98
ms) were obtained at a slice thickness of 8 mm. We evaluated the
lacunar and diffuse white matter lesions on the baseline MRI. Lacunae
were defined as lesions greater than 3 mm but less than 10 mm
in diameter and with low intensity on T1-weighted images but high
intensity on T2-weighted and proton density images. The number of
lacunae was counted and graded as 0, absent; 1, one to two lacunae; 2,
three to five lacunae; and 3, more than six lacunae. Diffuse white
matter lesions were defined as diffuse hyperintensities on T2-weighted
images and proton density images, which were located in the white
matter and were specified and graded according to Fazekas's
classification32 into 0, absent; 1, punctuate; 2,
becoming confluent; and 3, confluent. Hyperintense
periventricular caps and smooth halos were not counted as
diffuse white matter lesions.33 Both baseline MRI
and final MRI were evaluated by two authors (Y.Y. and I.A.) who were
blinded to the BP data and the outcome data. The mean period between
the first and last MRI was 3.2±2.6 years (mean±SD).
We followed up the subjects prospectively at our outpatient
clinic until March 31, 1997. Most patients (90) were seen once a month
and some patients (15) every 2 or 3 months in outpatient clinic. Those
who had new neurological deficits that continued for more than 24 hours
were estimated as having symptomatic cerebrovascular
disease. In those patients with no symptomatic
cerebrovascular disease, we compared the final MRI with the first MRI
to detect whether new lesions, including lacunae and diffuse white
matter lesions, had developed. Patients were divided into five groups
according to their prognosis as follows: group 1, those who showed
neither symptomatic episodes nor the development of new
silent lesions as detected by repeated MRI; group 2, those who showed
the development of silent lacunae only; group 3, those who showed
development of diffuse white matter hyperintensities only; group 4,
those who showed the development of both silent lacunae and diffuse
white matter lesions; and group 5, those who showed
symptomatic cerebrovascular disease. Division of the
patients into five groups was based on the speculation that
asymptomatic and symptomatic infarcts or
lacunar infarcts and leukoaraiosis could be influenced differently by
BP. We ordered severity as follows: symptomatic infarcts,
asymptomatic lacune, and diffuse white matter lesions.
Statistical comparisons among the five groups were performed
with a one-way ANOVA for parametric values and with a
Kruskal-Wallis test for nonparametric categories. When
there were differences among the five groups, groups 2 through 5 were
each compared by Bonferroni's method with group 1, which had the best
prognosis. In analyzing the distribution of sex and risk factors among
the groups, a 
2 test was used. The values were
expressed as mean±SD. A value of P<.05 was considered
statistically significant, but a value of P<.0125 was
considered to be statistically significant by Bonferroni's method.
Results
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Classification by Outcomes
We obtained complete tracking data from 105 of the 182 patients
who entered the study from January 1991 through December 1997. The mean
duration of tracking was 3.2 years (range, 6 to 74 months). The 105
patients studied for the entire period were divided into five groups:
group 1, 50 patients in whom the MRI findings had not changed; group 2,
16 patients in whom a silent lacuna or lacunae had developed; group 3,
14 patients in whom white matter hyperintensities had developed; group
4, 11 patients in whom both silent lacunae and white matter
hyperintensities had developed; and group 5, 15 patients in whom
symptomatic cerebral infarctions had developed.
(Symptomatic cerebral infarctions consisted of 13 lacunar
infarcts and 2 cortical infarcts.) The patient characteristics for each
group, including age, sex, complications from diabetes mellitus and
hypercholesterolemia, smokers, and the degree
of lacunar and white matter lesions on baseline MRI findings, are given
in Table 1
. Groups 2 through 5 were then
compared with group 1 with respect to these items.
View this table:
[in a new window]
Table 1. Characteristics of Patients in Five Groups Divided
by Outcome
The mean values and standard deviations at which the
casual BPs were controlled, the average 24-hour BP, daytime BP,
nighttime BP, and the magnitude of the nocturnal BP dip are given in
Table 2. The patients whose casual BPs
were not controlled within the range that we had described in the
"Methods" section were as follows: three patients in group 1, three
in group 2, two in group 3, two in group 4, and two in group 5.
Compared with group 1, groups 2 through 5 had significantly higher
systolic nighttime BPs (group 4, P=.002, and group
5, P=.002), smaller magnitude of the nocturnal SBP dip
(group 4, P=.001, and group 5, P=.01), higher
nighttime BP (group 4, P=.003), and smaller magnitude of the
nocturnal DBP dip (group 4, P=.001, and group 5,
P=.005) (Table 2).
View this table:
[in a new window]
Table 2. Comparison of Blood Pressure Values Among the Five
Groups
All of the patients in each group were divided into male (72
patients) and female (33 patients) subgroups. The ABP values were then
compared across severity groups including both D(+) and D(-) within
each sex. In both men and women, there were no significant differences
among the five groups in any of the ABP values (ANOVA).
All of the patients studied were then divided into two groups:
group D(-), 35 patients who did not take antihypertensive agents, and
group D(+), 70 patients who took antihypertensive agents. Their mean
casual BP, average 24-hour BP, daytime BP, nocturnal BP, and the
magnitude of their nocturnal BP dip in group D(-) and group D(+) are
given in Table 2
.
Compared with group D(-)1, groups D(-)2 through D(-)5 had
significantly smaller magnitude of the nocturnal DBP dip [group D(-)4
(P=.002)]. The daytime and nighttime BPs for the five
groups are plotted in Fig 1.
View larger version (29K):
[in a new window]
Figure 1. ABPs (upper: daytime; bottom: nighttime; left:
SBP; right: DBP) in patients who did not take antihypertensive agents
[D(-)].
Compared with group D(+)1, groups D(+)2 through D(+)5 had
significantly higher 24-hour SBP [group D(+)4 (P=.001)],
higher nighttime SBP [groups D(+)4 (P=.0003) and D(+)5
(P=.005)], lower magnitude of nocturnal SBP dip [group
D(+)5 (P=.003)], higher 24-hour DBP [group D(+)4
(P=.002)], higher daytime DBP [group D(+)4
(P=.008)], higher nighttime DBP [group D(+)4
(P=.001)], and lower magnitude of the nocturnal DBP dip
[group D(+)5 (P=.006)] (Table 2). The daytime and
nighttime BPs for the five groups are plotted in Fig 2. There were no patients who showed an
excessively low BP in the daytime or at night in groups D(+)2 through
D(+)5.
View larger version (31K):
[in a new window]
Figure 2. ABPs (upper: daytime; bottom: nighttime; left:
SBP; right: DBP) in patients who took antihypertensive agents [D(+)].
Groups 2 through 5 are compared with group 1. 
P<.01,
P<.001.
Discussion
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
This study demonstrated that a high ambulatory BP, especially at
night, and a reduced nocturnal BP dip were both associated with the
development of silent ischemic lesions (both lacunar and
diffuse white matter lesion) and symptomatic
ischemic stroke recurrences in lacunar infarct
patients. No patients showed the development of new lesions caused by
an excessive lowering of their daytime or nighttime BP. Unlike other
studies, our study did not find that the J-curve
phenomenon14 was present or that an excessive
fall in the nighttime BP27 28 29 caused cerebral
ischemic lesions. ). It is likely that a reduced nocturnal BP dip may have a
high correlation with the high nighttime BP. Verdecchia et
al26 reported that ambulatory hypertension and an
absent nocturnal BP dip were independent predictors of
cardiovascular morbidity. Verdecchia and colleagues'
report may be the first longitudinal study to have demonstrated that
cardiovascular morbidity was higher in nondippers than
in dippers. However, Verdecchia and colleagues' study was performed on
the basis of baseline, off-therapy, ambulatory BP. It appears that
nondippers have a worse prognosis, as detected by their ABPs during
therapeutic intervention, which we have demonstrated in this study, as
well as by their baseline, off-therapy, ambulatory BP. indicates, a reduced nocturnal BP and/or high ABPs appeared
to be responsible for the new lesions and events observed in groups 4
and 5. 
1-adrenergic receptor stimulation might be one
of the primary causes of a high nighttime BP in nondippers. Thus it may
be safely assumed that central autonomic disturbances, which
are present in nondippers, might impair their ability to control
their BP and cerebral blood flow and thus might accelerate end-organ
damage. Therefore a reduced nocturnal BP dip, with or without high
average ambulatory BP, may have adverse effects on end organ
damage. ). Our results differ from
those in which the J-curve phenomenon was
recognized14 and in which an excessive nocturnal
BP dip was thought to cause new lesions.27 28 One
of the reasons for this difference may be the fact that the patient BP
was controlled at a relatively high level in this study. The high BP
levels in our study were due to control, based on the theory of
cerebral autoregulation, and we also had some patients in whom BP was
unresponsive to medication. Another reason our results differ from
those in which the J-curve phenomenon was recognized is that we
restricted our subjects to patients with lacunar infarcts and excluded
those with atherothrombotic lesions. Kario et
al27 and Watanabe et al28
hypothesized that in their cross-sectional studies, an excessive
nocturnal BP dip might have caused silent cerebrovascular lesions. Our
longitudinal study did not support this view. It is likely that a high
daytime BP in those patients with an excessive nocturnal BP dip, rather
than the nocturnal BP dip itself, accelerates silent cerebrovascular
lesions.46
Selected Abbreviations and Acronyms
ABP
=
ambulatory blood pressure
ABPM
=
ABP monitoring
BP
=
blood pressure
DBP
=
diastolic BP
SBP
=
systolic BP
References
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
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P. Verdecchia Prognostic Value of Ambulatory Blood Pressure : Current Evidence and Clinical Implications Hypertension, March 1, 2000; 35(3): 844 - 851. [Abstract] [Full Text] [PDF]
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S. L. Dawson, B. N. Manktelow, T. G. Robinson, R. B. Panerai, and J. F. Potter Which Parameters of Beat-to-Beat Blood Pressure and Variability Best Predict Early Outcome After Acute Ischemic Stroke? Stroke, February 1, 2000; 31(2): 463 - 468. [Abstract] [Full Text] [PDF]
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 C. Bassetti and M. Aldrich Night time versus daytime transient ischaemic attack and ischaemic stroke: a prospective study of 110 patients J. Neurol. Neurosurg. Psychiatry, October 1, 1999; 67(4): 463 - 467. [Abstract] [Full Text] [PDF]
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G. Y. H. Lip, C. R. Gibbs, and D. G. Beevers Ambulatory Blood Pressure Monitoring and Stroke : More Questions Than Answers Stroke, August 1, 1998; 29(8): 1495 - 1497. [Full Text] [PDF]
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A. Chamorro, Y. Yamamoto, and I. Akiguchi Ambulatory Blood Pressure in Lacunar Infarct Patients • Response Stroke, August 1, 1998; 29(8): 1740 - 1742. [Full Text]
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