(Stroke. 1998;29:1740-1742.)
© 1998 American Heart Association, Inc.
Ambulatory Blood Pressure in Lacunar Infarct Patients
A. Chamorro, MD
Neurology Service,
Hospital Clinic,
Barcelona, Spain
To the Editor:
We read with interest the recent paper by Yamamoto and
colleagues1 evaluating longitudinal changes in MRI in
patients with lacunar infarcts. The main conclusion reached by these
authors is that high average ambulatory blood pressure, especially
nighttime blood pressure, and a reduced nocturnal blood pressure dip
may facilitate the development of silent ischemic lesions as
well as symptomatic stroke recurrences in patients
with lacunar infarcts. Before accepting these important conclusions, we
believe that some comments are pertinent. We have also evaluated the
effects of blood pressure in patients with first-ever lacunar infarcts
and its association with the coexistence of silent lacunar
infarcts2 and periventricular white matter
intensities.3 Our main results suggest that both types of
radiological signals react to separate hemodynamic
mechanisms. Whereas silent lacunar infarcts seem to be related to
elevated diurnal diastolic blood pressure,
periventricular white matter intensities are better
explained by elevated diurnal systolic blood pressure. A
reduced heart rate, especially in lacunar infarct patients with a
previous history of heart disease (symptoms of coronary heart
disease, congestive heart failure, or electrocardiographic proof of
ischemic changes or nonvalvular atrial fibrillation),
is an additional factor associated with the severity of white matter
abnormalities. It is likely that the angioarchitectural characteristics
of the supplying vessels to the periventricular white
matter explain why this region is vulnerable to different components of
arterial blood pressure compared with the
arterial territory of the lenticulostriate,
thalamoperforant, or perforant branches of the basilar artery, where
most silent lesions are located. In opposition to Yamamoto and
colleagues, we did not find significant differences between the
nocturnal blood pressure dip and the extent of silent subcortical or
periventricular ischemic lesions. Yamamoto and
colleagues did not observe significant blood pressure differences
between patients who took antihypertensive agents and those in whom
blood pressure followed its natural course. However, if Yamamoto et al
are right, hypotensive medication should be increased at night to
augment the nocturnal blood pressure dip. Conversely, if our findings
prove correct, the medication should be adjusted mainly to avoid
elevated diurnal systolic and diastolic blood
pressure and to prevent an excessive reduction in heart rate, which
frequently occurs at night. Nevertheless, our results also suggest that
therapeutic decisions should be tailored to individual patients
according to the coexistence of other risk factors, such as the
presence of cardiac abnormalities.
The study of Yamamoto et al differs with our own work in several
methodological aspects that deserve attention. Although both our group
and Yamamoto et al examined patients with lacunar infarcts, they
evaluated Japanese patients and we studied a white population. Yamamoto
et al excluded patients with "obvious atheromatous
stenotic lesions as detected by MR angiography," but from the
methods of the study it is unclear whether this technique was
specifically performed to rule out the presence of
intracranial atherosclerosis, particularly
prevalent in this population.4 Unlike the Japanese study,
we performed multivariate analysis to test the
independent contribution of variables that in
univariate analysis showed a significant
association with the radiological abnormalities. Although we initially
observed a relationship between elevated nocturnal systolic
blood pressure and white matter disease, the association did not remain
significant when multivariate analysis was
performed. Finally, rather than a dichotomous classification of
the extent of white matter disease,5 we quantified the
total area of all lesions detected by MRI to obtain a volumetric value
for each subject.6 To what extent our conflicting results
obey methodological disparities is difficult to establish. Certainly,
we both agree that further investigation is necessary to clarify these
important issues.
References
1.
Yamamoto Y, Akiguchi I, Oiwa K, Hayashi M, Kimura
J. Adverse effect of nighttime blood pressure on the outcome of
lacunar infarct patients. Stroke.. 1998;29:570–576.[Abstract/Free Full Text]
2.
Chamorro A, Saiz A, Vila N, Ascaso C, Blanc R, Alday
M, Pujol J. Contribution of arterial pressure to the
clinical expression of lacunar infarction. Stroke.. 1996;27:388–392.[Abstract/Free Full Text]
3.
Chamorro A, Pujol J, Saiz A, Vila N, Vilanova JC,
Alday M, Blanc R. Periventricular white matter
lucencies in patients with lacunar stroke. A marker of too high or too
low blood pressure? Arch Neurol.. 1997;54:1284–1288.[Abstract/Free Full Text]
4.
Brust RW. Patterns of cerebrovascular disease
in Japanese and other population groups in Hawaii: an angiographical
study. Stroke.. 1975;6:539–542.[Abstract/Free Full Text]
5.
Fazekas F, Chawluk JB, Alavi A, Hurtig HI, Zimmerman
RA. MR signal abnormalities at 1.5 T in Alzheimer's
dementia and normal aging. AJNR Am J
Neuroradiol.. 1987;8:421–426.
6.
Pujol J, Vendrell P, Junqué C,
Martí-Vilalta JL, Capdevila A. When does human brain
development end? Evidence of corpus callosum growth up to
adulthood. Ann Neurol.. 1993;34:71–75.[Medline]
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Response
Yasumasa Yamamoto, MD
Department of Neurology,
Second Red Cross Hospital,
Kyoto, Japan
Ichiro Akiguchi, MD
Department of Neurology,
Kyoto University,
Kyoto, Japan
We thank Dr Chamorro for his interest in our recent
article1 and critical comments. We fully agree with Dr
Chamorro's concept that silent lacunar infarcts and
periventricular white matter intensities react to separate
hemodynamic mechanisms. While lacunar infarcts are
defined as the occlusion of a branch of perforating arteries, including
lenticulostriate and thalamoperforant arteries, the most
consistent histological substrate of
periventricular white matter intensities is considered to
be a diffuse pallor of the white matter attributed to rarefaction of
the myelin sheaths. The periventricular white matter is
considered to be an arterial borderzone in terms of the
pattern of vascularization and to be susceptible to low flow
ischemia. Thus, consistent with Dr Chamorro's
idea,2 we speculated before starting this study that
periventricular white matter intensities could be
accelerated by lowered blood pressure. However, the results were
unexpectedly contrary to this speculation. Periventricular
white matter intensities, with or without silent lacunes, developed in
patients with higher blood pressure than patients with a good outcome.
It looks like high blood pressure develops periventricular
white matter intensities by accelerating microvascular
disturbances accompanied by a breakdown of the blood-brain
barrier. Differences from in the results of Chamorro et
al2 and ours may be due to the fact that we carefully
excluded those patients who had heart disease and obvious
atheromatous stenosis (>30%) in carotid,
middle cerebral, and vertebrobasilar arteries.
Furthermore, there might be another difference between silent lacunar
infarcts and periventricular white matter intensities in
regard to their location. While periventricular white
matter intensities are located in the periventricular and
subcortical white matter, multiple lacunes involve deep and specific
cerebral regions, including the striatum, thalamus, diencephalon, and
their connections, which are strongly associated with control levels of
the autonomic regulation system.3 We have considered that
multiple lacunes, especially when accompanying injury to the central
autonomic nervous system, might play an important role in causing
reduced nocturnal blood pressure dip, whereas
periventricular white matter intensities do not relate to
nocturnal blood pressure dip.
The most remarkable finding in our study is that high diurnal
blood pressure values and reduced nocturnal dip were observed in those
patients who showed the development of both silent lacunes and diffuse
white matter lesions. If both silent lacunes and diffuse white matter
lesions develop, they might cause Binswanger's disease. The
relationship between reduced nocturnal dip and the development of both
these lesions might be explained by two possibilities: the first is
that sustained high nighttime blood pressure might accelerate
arteriolosclerosis in small penetrating arteries; the second is that
autonomic disturbances coexisting with nondippers might have
adverse effects on cerebral blood flow regulations. In the first
situation, hypotensive medication should be administered to control
nighttime blood pressure as well as daytime blood pressure. In this
case, however, we would not recommend only lowering nighttime blood
pressure in order to change to dipper pattern, but rather trying to
control blood pressure throughout the whole day. In the second
situation, controlling blood pressure would not be enough to prevent
the development of ischemic lesions. Because nondippers have
recently been shown to have an adverse prognosis,4 the
strategies for these patients, including the medication for
ameliorating autonomic disturbance and consequently normalizing
the diurnal blood pressure pattern, should be considered or developed.
We detected atheroscrelotic stenosis using MR angiography and
ultrasonography, and excluded large lacunes (>15 mm) to which
atherosclerotic changes are considered to contribute.5
Although it has been suggested, as Dr Chamorro pointed out, that
intracranial artery disease has tended to be frequently found in
Japanese, recent studies have shown extracranial atherosclerotic
changes are also increasing in Japanese. Actually, we found and
excluded a small number of patients with intracranial artery disease by
MR angiography.
Although we have demonstrated that high diurnal blood pressure values
accelerate the development of silent infarcts and diffuse white matter
lesions, longitudinal study suggested that blood pressure tends to
become lower over the course of development of vascular
dementia.6 Further longitudinal studies are necessary to
clarify these issues.
References
1.
Yamamoto Y, Akiguchi I, Oiwa K, Hayashi M, Kimura
J. Adverse effect of nighttime blood pressure on the outcome of
lacunar infarct patients. Stroke.. 1998;29:570–576.
2.
Chamorro A, Pujol J, Saiz A, Vila N, Vilanova JC,
Alday M, Blanc R. Periventricular white matter lucencies in
patients with lacunar stroke: a maker of too high or too low blood
pressure? Arch Neurol.. 1997;54:1284–1288.
3.
Yamamoto Y, Akiguchi I, Oiwa K, Satoi H, Kimura J.
Diminished nocturnal blood pressure decline and lesion site in
cerebrovascular disease. Stroke.. 1995;26:829–833.[Abstract/Free Full Text]
4.
Verdecchia P, Porcellati C, Schillaci G, Borgioni C,
Ciucci A, Battistelli M, Guerrieri M, Gatteschi C, Zampi I, Santucci A,
Santucci C, Reboldi G. Ambulatory blood pressure: an independent
predictor of prognosis in essential hypertension.
Hypertension.. 1994;24:793–801.[Abstract/Free Full Text]
5.
Caplan LR. Intracranial branch atheromatous
disease: a neglected, understudied, and underused concept.
Neurology.. 1989;39:1246–1250.[Free Full Text]
6.
Skoog I, Lernfelt B, Landahl S, Plamertz B, Andreasson
L, Nilsson L, Persson G, Oden A, Svanborg A. 15-year
longitudinal study of blood pressure and dementia.
Lancet.. 1996;347:1141–1145.[Medline]
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