CORRESPONDENCE

the fact that infectious brain tissue is

largely composed of lipid, it is clear
that the infectious agent replicates in
the non-lipid cell cytoplasm, and
therefore would not necessarily (or
even probably) be removed by
hydrocarbon solvents used to extract
the last 15% or so of tallow from
greaves.
Indeed,
Taylor
and
colleagues1 have reported experimental
evidence for the absence of infectivity
in tallow that has been obtained from
infectious greaves. Thus, the argument
that the BSE epidemic was caused by
infectivity in residual tallow which
after 1981 had been allowed to remain
in animal feed products is not
convincing.
Paul Brown
National Institute of Neurological Disorders and
Stroke Laboratory of Central Nervous System
Studies, Public Health Service, National
Institutes of Health, Bethesda,
MD 20892, USA
1

Taylor DM, Woodgate SL, Fleetwood AJ,

Cawthorne RJG. Effect of rendering
procedures on the scrapie agent. Vet Rec
1997; 141: 64349.

ACE inhibitors and

pneumonia
SirTadashi Arai and co-workers
(July 11, p 115) 1 report an
improvement
of
symptomless
dysphagia with use of angiotensinconverting enzyme (ACE) inhibitors in
patients with cerebral infarction or
cerebral haemorrhage. Although
dysphagia with aspiration is suggested
as the most important factor
contributing to the risk of pneumonia
in patients with stroke,2 their report
did not refer to the effect of ACE
inhibitors on the frequency of
pneumonia.
We prospectively compared the rate
of pneumonia in stroke patients treated
with ACE inhibitors with that in stroke
patients
treated
with
other
antihypertensive drugs. Patients were
selected from seven long-term care
facilities. Eligible patients were those
who received antihypertensive therapy,
had a history of stroke, but were not
bedridden. We excluded patients if
they were immunocompromisedfor
example,
patients
with
active
malignant disease, renal dialysis, or
HIV-1 infection.
We enrolled 468 patients in March,
1996, and investigated all patients for
2 years. Diagnosis of pneumonia was
made by two radiologists who were not
involved in the studies. However, 28
patients were excluded from the
analysis since they died from causes
other than pneumonia during follow-

THE LANCET Vol 352 September 26, 1998

up. Of the remaining 440 patients, 127

patients (mean age 76 [SD 7] years)
had
received
ACE
inhibitors,
(imidapril, enalapril, or captopril) at
study entry. 313 patients (mean age
77
[8]
years)
had
received
antihypertensive drugs other than ACE
inhibitors (calcium-channel blocker or
-blocker). Before the study, physical
examination and chest radiograph
were done. The patients then
continued to receive the same
antihypertensive drugs.
During follow-up, new pneumonia
was diagnosed in 56 (18%) of the 313
patients who did not take ACE
inhibitors, and nine (7%) of the 127
patients who took ACE inhibitors.
According to the Cox regression
model, these findings corresponded to
a relative risk for patients who did not
receive ACE inhibitors compared with
those receiving ACE inhibitors of 265
(95% CI 131535, p=0007).
Our findings suggest that the risk of
pneumonia is reduced by about a third
if ACE inhibitors are used for
hypertension, compared with the use
of other antihypertensive drugs in
patients with previous strokes. ACE
inhibitors, therefore, may have
beneficial effects on the prevention of
pneumonia in these patients.
Kiyohisa Sekizawa, Toshifumi Matsui,
Takuma Nakagawa,
Katsutoshi Nakayama *Hidetada Sasaki
Department of Geriatric Medicine, Tohoku
University School of Medicine, Aoba-ku Seiryomachi 1-1 Sendai 980, Japan
1

Arai T, Yasuda Y, Takaya T, et al. ACE

inhibitors and symptomless dysphagia.
Lancet 1998; 352: 11516.
Horner J, Massey EW, Riski JE,
Lathrop DL, Chase KN. Aspiration
following stroke: clinical correlates and
outcome. Neurology 1988; 38: 135962.

Decrease of blood pressure

by ventrolateral medullary
decompression in essential
hypertension
SirI read with interest the early
report by Helmut Geiger and
colleagues (Aug 8, p 446)1 about
decrease of blood pressure after
ventrolateral medullary decompression
in essential hypertension. Eight
severely hypertensive patients had
decompression
after
magnetic
resonance imaging (MRI) had
identified neurovascular compression
of the root entry zone of the left
glossopharyngeal (IX) and vagus (X)
nerves. Seven of eight patients were
normotensive on reduced medication
after 3 months. The investigators have
based selection of patients on the MRI

findings and do not challenge the

concept of vascular compression, or the
increasingly held belief that MRI is not
a good screening aid for neurogenic
hypertension.24
With a T2-weighted fast spin echo
sequence with interleaved 3 mm slices
we have examined 124 normotensive
and 38 hypertensive patients referred
for brainstem imaging. 42% (16/38) in
the hypertensive and 32% (40/124) in
the normotensive group had vascular
contact or compression of the left
ventrolateral medulla at the root entry
zone of cranial nerves IX and X. The
rate on the right was 47% (18/38) and
27%
(33/124),
respectively
(unpublished data). 2 analysis showed
no statistical difference between the
hypertensive and normotensive patients
on the left side.
These findings are similar to those
published by Colon3 and Watters,4 and
suggest that vascular contact or
compression of the ventrolateral
medulla is a common observation in
the normotensive population. Other
researchers describe a difference
between hypertensives and controls2,5
but none of these studies have more
than 20 controls.
Protagonists
of
neurogenic
hypertension will still cite higher rates
of
medullary
compression
in
hypertensive patients (7583%).5 They
will continue to be critical of the MR
technique and selection bias of studies
that do not show significant differences
between hypertensive and controls. It is
increasingly clear, however, that
vascular
compression
of
the
ventrolateral medulla cannot be
reproducibly evaluated by MRI. When
this finding is present, it can have no
diagnostic or therapeutic impact, since
the prevalence is high in healthy
individuals.
The investigators might be correct in
their belief that surgical decompression
is a treatment for severe hypertension,
but, at present, MRI cannot aid patient
selection for surgery.
*Declan Johnson, Stuart Coley
Lysholm Department of Neuroradiology,
National Hospital for Neurology and
Neurosurgery, London WC1N 3BG, UK
1

Geiger H, Naraghi R, Schobel HP, et al.

Decrease of blood pressure by ventrolateral
medullary decompression in essential
hypertension. Lancet 1998; 352: 44649.
Tatsuo A, Yasuhiro F, Yasutaka J, et al.
Essential hypertension and neurovascular
compression at the ventrolateral medulla
obligata: MR evaluation. AJNR 1995; 16:
40105.
Colon G, Quint D, Dickinson L, et al.
Magnetic resonance evaluation of
ventrolateral medullary compression in
essential hypertension. J Neurosurg 1998; 88:
22631.

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