2153
Middle Cerebral Artery Velocity Changes During
Transfusion in Sickle Cell Anemia
N. Venketasubramanian, MD; Isak Prohovnik, PhD; Ann Hurlet, MD;
J.P. Mohr, MD; S. Piomelli, MD
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Background and Purpose Sickle cell disease is associated
with cerebral hyperemia, which is therapeutically reduced by
transfusion; however, the process of transfusion-induced cerebral perfusion changes has heretofore not been observed.
Methods We document the acute changes of intracranial
arterial velocity in 10 patients (7 with strokes, 3 without)
undergoing transfusion therapy using transcranial Doppler
ultrasonography. Middle cerebral artery velocities were bilaterally measured every 30 minutes for the duration of transfusion (4 to 5 hours). Regional cerebral blood flow was quantified in 5 of these patients before the transfusion and 24 hours
later by the 133Xe technique.
Results Velocities in stroke-associated vessels (6433 ±18.65
cm/s; n=6) were significantly lower than in uninfarcted territories (99.54±27.39 cm/s; n=13), and both types of vessels
showed a robust reduction of blood flow velocities during
transfusion. The rates of reduction were not significantly different as a function of prior stroke but did correlate with pretransfusion velocities and with the rise in hematocrit (multiple
r=.887, /><.001). These reductions occurred rapidly within the
first 3 hours of transfusion. Velocities attained at the end of
transfusion were maintained in the hour after transfusion and
the next day.
Conclusions We conclude that transfusion induces rapid
changes in cerebral hemodynamics that are related to pretransfusion velocities and a rise in hematocrit. Transcranial
Doppler provides a safe, simple, and noninvasive technique of
monitoring these changes and may provide a means of making
therapeutic decisions regarding transfusion therapy in patients
with sickle cell anemia. (Stroke. 1994^5:2153-2158.)
Key Words • anemia, sickle cell • blood flow velocity •
blood transfusion • cerebral blood flow • Doppler
L
patients,25 confirming the relation of higher velocities with
lower hematocrit values.26 Further studies have Indicated
that TCD may be used to detect concomitant intracranial
vessel stenosis in the setting of anemia in sickle cell
disease27 and even to predict stroke in patients with sickle
cell anemia.28-29 Although initial studies demonstrated
poor agreement between regional CBF (rCBF) and TCD
velocities,30-34 more recent data suggest that the correlation is better at higher flow values.35 Thus, TCD may be
used to provide an indication of CBF and has previously
shown velocity changes after transfusion.3^37 In this study
we used TCD and 133Xe rCBF techniques to describe the
acute changes of cerebral perfusion during and immediately after transfusion in patients with sickle cell disease
and to relate them to stroke, baseline velocities, and
hematologic changes.
ong-term transfusion therapy is the standard
treatment for stroke in patients with sickle cell
anemia.1 It has been shown to reduce the
recurrence of stroke 27 and may reverse cerebral angiographic abnormalities in patients with sickle cell anemia.8 It is not without risk, and thus there is still debate
as to some aspects of its use,9 including levels at which
hemoglobin S (%HbS) may be safely maintained,10 the
length of time a patient needs to remain on transfusion
therapy,11 and the role of alternative, less intensive
transfusion regimens.1214 Cerebral blood flow (CBF)
abnormalities have been observed in patients with sickle
cell anemia. 1519 Most commonly hyperemia has been
described, with its severity strongly correlated with the
degree of anemia. This cerebral hyperemia is reduced
by transfusion, possibly providing a putative mechanism
for the reduction of stroke risk.
The acute time course of cerebral perfusion changes
during transfusion has never been observed, primarily
because of lack of appropriate technology. Transcranial
Doppler ultrasonography (TCD) techniques, now widely
used in the evaluation of cerebrovascular disease,2022 are
safe, noninvasive, inexpensive, repeatable, and exceedingly portable. Previous studies have established the range
of CBF velocities in normal subjects23-24 and in anemic
Received May 11, 1994; final revision received July 22, 1994;
accepted July 22, 1994.
From the Departments of Neurology (N.V., I.P., J.P.M.), Psychiatry (I.P.), Radiology (I.P.), and Pediatric Hematology (A.H.,
S.P.), Columbia-Presbyterian Medical Center, New York, NY.
Correspondence to Dr Isak Prohovnik, Department of Brain
Imaging, New York State Psychiatric Institute, 722 W 168th St,
New York, NY 10032.
© 1994 American Heart Association, Inc.
Subjects and Methods
We studied 11 consecutive patients (6 male and 5 female)
attending the Comprehensive Sickle Cell Center at the Columbia-Presbyterian Medical Center for routine transfusion. All
patients were on a long-term transfusion program, and none of
them were suffering from an acute illness at the time of the
study. Neither middle cerebral artery (MCA) could be insonated in 1 patient who had clinical and radiological evidence
of bilateral hemispheric infarct and bilateral MCA occlusion
by magnetic resonance angiography. The final study sample
therefore includes 10 patients.
Blood was drawn for hematocrit, total hemoglobin, and
%HbS estimations shortly before and at the end of transfusion
and on the next day. Hematocrit was determined by means of
the Coulter Counter Plus-4, and %HbS was determined after
elution by optical density techniques by means of the Gilford
Spectrophotometer-260. Six of the patients were undergoing
transfusion after known strokes, 3 others for acute chest
2154
Stroke
TABLE 1.
Vol 25, No 11 November 1994
Treatment Characteristics In 10 Patients With Sickle Cell Disease
Aga, y
Weight, kg
Sex
Baseline Hct
Baseline MCA
Vm (L, R)
Transfusion
Volume, mL/kg
1
11.2
28.5
M
26.1
94, 90
14.5
Recurrent acute chest
syndrome
2
23.8
75
M
28.3
76,72
6.8
Recurrent acute chest
syndrome
3
12.2
32
F
29.0
134, 140
15.2
Recurrent acute chest
syndrome
4
13.7
53.7
M
30.6
72,64
8.5
Pt
Reason for Transfusion
and CT/MRI
TIA
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5
12.7
57.5
F
31.1
86, 90
10.1
6
20.8
60
M
25.4
56, 134
8.4
7
16.2
39
F
28.6
...,108
13.1
Stroke: L frontal and
frontoparietal infarct
8
22.5
46
M
31.1
70, 66
13.2
Stroke: extensive R frontal, L
frontal, and parieto-occipital
infarct
9
10.4
32
F
32.6
134, 96
12.2
Stroke: R frontoparietal infarct
10
24.8
73.8
F
24.8
58, 40
7
Stroke: R and L frontal irrfarct
16.8±5.6
49.8±16.6
28.8±2.6
86.7+29.4,
90.0±31.4
10.9±3.1
Mean±SD
Stroke: small pontine infarct
Stroke: L caudate Irrfarct
Pt indicates patient; Hct, hematocrit; MCA, middle cerebral artery; Vm, mean velocity; L, left; R, right; CT, computed tomography; MRI,
magnetic resonance imaging; and TIA, transient ischemic attack.
syndrome, and 1 prophylacticaJly after a transient ischemic
attack. Cranial computed tomograms and magnetic resonance
images were recalled in those patients with stroke, and the side
of hemispheric infarct was recorded. The transfusion program
at the center is designed to maintain HbS concentrations
below 20% by keeping hematocrit levels above 30 mL/100 m L .
The patients undergo transfusion on an outpatient basis, and
from 5 to 15 mL/kg of blood is given (for the current sample,
498±66 mL), usually every 3 to 4 weeks. Blood is delivered via
an infusion pump at 100 to 150 mL/h (for the current sample,
125 ±24 mL/h) either through a peripheral vein or a central
catheter.
We did not obtain blood samples during the transfusions. To
predict hemodynamics, we calculated the changes expected in
hematocrit. Initial (pretransfusion) hematocrit was known.
Initial whole-body blood volume (in liters) was assumed to be
8% of body weight (in kilograms). The rate of infusion
(milliliters per hour) was also known, and the hematocrit of
infused blood was assumed to be 80 mL/100 mL. From these
values and assumptions, it follows that hematocrit can be
computed for any time during transfusion. Following the
baseline hematocrit of 28.76±2.65, these calculated values
were 30.45+2.76, 32.03+2.93, 33.5+3.14, and 34.88±336 after
1, 2, 3, and 4 hours, respectively.
TCD measurements were conducted with the EME TC
2-64B (Eden Medical Electronics), which used pulsed ultrasound beams at 2 MHz delivered by a small hand-held
transducer. This transducer was placed over the temporal
region of the scalp. Through this temporal window, the MCA
was insonated bilaterally at its junction with the anterior
cerebral artery.38 The children were kept supine in bed during
the time of insonation, with the head elevated at no more than
15 degrees to the horizontal. Measurements were performed
at half-hour intervals, beginning at the start of transfusion and
ending an hour after transfusion was completed. An additional
set of measurements was made in those returning the next day.
We recorded peak systolic, end-diastolic, and time-averaged
mean velocities, as well as Gosling's pulsatility index.39 Because the time-averaged mean velocity is considered the most
accurate indication of velocity by TCD,38 it was the principal
velocity parameter used in this study.
We performed rCBF measurements on the morning of
transfusion and the next day using the Novo Cerebrograph 32c
(Novo Diagnostics Systems) with 32 scintillation detectors
covering the cortex. By means of the l33Xe inhalation method,40 gray matter flow was derived with the six-unknown
model41 and expressed in milliliters per 100 mg per minute,
using a standard correction for hemoglobin.42 Blood pressures
and pulse rates were recorded at frequent intervals during
both TCD and rCBF procedures.
Results
Patient and Transfusion Variables
Patient and transfusion characteristics are provided
in Table 1; pretransfusion and posttransfusion hematocrit and %HbS values are listed in Table 2. Posttransfusion hematology was performed immediately after
TABLE 2. Systemic Hemodynamlc Variables
Immediately Before and After Treatment
Variable
Before
Transfusion
After
Transfusion
Hematocrit, ml_/100 mL
28.8±2.7
(24.8-32.6)
34.9±3.4
(30-38.9)
HbS, %
15.8±8
(0-26)
12.2±5.8
(0-18)
Systolic BP, mm Hg
107±6.3
(100-120)
DiastcJic BP, mm Hg
66.5±8.9
(50-80)
Pulse rate, bpm
79.6±11.8
(66-102)
106.5±7.9
(100-120)
70±6.7
(60-80)
78.4 ±13.1
(62-106)
HbS indicates hemoglobin S; BP, blood pressure; and bpm,
beats per minute. Values are mean±SD (range).
Venketasubramanian et al
TCD During Transfusion
2155
110-1
100
80
80
70
o
60
1
2
3
4
5
Transfusion Time [hours]
FIQ 1. Une graph shows rate of decline of middle cerebral
artery (MCA) mean velocity (Vm) as a function of transfusion
duration (mean of 19 vessels in 10 patients). Velocity values are
expressed as a ratio of baseline velocity and are very well fitted
by a linear function (6%/h) within the first 3 hours. There are no
further changes between 3 and 5 hours of transfusion.
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transfusion in 5 patients and in 3 the next day; in 2
patients posttransfusion hematology was not available.
In the 2 patients in whom it was available on both
occasions, hematocrit and %HbS immediately posttransfusion and the next day were identical.
Furthermore, when the hematocrit values during the
transfusion were theoretically calculated, we found that
the change was exponentially decelerating. Throughout,
hematocrit values rose by 6.1 units (from 28.8 pretransfusion to 34.9 posttransfusion); the change during the
first hour was calculated as 1.7 units, followed by 1.6 and
1.5 during the second and third hours, respectively.
Thus, 79% of the ultimate hematocrit change occurred
in the first 3 hours.
The mean rise in hematocrit was positively correlated
with weight-adjusted transfusion volume in milliliters per
kilogram (r=.823, P=.O1; n=8) but not with unadjusted
volume. A negative correlation was found between
adjusted transfusion volume and weight (r=-.934,
P<.001). These findings indicate that heavier children
were given less blood per kilogram due to constraints on
clinic time and that the acute increase of hematocrit was
highly predictable by the volume of blood transfused per
kilogram.
TCD Findings
Of the 20 MCAs investigated, one could not be
insonated, presumably due to complete occlusion (left
MCA, patient 7). For all vessels insonated (n=19),
MCA mean velocity was reduced within the first 30
minutes of transfusion and continued to fall linearly
during the first 3 hours at the rate of 6%/h (Fig 1). After
the first 3 hours, changes were minimal and nonsignificant (on average, a further drop of 2% between 3 and 5
hours). The ratios of velocities attained at 3 and 5 hours
to the pretransfusion mean velocity were 0.78 and 0.76,
respectively, in the non-stroke-related vessels and 0.82
and 0.80, respectively, in the stroke-related vessels.
Further analyses were performed to compare vessels in
infarcted territories with noninfarcted vessels. Six MCAs
were ipsilateral to historical and radiological evidence of
hemispheric cerebral infarct in the MCA-supplied territory (both MCAs in patients 8 and 10 with bilateral
50
40
-1
0
1 2
3
4
Transfusion Tim*
[hours]
FIG 2. Line graph shows middle cerebral artery (MCA) mean
velocities during transfusion (mean±SE), normalized to baseline
velocities. Although the nonstroke vessels are consistently lower
(indicating greater reduction from baseline), this difference is
nonsignificant The drop at 210 minutes is due to missing data,
as only 10 nonstroke vessels and 5 stroke vessels were assessed; all other points include 13 nonstroke vessels and 6
stroke vessels (no measurements were made at 4 hours).
strokes, the left MCA in patient 6, and the right MCA in
patient 9). The effect of prior infarction is shown in Fig 2,
which depicts mean velocities measured during the course
of transfusion in the vessels without (n=13) and with
(n=6) ipsilateral hemispheric infarct in the 10 patients. A
repeated-measures ANOVA on mean velocities (with
stroke as grouping factor and 10 time points as repeated
observations) yielded a significant effect of stroke
(F=11.83, P<.005) and time (F=23.80, /><.0001). This
analysis suggested that velocities were reduced with time
and were lower ipsilateral to stroke. Unpaired t tests
between the two groups were significant at all time points.
In particular, velocities before transfusion were lower
(t l7 =2.84, P=.Q\) in vessels in infarcted territories
(64.33 ±18.65 cm/s) than in vessels in noninfarcted territories (9954±27.39 cm/s). This difference was also observed after 5 hours (51.00±7i6 versus 75.23± 14.04 cm/s;
t,7=3.93, P=.00l). The lack of significant interaction between stroke occurrence and time during transfusion in
the ANOVA, as well as the all-significant / tests, suggests
that the slope of velocity reduction over time was equivalent in the two groups. To verify this similarity of slopes,
velocities were normalized to baseline (ie, expressed as
percentage of baseline velocity of each patient) for all time
points, and the repeated-measures ANOVA was again
performed. Only the effect of time was significant
(F8jKM=24.61, P<.000\), confirming the lack of difference
in velocity changes between the two groups of vessels.
Overall, therefore, vessels in infarcted territories had
lower mean velocities at baseline than vessels in noninfarcted territories, but the rate of reduction of velocity
during transfusion was the same.
Regression Analyses
Several determinants of baseline velocity in these
patients (in addition to stroke) were suggested by
significant correlations. These included the patients' age
(r=-.58, P<.01), weight (r=-.62, P=.005), and dia-
2156
Stroke
Vol 25, No 11 November 1994
NOD Stroke!
Strok
uo
110
D
D
a
y.
-4.484X + 227.321
r • 0.989
100-
00
a
HO
B "
"^-\B
>
80
a
m
B
80'
V
D
%
70'
r
60'
•
«
y .
i
*
*
WrighlCkg)
FIG 3. Plot shows baseline middle cerebral artery mean
velocity (Vm) before transfusion as a function of the patients'
weight. The symbol • indicates Infarcted territories; n, noninfarcted territories.
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stolic blood pressure (r= —.49, P<.05). Of note, hematocrit and HbS fraction did not significantly predict
baseline velocity within their ranges of 24.8 to 32.6 and
0% to 26%, respectively. Furthermore, when interrelations were addressed by stepwise multiple regression
analysis, only the patients' weight remained significant.
This relation (mean velocity = 143 -1.09 kg), which appeared similar in both infarcted and noninfarcted territories, is shown in Fig 3.
The final velocity obtained after 5 hours of transfusion was strongly predictable by baseline velocity
(r=.91, P<.0001). The reduction of flow after transfusion (velocity at 5 hours normalized to baseline velocity)
was negatively related to baseline velocity (Fig 4). The
only other baseline variable accepted into a stepwise
multiple regression was the patients' weight, which
brought the multiple r to .79. In addition, the drop of
velocities during transfusion was significantly correlated
with the rise of hematocrit (r=.55, P<.05). When all
predictive variables were combined into a stepwise
multiple regression (baseline velocity, weight, and increase of hematocrit), weight was rejected, and initial
velocity and hematocrit change yielded a multiple r of
.86. Furthermore, there was a very strong relation at all
40
80
80
1D0
120
Pre-Traniftirinn MCA Velocity
-2.545X + 138.117
r - 0.991
40
140
160
FIG 4. Plot shows final posttransfusion (5 hours) middle cerebral artery (MCA) velocity normalized to baseline values as a
function of baseline values. Transfusion caused a reduction of
velocity inversely proportional to initial velocity in both infarcted
territories (•) and noninfarcted territories (D).
Hct Daring Transfusion
FK3 5. Line graph shows relation between hematocrtt (Hct)
values (measured before transfusion, calculated during the first
3 hours) and middle cerebral artery (MCA) mean blood flow
velocity in infarcted (n=6) and normal (n=13) hemispheres.
time points between the measured MCA velocity and
the calculated hematocrit (Fig 5).
Velocities attained at the end of transfusion were
maintained into the next hour in all 10 patients and into
the next day in all 5 who were seen the next morning.
The pulsatility index was variable before and during
transfusion without any clear pattern of change. Blood
pressure and heart rate did not change significantly
during transfusion (Table 2).
Regional CBF
rCBF was elevated in all 5 children in whom the
procedure was performed (2 with stroke, 3 without). It
fell by the next day in 4 of the 5, parallel to the falls in
mean velocity in these patients. No change was seen in
the rCBF of 1 child who had shown a fall in mean
velocity but no detectable levels of HbS pretransfusion
or posttransfusion. A patient with bilateral extensive
infarction (patient 8) had the lowest rCBF values (64
and 66 mL/100 g per minute) and the lowest velocities
(70 and 66 cm/s).
Discussion
This is the first demonstration of the immediate
hemodynamic effect of transfusion in patients with
sickle cell disease, although this effect was indirectly
inferred and predicted by us16 and observed in other
circumstances by others.36-37 Additional novel aspects of
this experiment include the precise rate and time course
of this reduction, its predictors, and the differences
between infarcted and noninfarcted vascular territories.
MCA mean velocity was found to fall immediately
(within 30 minutes) on initiation of transfusion and to
maintain a constant rapid rate of decline (6%/h) during
the first 3 hours. It did not continue to decline appreciably for the remaining duration of transfusion (up to 5
hours) and remained stable for the next 24 hours in both
patients in whom it was monitored. Furthermore, despite marked effects of stroke on initial velocity, the
relative rate of decline was uniform across both noninfarcted and infarcted territories.
Venketasubramanian et al TCD During Transfusion
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Because these patients were all transfused on a
long-term basis, the small change in HbS fraction during
a single transfusion is improbable as the hemodynamic
effector. The most likely explanation of the rapid drop
of velocities is the rise of hematocrit. Previous studies
have reported cross-sectional correlations between hematocrit and TCD velocities.23-2542 It follows that as
hematocrit rises, velocities should fall, which is in
agreement with our findings. Our theoretical calculations suggest that the rise of hematocrit during the first
hour was similar in magnitude to the fall of velocity (6%
in both cases). Furthermore, there was a near-perfect
correlation between hematocrit and velocity values at
all time points (Fig 5), and velocities did not change
appreciably toward the end, when hematocrit was stable. From these observations we conclude that CBF
velocity was rapidly and precisely being adjusted by the
rising hematocrit.
The high velocities seen in sickle cell anemia may be
due to a combination of factors, including the lowered
viscosity of anemic blood, local stenoses, and cerebral
vasodilation of cortical blood vessels caused by the
requirement to maintain oxygen delivery. The present
data cannot discriminate between the hemodynamic
effects of viscosity and oxygen content, but it is extremely improbable that obstructive stenoses were being
removed during transfusion. Rather, we propose that
the high pretransfusion velocities merely reflect the
hyperemia we previously reported by other techniques,16 and its reduction indicates normalized CBF.
Mean MCA velocity in this study was approximately 64
cm/s in infarcted territories and 100 cm/s in noninfarcted hemispheres, dropping to approximately 75 cm/s
after treatment. Previous studies of TCD did not specifically investigate this difference. Adams et al24 reported an expected velocity of approximately 70 cm/s in
healthy children aged 14 to 16 years and approximately
100 cm/s for hematocrit values equivalent to our sample
in patients with sickle cell disease.25 Thus, our noninfarcted values are in extremely good agreement with
theirs but are here shown to exist in disparate territories
within the same brain. That the velocity in infarcted
territories is similar to that observed in normal, nonanemic subjects is probably coincidental. Lower velocity in
infarct areas is consistent with the well-documented
tendency of stable stroke to lower parenchymal metabolic demand, and therefore tissue perfusion, in patients with sickle cell disease16 as well as in other
populations. In this case, the flow elevation due to
anemia and flow reduction due to infarct approximately
balanced each other to result in velocity values that
were close to normal.
In contrast to previous reports, however, our study
failed to show a clear correlation between pretransfusion
velocities and hematocrit. That is not surprising for the
vessels in infarcted hemispheres, because the effects of
disease, both stenosis-induced acceleration and infarctinduced metabolic reduction, can easily mask the influence of anemia. The lack of correlation does, however,
appear unexpected for the vessels in noninfarcted territories. One likely explanation is the fairly limited range of
hematocrit values in this study (between 25 and 31)
compared with the study by Adams et al,25 which included
patients with hematocrit of 17 to 38; the very large
variation shown in that study makes it unlikely that
2157
restricted ranges will have the power to demonstrate
significant correlations. Similarly, our own previous
study,17 which did report significant correlations, had a
hematocrit range of 10 to 38. The restricted range hypothesis is also supported by the findings in another study,43
which reported nonsignificant correlations between CBF
and hematocrit in three patients (n=12 procedures) while
they were being treated with long-term transfusion (mean
hematocrit, 29; range, 24 to 33). Finally, the current study
was performed in patients in the lower ranges of HbS.
Although HbS levels were not reported in previous studies
of patients with sickle cell disease,24-25 it would appear that
our patients were more like normal patients in that they
had higher hematocrit and low %HbS. It is possible that
vasoregulatory mechanisms are altered by age, HbS concentrations, and long-term transfusion. This is corroborated by the significant correlations we found between
baseline velocities and the patients' age and weight.
The decline of MCA velocity during transfusion was
strongly predicted by initial velocity and hematocrit
change (multiple r=.86). Patients with higher levels of
pretransfusion mean velocity (mostly noninfarcted territories) registered greater falls than those with lower
levels (mostly infarcted territories). It is unclear why
vessels with lower pretransfusion mean velocity show a
less marked change. Also, despite marked differences of
initial velocity between stroke-related vessels and noninfarcted territories and the relation between initial
velocity and velocity decrease, there was no significant
difference in the rates of decline between the two
groups of vessels. Thus, although stroke tends to lower
MCA velocity as well as rCBF (eg, Reference 16), an
additional mechanism, as yet undefined, is present.
Tissue perfusion and MCA velocity are probably affected by the presence and severity of anatomic abnormalities, such as stenoses, as well as oxygen delivery and
viscosity. Because angiograms were not available for
these patients, we can only speculate regarding the
relevance of such factors. Of interest are patients 6 and
9, who had unilateral hemispheric infarct. Both had
remarkably higher pretransfusion velocities in the noninfarcted hemisphere, presumably due to the metabolic
suppression of the stroke side. The relative decline of
velocity, however, was bilaterally similar for patient 9,
reaching approximately 70% of baseline at 90 minutes
and approximately 60% after 5 hours. In contrast, the
symptomatic hemisphere of patient 6 showed no decline
whatsoever due to transfusion, while the noninfarcted
side showed the usual drop. Thus, within the same
patient, a radically different response to transfusion can
be seen in the left and right MCAs. The reason for the
lack of response in the left MCA of patient 6 is currently
unknown, partly because we are not sure about the
nature and anatomic origin of the vascular regulatory
mechanisms.
In conclusion, our data further validate the TCD
technique as uniquely appropriate for evaluation of the
cerebrovascular system. They suggest that TCD may be
used to aid the physician in deciding the timing and
adequacy of transfusion and the efficacy of different
transfusion regimens in the determination of optimal
treatment in patients with sickle cell anemia. It is
conceivable that patients with high TCD velocities
would benefit from transfusion in the prevention of
stroke and that decreases in the velocities into the
2158
Stroke
Vol 25, No 11 November 1994
normal range after transfusion may indicate that the
patient has been adequately transfused. This hypothesis
requires further study. Another study of particular
interest would attempt to isolate the precise correlations between velocity and tissue perfusion, unconfounded by anatomic vascular abnormalities.
Acknowledgments
This study was supported in part by grant HL-28381 from
the National Institutes of Health. We thank Wendy Winer,
RN, Amy Wu, MD, and Dorothy Patterson, AA, for their help
with this project.
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doi: 10.1161/01.STR.25.11.2153
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