(Stroke. 1998;29:874-880.)
© 1998 American Heart Association, Inc.
Abstracts of Literature
Askiel Bruno;
Alfredo M. Lopez-Yunez
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Cerebral Aneurysms
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AB-14040-98
Some Patients With Intracranial Aneurysms Have
a Reduced Type III/Type I Collagen Ratio: A Case-Control
Study—van den Berg JSP, Limburg M (Dept of Neurology, Academic
Medical Center, PO Box 22660, 1100 DD Amsterdam, Netherlands), Pals G,
Arwert F, Westerveld A, Hennekam RCM, Albrecht
KW—Neurology. 1997;49:1546–1551.
A reduced production of type III collagen has been reported in
previous studies to be associated with intracranial aneurysms.
The purpose of this prospective case-control study was to assess the
possible role of a reduced type III collagen production as a
risk factor for having an intracranial aneurysm. The study
group consisted of 41 consecutively admitted patients with intracranial
aneurysms. Intracranial aneurysms were demonstrated by
intraarterial digital subtraction cerebral angiography or
during operation. The control group consisted of 41 healthy volunteers
matched for age and sex. Fibroblasts were cultured from skin biopsies
from patients and control subjects, and the type III/type I collagen
ratios were determined. The type III/type I collagen ratios in the
controls ranged from 5.5 to 19.8%, with a median ratio of 10%, and
none had a ratio below 5.5%. The type III/type I collagen ratios in
patients ranged from 1.1 to 25.1%, with a median ratio of 10.5%, and
eight patients (19.5%) had a low (<5.5%) ratio (p=0.005,
Fisher's exact test). Our findings support the hypothesis that a
reduced production of type III collagen may contribute to the
formation of intracranial aneurysms in some patients.
Key Words: aneurysm, collagen
AB-14041-98
Intracranial Aneurysm: Anatomic Factors That Predict the
Usefulness of Intraoperative Angiography—Derdeyn CP (Section of
Neuroradiology, Mallinekrodt Institute of
Radiology, Washington University School of Medicine, 510 S Kingshighway
Blvd, St Louis, MO 63110), Moran CJ, Cross III DT, Sherburn EW, Dacey
Jr RG—Radiology. 1997;205:335–339.
Purpose: To correlate the size and location of intracranial
aneurysm with the need to reposition the aneurysm clip
after intraoperative angiography.
Materials and Methods: In 199 consecutive patients with 234
clipped intracranial aneurysms, 273 intraoperative angiographic
studies were retrospectively reviewed. Aneurysm size and
location, determined with preoperative angiographic and surgical
reports, were correlated with the frequency of clip repositioning
because of parent- or branch-vessel compromise or unexpected residual
aneurysm.
Results: Findings from intraoperative angiograms resulted in
clip repositioning in 46 of 273 (16.8%) studies. Clip repositioning
was statistically significantly less frequent with aneurysms of
the posterior communicating (three of 52 [5.7%] studies) and
anterior choroidal (none of 12 studies) arteries. High rates of clip
repositioning were found in aneurysms of the superior
hypophyseal artery (seven of 18 [38.9%] studies), superior
cerebellar artery (three of five [60.0%] studies), and bifurcation
of the internal carotid artery (three of nine [33.3%]
aneurysms). In 98 conventional follow-up angiographic studies,
seven (7%) false-negative cases with unsuspected aneurysm neck
remnant were found.
Conclusion: The rate of clip repositioning in
aneurysms of the posterior communicating or anterior choroidal
arteries was less than that at other locations (P<.05).
Intraoperative angiography may not be necessary when aneurysms
are at these two locations.
Key Words: aneurysm, angiography,
intraoperative
AB-14042-98
Remote Effect of Brain Retraction on Regional Cerebral Blood Flow
and Cerebrovascular Reserve on Single Photon Emission Computed
Tomography—Sloniewski P, Zieliñski P (Dept of Neurosurgery,
Medical University of Gdansk, Debinki Str 7, 80-211 Gdansk,
Poland)—Surg Neurol. 1997;48:511–513. ©1997 by
Elsevier Science Publishing Co, Inc.
Background The purpose of this study is to evaluate the effect of
brain retraction 1 year or more after intracranial aneurysm
clipping, demonstrated by a regional cerebral blood flow (rCBF) imaging
technique.
Methods and Results rCBF and cerebrovascular reserve (CV) were
evaluated in 40 patients 12–25 months after operation, using single
photon emission computed tomography (SPECT) with
Tc-99m-hexamethylpropylene amine oxime (HMPAO) combined with
acetazolamide test. The images were analysed
semiquantitatively, focusing on regions of interest (ROIs) chosen for
places retracted during the operation. The regions of hypoperfusion in
the retracted tissue were clearly visible in 26 cases. Assymmetry of
measured activity, expressed in the Assymmetry Index, reached 12%
(SEM±8). After injection of acetazolamide during
hypercapnia, the assymmetry decreased.
Conclusions The results confirm the negative role of brain retraction.
However, these consequences seem to be diminished by good
vasoreactivity. ©1997 by Elsevier Science Inc.
Key Words: surgery, cerebral blood flow
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Clinical
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AB-14043-98
Early Carotid Atherosclerosis of the Internal and
External Carotid Artery Related to Twenty-Four-Hour Blood Pressure
Variability—Sander D, Klingelhöfer J (Dept of Neurology,
Technical University of Munich, Möhlstrasse 28, D-81675
München, Germany)—Cerebrovasc Dis. 1997;7:338–344.
Reprinted with permission of S. Karger AG, Basel.
We analyzed the relationship between 24-hour blood pressure
variability and spatial distribution and extent of early carotid
atherosclerosis in 208 hypertensive and 216
normotensive patients aged over 55 years. Circadian blood pressure
patterns were evaluated noninvasively with a long-term blood pressure
monitor. The extent of atherosclerosis was measured as
the intima-to-media wall thickness (IMT) of the internal (ICA) and
external carotid artery (ECA). No significant differences regarding
age, sex, smoking, diabetes, cholesterol and
triglycerides were found in either patient group. In both
groups, a linear correlation between ICA and ECA IMT was observed.
However, the slope of the regression line was clearly increased in
hypertensive patients [0.563 (95% confidence interval 0.522, 0.604)
vs. 0.436 (0.364, 0.509); p<0.01]. Multivariate
regression analysis revealed the strongest correlation between
the IMT of the ICA and the diurnal systolic blood pressure
variability; this parameter was not significantly
associated with the ECA IMT. The odds ratio of having ischemic
heart disease was significantly raised in patients with early
atherosclerosis of the ICA but not the ECA [4.7 (2.5,
8.8); p<0.001 vs. 1.6 (0.7, 3.6)]. Our results show that the diurnal
systolic blood pressure variability is closely correlated with
early carotid atherosclerosis of the ICA but not the
ECA territory. The analysis of circadian blood pressure
patterns is useful to explain the focal effects of blood pressure on
the development of atherosclerosis.
Key Words: blood pressure, carotid artery
stenosis
AB-14044-98
Aortic Plaque Morphology and Vascular Events: A Follow-up Study in
Patients With Ischemic Stroke—Cohen A (Service de
Cardiologie, Saint-Antoine University and Medical School,
Université Pierre et Marie Curie, 184 rue du faubourg St-Antoine,
75571 Paris Cedex 12, France), Tzourio C, Bertrand B, Chauvel C,
Bousser M-G, Amarenco P—Circulation.
1997;96:3838–3841.
Background Atherosclerotic disease of the aortic arch has
been found to be associated with the risk of ischemic stroke.
We have shown that atherosclerotic plaques 
4 mm in thickness in
the ascending aorta and proximal arch detected by
transesophageal echocardiography
are a risk factor for ischemic stroke. The purpose of this
study was to evaluate the impact, if any, of plaque morphology
(ulceration, hypoechoic plaques or calcification) on the risk of
subsequent vascular events.
Methods and Results We followed for a period of 2 to 4
years, a cohort of 334 patients 60 years or older who were
consecutively admitted with brain infarction and who had
transesophageal echocardiography.
The risk of vascular events in patients with plaques in the aortic arch
according to the presence of surface ulceration, calcifications, and
sessile or mobile thrombus was estimated during a total of 788
person-years of follow-up. Hypoechoic plaques, calcifications, and
ulceration were more frequently found in patients with plaques 4
mm as compared with those with plaques <4 mm. The presence of
ulceration did not increase the relative risk of vascular events in
patients with plaque 4 mm (the relative risk was 4.3
[P<.001] in those with ulceration and 5.7
[P<.001]) in those without ulceration. The lack of
calcification did increase the risk of vascular events in patients with
plaque 4 mm. The highest relative risk of events was found among
the patients with noncalcified plaques (relative risk, 10.3; 95%
confidence interval, 4.2 to 25.2; P<.001). The risk of
events was systematically higher in patients without calcifications
than in patients with calcifications regardless of what other
morphological features were considered.
Conclusions In patients with brain infarction, the risk
associated with aortic plaque thickness (4 mm) is markedly
increased by the absence of plaque calcifications. These findings are
important for the design of therapeutic trials in such patients.
Key Words: aortic arch, stroke, ischemic
AB-14045-98
Hypokalemia and Potassium Excretion in Stroke Patients—Gariballa
SE, Robinson TG, Fotherby MD (University Dept of Medicine for the
Elderly, The Glenfield Hospital, Leicester LE3 9QP, UK)—J
Am Geriatr Soc. 1997;45:1454–1458.
Objectives: To determine (1) the prevalence of hypokalemia
(plasma potassium 
3.4 mmol/L) in a group of stroke patients in
comparison with age- and sex-matched groups of patients having
sustained a myocardial infarction or having mild hypertension and (2)
the association between plasma potassium concentration and stroke
outcome.
Design: Observational study.
Participants: A total of 421 consecutive stroke patients
admitted to a teaching hospital, 150 consecutive patients 50 years or
older with myocardial infarction admitted to the hospitals
Coronary Care Unit, and 161 out-patients 60 years or older with
borderline and established hypertension.
Measurements: All stroke and cardiac patients had plasma
urea and electrolytes estimated within 2 hours of hospital admission;
in the hypertensive group blood samples were taken in clinic. Stroke
patients had blood pressure, stroke severity (Barthel score) and
smoking status recorded. A sub-group of 61 stroke patients and all
79 hypertensive patients not taking antihypertensive medication had
24-hour urine electrolyte excretion measured. Outcome (independent,
dependent, or dead) at 3 months post-stroke was established in 349
patients.
Results: Hypokalemia occurred more frequently in stroke
patients than in patients with myocardial infarction (84 (20%) vs 15
(10%), P=.008) or patients with hypertension (84 (20%) vs
13 (8%), P<.001), even when patients taking
diuretics were excluded from analysis (56 (19%) vs 12
(9%) of cardiac group, P=.014 and 56 (19%) vs 4 (5%) of
hypertensive group, P=.005, respectively). 24-hour urine
excretion of potassium and the potassium: creatinine ratio
was lower in stroke patients than in hypertensive patients (41±21 vs
62±25 mmol/24 hour, P=.001, 5.5±2.2 vs 7.4±2.6
mmol/24 hour, P=.001, respectively). On survival
analysis, a lower plasma potassium on admission to hospital was
associated with an increased chance of death, independent of age,
stroke severity, history of hypertension, blood pressure level, or
smoking history (hazard ratio 1.73 (95% CI: 1.03–2.9) for a 1
mmol/L lower plasma potassium concentration).
Conclusions: Hypokalemia post stroke is common and may be
associated with a poor outcome.
Key Words: potassium, stroke, acute
AB-14046-98
Stroke Mechanisms and Clinical Presentation in Large
Subcortical Infarctions—Horowitz DR (Dept of Neurology, Box 1052,
The Mount Sinai School of Medicine, One Gustave L. Levy Place, New
York, NY 10029), Tuhrim S—Neurology.
1997;49:1538–1541.
Large subcortical infarctions may be due to cerebral embolism and cause
cortical signs more frequently than small subcortical infarctions,
which usually result from small-vessel disease and are not associated
with cortical findings. We evaluated 51 consecutive patients with a
subcortical infarct on CT that was 1.5 cm or larger for a potential
carotid or cardiac source of embolism and determined how frequently
aphasia, hemineglect, or gaze paresis occurred. A carotid or cardiac
embolic source was identified in 63% of the total population with a
carotid source occurring in 23% and a cardiac source occurring in
49%. More than one-half of the patients with hypertension or diabetes
mellitus had an embolic source, whereas all patients without these risk
factors had a possible carotid or cardiac source of embolism. Aphasia
or hemineglect occurred in 39% of patients and gaze paresis occurred
in 41%. Large subcortical strokes frequently result in a different
clinical syndrome and from a different mechanism than small subcortical
strokes.
Key Words: subcortical infarction, cerebral
embolism
AB-14047-98
Dichotomizing Stroke Outcomes Based On Self-Reported
Dependency—Kay R (Dept of Medicine, Prince of Wales Hospital,
Shatin, Hong Kong), Wong KS, Perez G, Woo J—Neurology.
1997;49:1694–1696.
Patients participating in a clinical trial of stroke therapy were
assessed 3 months after randomization using the Barthel Index, the
Modified Rankin Scale, questions on activities of daily living, and
extent of recovery. Those who needed help in performing the activities
of daily living and had not recovered completely were classified as
dependent. Self-reported dependency had a sensitivity of 94% and
specificity of 80% against the Barthel Index dichotomized at 16 or
below, or a sensitivity of 85% and specificity of 87% against the
Modified Rankin Scale dichotomized at 2 or above.
Key Words: stroke outcome, activities of daily
living
AB-14048-98
von Willebrand Factor and Risk of Ischemic
Stroke—Qizilbash N (Memory Trials Research Group, Dept of
Clinical Geratology, University of Oxford, Radcliffe Infirmary, Oxford
OX2 6HE, UK), Duffy S, Prentice CRM, Boothby M, Warlow
C—Neurology. 1997;49:1552–1556.
We carried out a case-control study to determine whether von
Willebrand factor (vWF) antigen (and factor VII and tissue
plasminogen activator [tPA] antigens) are
associated with ischemic stroke. Ninety-five patients with
transient ischemic attack or minor ischemic stroke
recruited from the Oxfordshire Community Stroke Project and one
neurology clinic were compared with 236 controls, group-matched for age
and sex, from the same general practitioners as the
incident cases. In crude analyses, concentrations of vWF
antigen were significantly higher in cases than in controls
(p=0.004). The age- and sex-adjusted odds ratios from lowest
(referent) to highest quartile of vWF antigen were 1.00, 1.15, 2.34,
and 2.36. (trend test, p=0.006). Factor VII antigen and tPA
antigen were not significantly different between cases and controls.
Although adjustment for other potential risk factors abolished the
statistical significance of the association between vWF and disease,
this was largely due to the influence of history of ischemic
heart disease. We conclude that vWF is a potent and independent risk
factor for transient ischemic attack, minor ischemic
stroke, and, by extrapolation, ischemic stroke in general. The
data also suggest that vWF may be a risk factor for both
ischemic stroke and ischemic heart disease. We found no
evidence to implicate factor VII and tPA as risk factors for
ischemic stroke.
Key Words: von Willebrand factor, risk
factors
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Epidemiology
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AB-14049-98
Hemostatic Factors as Predictors of Ischemic Heart Disease and
Stroke in the Edinburgh Artery Study—Smith FB (Wolfson Unit for
Prevention of Peripheral Vascular Diseases, Dept of Public
Health Sciences, University of Edinburgh, Medical School, Teviot Place,
Edinburgh EH8 9AG, Scotland, UK), Lee AJ, Fowkes FGR, Price JF, Rumley
A, Lowe GDO—Arterioscler Thromb Vasc Biol.
1997;17:3321–3325.
Plasma fibrinogen is a consistent predictor of ischemic
heart disease (IHD) in prospective studies, but there are fewer data
relating other hemostatic variables to IHD and also to stroke. We
therefore studied the relationships of plasma fibrinogen, von
Willebrand factor antigen, tissue plasminogen
activator (TPA) antigen, factor VII, and fibrin D-dimer to
incidence of IHD and stroke and determined whether any associations
could be explained by conventional risk factors and baseline heart
disease. In the Edinburgh Artery study, 1592 men and women aged 55 to
74 years, randomly sampled from the general population, were followed
prospectively over 5 years to detect fatal and nonfatal IHD and stroke
events. During the 5 years, 268 new vascular events were identified.
Baseline plasma fibrinogen was independently related to risk of stroke
in multivariate analysis that adjusted for
cigarette smoking, LDL-cholesterol, systolic blood
pressure, and preexisting IHD (relative risk [RR] 1.52, 95%
confidence interval [CI] 1.17, 1.98). TPA antigen, and fibrin D-dimer
were also independently associated with risk of stroke (RR 1.69, 95%
CI 1.22, 2.35 and RR 1.96, 95% CI 1.12, 3.41, respectively).
Significant relationships were found between TPA antigen and myocardial
infarction (P.05). In older men and women, increased
coagulation activity and disturbed fibrinolysis are
predictors of future vascular events (both IHD and stroke).
Key Words: tissue plasminogen
activator, cerebral ischemia
AB-14050-98
Body Iron Stores and the Risk of Carotid
Atherosclerosis: Prospective Results From the Bruneck
Study—Kiechl S (Dept of Neurology, Innsbruck University Hospital,
Anichstr 35, A-6020 Innsbruck, Austria), Willeit J, Egger G, Poewe W,
Oberhollenzer F—Circulation. 1997;96:3300–3307.
Background Fe2+ released from tissue iron
stores may accelerate lipid peroxidation by virtue of its pro-oxidant
properties and thus promote early atherogenesis.
Methods and Results The present prospective survey
addresses the potential association between serum ferritin
concentrations and the 5-year progression of carotid
atherosclerosis as assessed by ultrasonographic
follow-up evaluations. The study population comprises a random sample
of 826 men and women 40 to 79 years old. Serum ferritin was one of the
strongest risk predictors of overall progression of
atherosclerosis. The main part of this association
appeared to act through modification of the atherogenic potential of
LDL cholesterol (OR [95% CI] for a 1-SD unit increase in
ferritin at LDL levels of 2.5, 3.6, and 4.9 mmol/L: 1.55 [1.30 to
1.85], 1.77 [1.40 to 2.24], and 2.05 [1.50 to 2.80]:
P=.0012 for effect modification). Changes in iron stores
during the follow-up period modified atherosclerosis
risk, in that a lowering was beneficial and further iron accumulation
exerted unfavorable effects. All these findings applied equally to
incident atherosclerosis and the extension of
preexisting atherosclerotic lesions. The significance of prominent iron
stores in the development of carotid stenosis was clearly less
pronounced. Finally, ferritin and LDL cholesterol showed a
synergistic association with incident cardiovascular
disease and death (n=59).
Conclusions The present study provided strong
epidemiological evidence for a role of iron stores in early
atherogenesis and suggests promotion of lipid peroxidation as the main
underlying pathomechanism. This hypothesis could in part explain the
sex difference in atherosclerotic vascular disease.
Key Words: carotid artery diseases, iron
AB-14051-98
Atrial Fibrillation in Older Stroke Patients: Association With
Recurrence and Mortality After First Ischemic
Stroke—Kaarisalo MM (Rykmentintie 26, 20810 Turku, Finland),
Immonen-Räihä P, Marttila RJ, Lehtonen A, Salomaa V, Sarti
C, Sivenius J, Torppa J, Tuomilehto J—Am Geriatr Soc.
1997;45:1297–1301.
Objectives: The objective of this study was to determine the
association of atrial fibrillation (AF) with stroke recurrence
and mortality and with the causes of death in ischemic stroke
patients aged 75 years and older.
Design: A population-based study.
Setting: The cities of Turku and Kuopio in Finland.
Participants: The study cohort consisted of 2635 consecutive patients
aged 75 years and older, with a first ischemic stroke,
registered in the FINMONICA Stroke Register.
Measurements: 28-day and 1-year stroke mortality, causes of death, and
recurrence of stroke.
Results: There were 767 stroke patients with AF (mean age 82.2) and
1868 patients without AF (mean age 81.4). Mortality was higher in the
AF group both 28 days (33.9% vs 28.1%, P=.003) and 1 year
after the attack (52.7% vs 43.0%, P<.001). The age- and
sex-adjusted relative risk of death at 28 days was 1.25 in the AF group
(95% confidence interval (CI) 1.04–1.50, P=.018), and at 1
year it was 1.41 (95% CI 1.18–1.67, P<.001). In a Cox
proportional hazards model, 1-year mortality risk comparing the
AF-group with non-AF group was 1.24 (95% CI 1.10–1.39,
P<.001). The strongest risk factor predicting 1-year
mortality was recent myocardial infarction (MI) (RR 1.90, 95% CI
1.49–2.42). Myocardial infarction was more often the underlying cause
of death in the AF group during the period of 28 days, but not from 28
days up to 1 year. The 1-year recurrence rate among those alive
at day 28 was 11.5% in the AF group and 9.4% in the non-AF group
(P=.240).
Conclusion: Recent MI and AF are independent negative prognostic
factors in older patients with stroke. Although the relative risk
estimates attributable to AF are of the same magnitude in older as in
middle-aged stroke patients, the much higher prevalence of AF in the
older patients emphasizes its absolute impact on the mortality and
recurrence after the first ischemic stroke in the age
group 75 years and older. The treatment of coexisting cardiac disease
also has the potential to prevent deaths and recurrent stroke events in
older persons.
Key Words: atrial fibrillation, stroke outcome
AB-14052-98
Inverse Association of Dietary Fat With Development of Ischemic
Stroke in Men—Gillman MW (Dept of Ambulatory Care and Prevention,
Harvard Medical School and Harvard Pilgrim Health Care, 126 Brookline
Ave, Suite 200, Boston, MA 02215), Cupples LA, Millen BE, Ellison RC,
Wolf PA—JAMA. 1997;278:2145–2150.
Context.—A few ecological and cohort studies in Asian
populations suggest an inverse association of the intake of both fat
and saturated fat with risk of stroke. However, data among western
populations are scant.
Objective.—To examine the association of stroke incidence
with intake of fat and type of fat among middle-aged US men during 20
years of follow-up.
Design and Setting.—The Framingham Heart Study, a
population-based cohort study.
Participants.—A total of 832 men, aged 45 through 65 years,
who were free of cardiovascular disease at baseline
(1966–1969).
Measurements and Data Analysis.—The diet of each
subject was assessed at baseline by a single 24-hour dietary recall,
from which intakes of energy and macronutrients were estimated. In
Kaplan-Meier analyses, we calculated age-adjusted cumulative
incidence rates of stroke. Using Cox regression, we estimated stroke
incidence relative risks during 20 years of follow-up.
Main Outcome Measure.—Incidence of ischemic stroke,
which occurred in 61 subjects during the follow-up period.
Results.—Mean intakes were 10 975 kJ for energy; 114
g (39% of energy) for total fat; 44 g (15%) for saturated fat;
46 g (16%) for monounsaturated fat; and
16 g (5%) for polyunsaturated fat. Risk of ischemic
stroke declined across the increasing quintile of total fat (log-rank
trend P=.008), saturated fat (P=.002), and
monounsaturated fat (P=.008) but not
polyunsaturated fat (P=.33). The age- and energy-adjusted
relative risk for each increment of 3% of energy from total fat was
0.85 (95% confidence interval [CI], 0.78–0.94); for an increment of
1% from saturated fat, 0.91 (95% CI, 0.85–0.98); and for 1% from
monounsaturated fat, 0.89 (95% CI, 0.83–0.96).
Adjustment for cigarette smoking, glucose intolerance, body mass index,
blood pressure, blood cholesterol level, physical activity,
and intake of vegetables and fruits and alcohol did not materially
change the results. Too few cases of hemorrhagic stroke (n=14) occurred
to draw inferences.
Conclusion.—Intakes of fat, saturated fat, and
monounsaturated fat were associated with reduced
risk of ischemic stroke in men.
Key Words: cerebral infarction, diet
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Experimental Pathology
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AB-14053-98
Lifetime Smoking Exposure Affects the Association of C-Reactive Protein
With Cardiovascular Disease Risk Factors and
Subclinical Disease in Healthy Elderly Subjects—Tracy RP
(University of Vermont, Aquatec Bldg T205, 55 A S Park Drive,
Colchester, VT 05446), Psaty BM, Macy E, Bovill EG, Cushman M, Cornel
ES, Kuller LH—Arterioscler Thromb Vasc Biol.
1997;17:2167–2176.
Blood levels of C-reactive protein (CRP), a marker of inflammation, are
related to cardiovascular disease risk. To determine
cross-sectional correlates in the elderly, we measured CRP in 400 men
and women older than 65 years and free of clinical
cardiovascular disease at baseline as part of the
Cardiovascular Health Study. Only 2% of the values
were greater than 10 mg/L, the cut-point usually used to identify
inflammation. CRP levels appeared tightly regulated, since there were
strong bivariate correlations between CRP and the following:
inflammation-sensitive proteins such as fibrinogen (r=.52);
measures of fibrinolysis such as plasmin-antiplasmin
complex (r=.23); pack-years of smoking (r=.30);
and body mass index (r=.24; all P values.001).
The association with pack-years was independent of the length of time
since cessation of smoking. CRP levels were also associated with
coagulation factors VIIc, IXc, and Xc; HDL cholesterol
(negative) and triglyceride; diabetes status;
diuretic use; ECG abnormalities; and level of exercise. Because
of effect modification, two multiple linear regression prediction
models were developed for CRP, one each for never smokers and ever
smokers. An a priori physiologic model was used to guide these
analyses, which disallowed the use of other
inflammation-sensitive variables such as fibrinogen. In never
smokers, the independent predictors were body mass index (+), diabetes
status (+), plasmin-antiplasmin complex (+), and the presence of ECG
abnormalities (+): this model predicted 15% of the CRP population
variance. In ever smokers, the predictors were body mass index (+),
plasmin-antiplasmin complex (+), pack-years of smoking (+), HDL
cholesterol (-), and ankle-arm blood pressure index (-):
this model predicted 42% of the population variance. We conclude that
levels of CRP in the healthy elderly are tightly regulated and reflect
lifetime exposure to smoking as well as level of obesity, ongoing level
of fibrinolysis, diabetes status, and level of
subclinical atherothrombotic disease. Moreover, exposure to smoking
affects the relation of CRP to these other factors.
Key Words: inflammation, cigarette smoking
AB-14054-98
Transient Middle Cerebral Artery Occlusion by Intraluminal Suture: I.
Three-Dimensional Autoradiographic Image-Analysis
of Local Cerebral Glucose Metabolism-Blood Flow
Interrelationships During Ischemia and Early
Recirculation—Belayev L, Zhao W, Busto R, Ginsberg MD (Dept of
Neurology [D4–5], University of Miami School of Medicine, PO Box
016960, Miami, FL 33101)—J Cereb Blood Flow Metab.
1997;17:1266–1280.
Using autoradiographic image-averaging strategies, we
studied the relationship between local glucose utilization (LCMRglc)
and blood flow (LCBF) in a highly reproducible model of transient
(2-hour) middle cerebral artery occlusion (MCAO) produced in
Sprague-Dawley rats by insertion of an intraluminal suture coated with
poly-L-lysine. Neurobehavioral examination at 60 minutes after
occlusion substantiated a high-grade deficit in all animals. In two
subgroups, LCBF was measured with 14C-iodoantipyrine at
either 1.5 hours of MCAO, or at 1 hour of recirculation after suture
removal. In two other matched subgroups, LCMRglc was measured with
14C-2-deoxyglucose at 1.5 to 2.25 hours of MCAO, and at
0.75 to 1.5 hours of recirculation after 2 hours of MCAO. Average image
data sets were generated for LCBF, LCMRglc, and the LCMRglc/LCBF ratio
for each study time. Middle cerebral artery occlusion for 2 hours
induced graded LCBF decrements affecting ipsilateral cortical and basal
ganglionic regions. After 1 hour of recirculation, LCBF in previously
ischemic neocortical regions increased by 40% to 200% above
ischemic levels, but remained depressed, on average, at about
40% of control. By contrast, frank hyperemia was noted in the
previously ischemic caudoputamen. Mean cortical
LCBF values during MCAO correlated highly with their respective LCBF
values after 1 hour of recirculation (R=0.93), suggesting that
postischemic LCBF recovery is related to the depth of
ischemia. Despite focal ischemia, LCMRglc during ~2
hours of MCAO was preserved, on average, at near-normal levels; but
following ~1 h of recirculation, LCMRglc became markedly depressed
(on average, 55% of control in previously densely ischemic
cortical regions). Regression analysis indicated that this
depressed glucose utilization was determined largely by the intensity
of antecedent ischemia. By pixel analysis, the
ischemic core (defined as LCBF 0% to 20% of control)
comprised 33% of the ischemic hemisphere, and the penumbra
(LCBF 20% to 40%) accounted for 26%. The penumbra was concentrated
at the coronal poles of the ischemic lesion and formed a thin
shell around the central ischemic core. During 2 hours of MCAO,
the LCMRglc/LCBF ratio within the ischemic penumbra was
increased four-fold above normal (average, 179 umol/100 mL). In marked
contrast, after ~1 h recirculation, this uncoupling had almost
completely subsided. The companion study (Zhao et al., 1997) further
analyzes these findings in relation to patterns of infarctive
histopathology.
Key Words: cerebral ischemia, cerebral
metabolism
AB-14055-98
Transient Middle Cerebral Artery Occlusion by Intraluminal Suture: II.
Neurological Deficits, and Pixel-Based Correlation of Histopathology
With Local Blood Flow and Glucose Utilization—Zhao W, Belayev L,
Ginsberg MD (Dept of Neurology [D4–5], University of Miami School of
Medicine, PO Box 016960, Miami, FL 33101)—J Cereb Blood Flow
Metab. 1997;17:1281–1290.
We conducted a pixel-based analysis of the acute
hemodynamic and metabolic determinants of
infarctive histopathology in a reproducible model of temporary (2-hour)
middle cerebral artery occlusion (MCAO) produced in rats by an
intraluminal suture. Three-dimensional averaged image data sets of
local cerebral blood flow (LCBF) and glucose utilization (LCMRglc)
acquired in the companion study (Belayev et al., 1997) either at the
end of a 2-hour period of MCAO or after 1 hour of recirculation were
comapped (using digitized atlas-templates) with data sets depicting the
frequency of histological infarction in a matched
animal group (n=8) in which 2 hours of MCAO was followed by 3-day
survival, sequential neurobehavioral examinations, and
perfusion-fixation and paraffin-embedding of brains for
light-microscopic analysis. All rats developed marked
postural-reflex and forelimb-placing deficits at 60 minutes of MCAO,
signifying high-grade ischemia. Tactile placing deficits
persisted during the 72-hour observation period while visual placing
and postural-reflex abnormalities variably improved. Comapping of LCBF
and histopathology showed that in those pixels destined to undergo
infarction, LCBF measured at 2 hours of MCAO showed a sharp
distributional peak centered at 0.14 mL/g/min. In 70% of pixels
destined to infarct, LCBF at 2 hours of MCAO was 0.24 mL/g/min or
below, and in 89% LCBF was below 0.47 mL/g/min (the upper limits of
the ischemic core and penumbra, respectively, as defined in the
companion study [Belayev et al., 1997]). Local cerebral glucose
utilization measured at ~1 hour after 2 hours of MCAO was distributed
bimodally in the previously ischemic hemisphere. The major
peak, at 22 µmol/100 g/min, coincided exactly with the
distribution peak of pixels destined to undergo infarction, while in
pixels with a zero probability of infarction, LCMRglc was higher by 12
to 13 µmol/100 g/min. These results indicate that local blood
flow at 2 hours of MCAO is a robust predictor of eventual infarction.
Pixels with ischemic-core levels of LCBF (0% to 20% of
control) have a 96% probability of infarction, while the fate of the
penumbra is more heterogeneous: below LCBF of 0.35
mL/g/min, the probability of infarction is 92%, while approximately
20% pixels in the upper-penumbral LCBF range (30% to 40% of control)
escape infarction. Our data strongly support the view that the
likelihood of infarction within the ischemic penumbra is highly
influenced by very subtle differences in early perfusion.
Key Words: cerebral ischemia, histology
AB-14056-98
Delayed Reduction of Ischemic Brain Injury and Neurological
Deficits in Mice Lacking the Inducible Nitric Oxide Synthase
Gene—Iadecola C (Dept of Neurology, University of Minnesota, Box
295 UM HC, 420 Delaware St SE, Minneapolis, MN 55455), Zhang F, Casey
R, Nagayama M, Ross ME—J Neurosci.
1997;17:9157–9164.
Inducible nitric oxide synthase (iNOS), an enzyme that produces toxic
amounts of nitric oxide, is expressed in a number of brain pathologies,
including cerebral ischemia. We used mice with a null mutation
of the iNOS gene to study the role of iNOS in ischemic brain
damage. Focal cerebral ischemia was produced by occlusion of
the middle cerebral artery (MCA). In wild-type mice, iNOS mRNA
expression in the post-ischemic brain begun between 24 and 48
hr peaked at 96 hr and subsided 7 d after MCA occlusion. iNOS mRNA
induction was associated with expression of iNOS protein and enzymatic
activity. In contrast, mice lacking the iNOS gene did not express iNOS
message or protein after MCA occlusion. The infarct and the motor
deficits produced by MCA occlusion were smaller in iNOS knockouts than
in wild-type mice (p<0.05). Such reduction in
ischemic damage and neurological deficits was observed 96 hr
after ischemia but not at 24 hr, when iNOS is not yet expressed
in wild-type mice. The decreased susceptibility to cerebral
ischemia in iNOS knockouts could not be attributed to
differences in the degree of ischemia or vascular reactivity
between wild-type and knockout mice. These findings indicate that iNOS
expression is one of the factors contributing to the expansion of the
brain damage that occurs in the post-ischemic period. iNOS
inhibition may provide a novel therapeutic strategy targeted
specifically at the secondary progression of ischemic brain
injury.
Key Words: cerebral ischemia, nitric oxide
synthase
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Imaging
|
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AB-14057-98
Brief Episodes of Ventricular Fibrillation Do Not Influence
Postischemic Cerebral Perfusion Assessed by Positron
Emission Tomography—Runsiö M (Dept of Cardiothoracic
Surgery, Karolinska Hospital, 171 76 Stockholm, Sweden) Brodin L-Å,
Eriksson L, Rosenqvist M, Samuelsson S, Stone-Elander S, Öwall A,
Ingvar M—Crit Care Med. 1997;25:1827–1830.
Objectives: To establish the defibrillation threshold in
patients receiving an implantable cardioverter defibrillator, at least
three episodes of ventricular fibrillation are induced and
converted back to regular rhythm, using direct current countershocks.
The aim of this study was to examine the influence of repeated short
episodes of ventricular fibrillation on global and regional
cerebral perfusion.
Design: A prospective, descriptive study.
Setting: A positron emission tomography laboratory at a
university hospital.
Patients: Four patients, admitted for defibrillation
threshold tests 2 yrs after the implantation of a cardioverter
defibrillator, were included in the study. Global and regional cerebral
blood flow was measured by cerebral positron emission tomography, using
an 15O-labeled tracer under propofol-induced general
anesthesia. Electroencephalograms (EEGs) were concomitantly
recorded.
Interventions: Induction and conversion of
ventricular fibrillation.
Measurements and Main Results: No effect on global cerebral
perfusion was observed after induced ventricular
fibrillation lasting 21±3 secs. The average global cerebral perfusion
was 23±1 mL/100 g/min after induction of anesthesia and
31±8 mL/100 g/min and 24±2 mL/100 g/min immediately after the
termination of the first and second ventricular
fibrillation episodes, respectively. Ten minutes after the second and
the third threshold tests, global cerebral perfusion was 21±1 mL/100
g/min and 21±2 mL/100 g/min, respectively. Regional cerebral perfusion
and EEGs were not influenced.
Conclusion: Short episodes of ventricular
fibrillation did not induce any measurable effects on global and
regional cerebral perfusion detectable by positron emission tomography
30 secs and 10 mins after restitution of sinus rhythm.
Key Words: tomography, emission
computed, ventricular fibrillation
AB-14058-98
Cerebral White Matter Changes (Leukoaraiosis), Stroke, and Gait
Disturbance—Briley DP (Stoke Mandeville Hospital NHS
Trust, Mandeville Rd, Aylesbury, Bucks, HP21 8AL, UK), Wasay M, Sergent
S, Thomas S—J Am Geriatr Soc.
1997;45:1434–1438.
Objectives: Leukoaraiosis, a radiological change of cerebral white
matter thought to be caused by ischemia, is associated with
gait disturbance. However, because of concomitant stroke and
cerebral atrophy, the clinical relevance of leukoaraiosis is uncertain.
We, therefore, sought to determine if leukoaraiosis is a predictor of
gait disturbance after accounting for cerebral atrophy and
stroke in patients with a high prevalence of cerebrovascular
disease.
Design: Cross-sectional observational study.
Setting: Neurology service (inpatient and outpatient) of a Department
of Veterans Affairs Hospital.
Participants: Consecutive sample of 130 patients, 127 men and three
women.
Measurements: The findings of a gait scale were correlated to vascular
risk factors, neurological examination as quantified by the NIH stroke
scale and supplemental motor scale, and to brain CT findings. Brain CT
scans were rated for leukoaraiosis, cerebral infarction, and cerebral
atrophy.
Results: Gait disturbance was more frequent and more severe in
subjects with leukoaraiosis, of whom 31% had mild and 49%
moderate/severe gait disturbance compared with 27% with mild
and 12% with moderate/severe gait disturbance in subjects
without leukoaraiosis (P<.001). Leukoaraiosis, cerebral
atrophy, a history of multiple strokes, and weakness and ataxia of the
legs were independent predictors of gait disturbance. The
proportion and severity of leukoaraiosis increased with increasing gait
disturbance in subgroups without leg deficit
(P<.001) and without multiple strokes (P<.001),
but no association with leukoaraiosis was shown in patients with leg
deficit or a history of multiple strokes (P=.037 and
P=.186, respectively). Gait disturbance was more
severe when both leukoaraiosis and cerebral atrophy were present
(P=.019).
Conclusion: In our Veteran population, leukoaraiosis is an independent
predictor of gait disturbance after accounting for stroke and
cerebral atrophy. Although leukoaraiosis is a form of cerebrovascular
disease, it appears to be most closely associated to gait
disturbance in the absence of symptomatic stroke or
leg deficit.
Key Words: leukoaraiosis, gait
AB-14059-98
Changes In Cerebral Blood Flow and Vasoreactivity in Response to
Acetazolamide in Patients With Transient Global
Amnesia—Sakashita Y (Dept of Neurology, Tonami General Hospital,
1-61 Shintomi-cho, Tonami, Toyama 939-13, Japan), Kanai M, Sugimoto T,
Taki S, Takamori M—J Neurol Neurosurg Psychiatry.
1997;63:605–610.
Objective—Previous reports about changes in cerebral blood
flow (CBF) in transient global amnesia disclosed decreased flow in some
parts of the brain. However, CBF analyses in most reports were
qualitative but not quantitative. The purpose of this study was to
determine changes in CBF in transient global amnesia.
Methods—The CBF was measured and the vasoreactive response
to acetazolamide was evaluated in six patients with
transient global amnesia using technetium-99m
hexamethylpropylene amine oxime single-photon emission computed
tomography (SPECT). The CBF was measured during an attack in two
patients and soon after an attack in the other four. About one month
later, CBF was re-evaluated in each patient.
Results—Two patients examined during an attack and
one patient examined five hours after an attack had increased blood
flow in the occipital cortex and cerebellum. Three patients examined at
six to 10 hours after an attack had decreased blood flow in the
thalamus, cerebellum, or putamen. These abnormalities of blood flow
almost disappeared in all patients one month after onset. The
vasodilatory response to acetazolamide, which was evaluated
initially using SPECT, was poor in areas of increased blood flow. By
the second evaluation of CBF with acetazolamide, the
vasodilatory response had returned to normal.
Conclusions—In a patient with transient global amnesia, CBF
increased in the vertebrobasilar territory during the attack and
decreased afterwards. The vasodilatory response to
acetazolamide may be impaired in the parts of the brain
with increased blood flow. It is suggested that transient global
amnesia is distinct from migraine but may share the same underlying
mechanism.
Key Words: cerebral blood flow, amnesia
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Neurosonology
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AB-14060-98
Cerebral Microembolism in Patients With Stroke or Transient Ischaemic
Attack as a Risk Factor for Early Recurrence—Valton L,
Larrue V (Service de Neurologie, Hôpital de Rangueil, CHU de
Toulouse, 31403 Toulouse Cedex 04, France), Pavy Le Traon A,
Géraud G—J Neurol Neurosurg Psychiatry.
1997;63:784–787.
The incidence of early recurrence in 32 patients who had had a
transient ischaemic attack or stroke in the anterior circulation was
studied. Patients with a potential cardiac source of embolism were
excluded from the study. All patients had transcranial
Doppler (TCD) monitoring of the symptomatic middle
cerebral artery for microembolic signal detection
within seven days from the onset of symptoms. Four patients had early
recurrence during a mean follow up of 15 (SD11) days. All early
recurrences occurred in the same arterial territory
as the initial ischaemic event. Three of the four patients with early
recurrence had prior microembolic signals. The
incidence of early recurrence was 50% (3/6) in patients with
microembolic signals and 3.8% (1/26) in patients
without microembolic signals (P=0.02). The findings
suggest that TCD monitoring of patients with recent cerebral ischaemia
of presumed arterial origin allows recognition of a subset
of patients at high risk for early recurrence.
Key Words: cerebral embolism, ultrasonography,
Doppler
AB-14061-98
Carotid Artery Stents: Early and Intermediate Follow-up With
Doppler US—Robbin ML (Dept of Radiology, The University of
Alabama at Birmingham, 619 S 19th St, New Hillman Bldg 623, Birmingham,
AL 35233-1924), Lockhart ME, Weber TM, Vitek JJ, Smith JK, Yadav J,
Mathur A, Iyer SS, Roubin GS—Radiology.
1997;205:749–756.
Purpose: To determine whether ultrasound (US) is a sensitive
follow-up method after placement of a carotid artery stent for the
detection of significant stenosis, occlusion, and other
complications at early and intermediate follow-up.
Materials and Methods: Doppler US examinations were
performed after stent placement in 170 carotid arteries in 119 patients
with angiographic correlation. Prospective diagnostic US
criteria for stenosis were peak-systolic velocity
greater than 1.25 m/sec, internal carotid artery (ICA) to common
carotid artery (CCA) peak-systolic velocity ratio of greater
than or equal to 3:1, and intrastent doubling of
peak-systolic velocity. Retrospective criteria for
stenosis were also applied: peak-systolic velocity
greater than 1.7 m/sec, ICA end-diastolic velocity greater
than 0.4 m/sec, ICA/CCA peak-systolic velocity ratio greater
than 2.0, and ICA/CCA end-diastolic velocity ratio greater
than 2.4.
Results: Eighty-seven immediate and 83 intermediate
(average, 7.3 months) follow-up US examinations were performed. Two
stent occlusions were detected. One or more prospective US criteria
were abnormal in 26 arteries with a stent. One or more retrospective
criteria were positive in 47 arteries. Angiography showed corresponding
findings, with only one significant stenosis (63%) in the ICA
stents. Moderate collapse of a CCA stent was depicted at US.
Conclusion: Only one significant recurrent stenosis
was detected, and no significant stenoses were missed at US. US
successfully depicted carotid artery stent occlusion and a moderate
stent collapse. Sensitivity in the detection of intrastent
stenosis is promising. Further study to refine US criteria in a
study with longer term follow-up is needed owing to the lack of
significant recurrent stenosis in the intermediate follow-up
group.
Key Words: stents, carotid artery
stenosis
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Pharmacology/Therapeutics
|
|---|
AB-14062-98
Evolving Indications For and Early Results of Carotid Artery
Stenting—Criado FJ (Johnston Professional Building, Suite 570,
3333 N Calvert St, Baltimore, MD 21218), Wellons E, Clark
NS—Am J Surg. 1997;174:111–114.
BACKGROUND: While carotid endarterectomy
continues to be the gold standard of treatment for most patients with
significant carotid artery disease, there are cases where lesion or
anatomy-related factors create situations less than ideal for
conventional surgery. Other therapeutic modalities, such as endoluminal
stenting, may represent reasonable options for such
patients.
METHODS: Thirty-three patients with 70% or greater internal
carotid artery lesions were treated by endovascular stent placement
from July 1994 through June 1996. Indications included transient
ischemic attacks in 20 and previous stroke in 4; and 9 were
asymptomatic.
RESULT: Stents were placed successfully in all instances.
Mortality and stroke rates were zero. All patients remained
asymptomatic during follow-up (mean 8 months), and stent
patency by duplex ultrasound has been 100%. A single instance of
intrastent restenosis has been observed.
CONCLUSIONS: Endoluminal stenting is an investigational
technique of unproven efficacy and long-term durability. Yet it appears
technically feasible, and possibly reasonable, as an alternate option
for cases unfavorable for standard surgery.
Key Words: stents, carotid artery
stenosis
AB-14063-98
Intra-arterial Thrombolysis in Acute Basilar
Artery Thromboembolism: The Intial Mayo Clinic
Experience—Wijdicks EFM (Dept of Neurology, Mayo Clinic
Rochester, 200 First St SW, Rochester, MN 55905), Nichols DA, Thielen
KR, Fulgham JR, Brown RD, Meissner I, Meyer FB, Piepgras DG—Mayo
Clin Proc. 1997;72:1005–1013.
Objective: To investigate the feasibility of
intra-arterial thrombolysis in acute
basilar artery thrombosis.
Design: We reviewed a consecutive series of patients in whom
intra-arterial thrombolysis was performed
during the period from 1994 to 1996.
Material and Methods: Intra-arterial
thrombolysis with urokinase was done in an attempt to
recanalize the basilar artery in a series of nine patients with basilar
artery thrombosis admitted to the neurologic intensive-care unit. At
the time of initial assessment, all nine patients had major neurologic
deficits attributable to brain-stem ischemia, including two
patients with locked-in syndrome.
Results: Recanalization of the basilar
artery system was successful in seven of the nine patients (a range of
2 to 13 hours after the ictus). Failure to recanalize the basilar
artery occurred in two patients, who died after progressing to coma.
Complete recovery or only minimal neurologic deficits were demonstrated
in five of the nine patients. Despite
recanalization of the basilar artery, two patients
had no major change in their neurologic function, and both ultimately
had severe ataxia and were fully dependent on others. A cerebellar
hemorrhage occurred in one patient but without clinical
worsening. Two patients had a retroperitoneal hematoma.
Conclusion: Intra-arterial
thrombolysis with urokinase in acute basilar artery
occlusion resulted in recanalization in seven of
the nine patients (78%). Five of the nine patients recovered fully,
including two patients who had had locked-in syndrome. In light of the
devastating natural course of acute basilar artery occlusion, these
initial results are encouraging and indicate that
intra-arterial thrombolysis may be a useful
emergency treatment, even in patients with prolonged symptoms of
ischemia (up to 12 hours).
Key Words: thrombolytic
therapy, basilar artery
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Surgery
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AB-14064-98
Carotid Endarterectomy in the U.K. and Ireland:
Audit of 30-day Outcome—McCollum PT (Consultant Vascular
Surgeon, Vascular Unit, Ninewells Hospital, Dundee DD1 9SY, UK), da
Silva A, Ridler BDM, de Cossart L—Eur J Vasc Endovasc
Surg. 1997;14:386–391.
Objectives and Design: A prospective study of 709 patients
undergoing carotid surgery in the U.K. and Ireland was performed to
evaluate the performance of vascular surgeons.
Materials and Methods: Fifty-nine surgeons (range
2–39 cases each) were sampled and all patients undergoing surgery over
a 6-month period (1 March 1994–31 August 1994) were included in the
study. Indications for surgery were TIA (35.9%), AF (23.3%), CVA
(21.4%) and "others" (19.6%).
Results: Mean ipsilateral stenosis was 82%
(30%–99%). Thirty-one percent of patients had preoperative
neurological consults. Shunts were used in 67.6%, tacking sutures in
40.1%, drains in 71.9% and patches in 54.4% of cases. At 30 days
there were nine (1.3%) deaths (four cardiac, three neurological).
There were 15 ipsilateral postoperative CVAs (2.1%); 19% of patients
had one or more complication, usually minor. Statistical
analysis showed no independent risk factor for CVA other than
seniority of the surgeon.
Conclusions: A combined stroke/death rate of 3% for
the series was obtained at 30 days for all cases. This large, validated
study suggests that members of the Vascular Society of G.B. and Ireland
currently have a very low morbidity/mortality rate for performing
carotid surgery. Continued audit is required to ensure that this
quality of service does not deteriorate.
Key Words: outcome, carotid
endarterectomy
AB-14065-98
Middle Cerebral Artery Blood Velocity, Embolisation, and Neurological
Outcome During Carotid Endarterectomy: A
Prospective Comparison of the Javid and the Pruitt-Inahara
Shunts—Wilkinson JM, Rochester JR, Slvaguru A, Cameron IC, Fisher
R, Beard JD (Sheffield Vascular Institute, Northern General Hospital,
Herries Road, Sheffield, S5 7AU)—Eur J Vasc Endovasc Surg.
1997;14:399–402.
Objectives: To investigate the in vivo
haemodynamic performance and neurological outcome of two types
of carotid shunt.
Design: Randomised single surgeon study of consecutive
symptomatic patients.
Setting: 163 consecutive patients undergoing carotid
endarterectomy for symptomatic carotid
disease were randomised to the Javid or Pruitt shunt.
Chief outcome measures: Middle cerebral artery velocity
(MCAV), preoperatively, during clamping, during shunting and
post-restoration of flow, embolic episodes, neurological outcome.
Main results: The MCAV preoperatively, at carotid clamping,
and postoperatively was the same for both groups (p>0.15).
During shunting the MCAV was significantly lower in the Pruitt group,
p<0.005, 59% of the Javid and 34% of the Pruitt shunts
maintained MCAV at preoperative levels p<0.005,
2=8.92. The Javid shunt produced significantly more
emboli (73% of cases) at declamping than the Pruitt (41%),
p<0.0002, 2=14.7. Four Javid patients and
one Pruitt had disabling thromboembolic strokes; overall thromboembolic
stroke rate 3.7%. The difference in stroke rates was not statistically
significant (p=0.14).
Conclusions: The Pruitt shunt was unable to maintain
preoperative MCAV in 66% of cases, the Javid shunt had a higher
incidence of emboli on declamping. These factors may lead to an
increased risk of stroke; however, the numbers required for statistical
confirmation would be large.
Key Words: carotid
endarterectomy, shunt
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Items of Interest
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Emergency Identification and Treatment of Acute Ischemic
Stroke
—Kasner SE (Dept of Neurology, University of Pennsylvania
Medical Center, 3400 Spruce St, Philadelphia, PA 19104), Grotta
JC—Ann Emerg Med. 1997;30:642–653.
Total Quality Improvement Method for Reduction of Delays Between
Emergency Department Admission and Treatment of Acute Ischemic
Stroke—Tilley BC (Division of Biostatistics and Research
Epidemiology, Henry Ford Health Sciences
Center, 1 Ford Pl, Suite 3 E, Detroit, MI 48202), Lyden PD, Brott TG,
Lu M, Levine SR, Welch KMA—Arch Neurol.
1997;54:1466–1474.
Rational Approach to Combined Carotid and Ischaemic Heart
Disease—Renton S, Hornick P, Taylor KM, Grace PA (University of
Limerick, Regional General Hospital, Dooradoyle, Limerick,
Ireland)—Br J Surg. 1997;84:1503–1510.
Ticlopidine and Clopidogrel in Secondary Stroke
Prevention—Bousser MG (Service de Neurologie, Hôpital
Saint-Antoine 184, rue du Faubourg Saint-Antoine, F-75571 Paris Cedex
12, France), Roberts RS, Gent M—Cerebrovasc Dis.
1997;7:17–23.
Aspirin With and Without Dipyridamole—Dyken
ML (Indiana University Medical Center, Neurology, 545 Barnhill Dr,
Indianapolis, IN 46202-5124)—Cerebrovasc Dis.
1997;7:10–16.
The Role of Chronic Brain Edema in the Formation of Lacunes in
Binswanger's Encephalopathy: Histopathological and Immunohistochemical
Observations—Ma K-C (Laboratory of Neuropathology, University
Hospital, S-751 85 Uppsala, Sweden), Olsson
Y—Cerebrovasc Dis. 1997;7:324–331.
Platelet Function and Pharmacology of Antiplatelet
Drugs—Nurden AT (Director, UMR 5533 CNRS, Hôpital
Cardiologique, Ave de Magellan, F-33604 Pessac, France), Duperat VG,
Nurden P—Cerebrovasc Dis. 1997;7:2–9.
Status of Patent Foramen Ovale, Atrial Septal Aneurysm,
Atrial Septal Defect and Aortic Arch Atheroma as Risk
Factors for Stroke—Devuyst G (Hôpital de Jolimont, Dept of
Neurology, rue Ferrer 159, B-7100 Haine-St-Paul, Belgium),
Bogousslavsky J—Neuroepidemiology.
1997;16:217–223.
Patterns of Sensory Dysfunction in Lateral Medullary Infarction:
Clinical-MRI Correlation—Kim JS (Dept of Neurology, Asan Medical
Center, Song-Pa PO Box 145, Seoul 138-600, South Korea), Lee JH, Lee
MC—Neurology. 1997;49:1557–1563.
Treatment of Cerebral Vasospasm Due to Aneurysmal
Subarachnoid Hemorrhage: Past, Present, and Future
of Hyperdynamic Therapy—Pritz MB (Section of Neurological
Surgery, Indiana University School of Medicine, 545 Barnhill Dr,
Emerson 139, Indianapolis, IN 46202-5124)—Neurosurg Q.
1997;7:273–285.
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Footnotes
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The abstracts in this section have been typeset for consistency with journal format but otherwise appear as in the original articles.
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Cerebral Aneurysms
Clinical