From the Department of Neurology, Segovia General Hospital (Spain).
Correspondence to Angel Pérez Sempere, PO Box 43 (Aptdo 43), 03800 Alcoy, Spain. E-mail aperezs{at}meditex.es
Methods—We prospectively studied the vascular risk factors and
etiologic categories in 235 patients with TIAs and MISs from a
community-based register in a rural area of Spain. Five etiologic
categories were considered: (1) cardioembolism, (2)
large-artery atherosclerosis, (3) small-artery disease,
(4) other etiologies, and (5) undetermined etiology. Systematic
investigations included neuroimaging (CT/MRI) and vascular studies
(duplex scan/MR angiography and angiography in selected cases).
Results—The two most frequent etiologic categories were
small-artery disease (31%) and cardioembolism (26%).
Large-artery atherosclerosis was detected in 11% of
the patients. Significant carotid stenosis (
Conclusions—An etiologic classification of TIAs and MISs is
feasible. The two most frequent pathogenetic mechanisms in our study
were small-artery disease and cardioembolism. The
prevalence of large-artery atherosclerosis was low.
The aim of this study was to analyze the underlying vascular
risk factors and causes of TIAs and MISs in a community-based
study.
TIA was defined as an acute loss of ocular or focal cerebral function
lasting less than 24 hours that was presumed to be due to
ischemic vascular disease. A stroke was considered minor if the
score on the modified Rankin Scale was 1 at the first evaluation or if
the score was 0 or 1 at the 1-month follow-up (ie, no symptoms or minor
symptoms that did not interfere with normal lifestyle).
All patients underwent a thorough physical and neurological
examination, including neck auscultation to search for carotid bruits.
Systematic investigations included cranial CT scan, 12-lead ECG, chest
radiography, routine blood tests that included complete
blood count, fasting glucose and cholesterol
concentrations, and luetic serology. MRI of the head, with the use of a
1-T system, was performed in all patients except the carriers of
pacemakers or metallic devices, claustrophobic patients, and those who
were not cooperative enough for MRI. MRI consisted of conventional
sagittal and transverse T1- and T2-weighted images, with 5-mm-thick
slices.
Criteria for the diagnosis of carotid distribution included any of the
following features: transient monocular blindness, dysphasia, and
unilateral weakness or sensory disturbance. Criteria for the
diagnosis of vertebrobasilar distribution were weakness or numbness
involving both sides of the body, loss of vision in one or both
homonymous fields, loss of balance, vertigo, diplopia, dysarthria, and
dysphagia. Vertigo, dysphagia, dysarthria, and diplopia were not
considered if they occurred in isolation. Unilateral weakness and/or
sensory disturbance was considered carotid unless CT/MRI showed
an appropriate lesion in the vertebrobasilar territory. For instance,
if clinical criteria were suggestive of carotid distribution (ie, pure
left hemiparesis) but MRI showed a relevant pontine infarction, the
vascular event was finally classified as vertebrobasilar.
Evaluation of the carotid artery was undertaken if the carotid
territory was affected. Duplex ultrasound and MRA were used as
screening tests for extracranial carotid artery stenosis of
>50%. In our center, the negative predictive value of duplex and MRA
for the presence of
The posterior circulation was evaluated in patients with
vertebrobasilar events by three-dimensional TOF MRA. MRA images of the
posterior circulation included the vertebral, basilar, and proximal
posterior cerebral arteries. A diagnosis of significant
stenosis was made when the lumen diameter was reduced by
Other diagnostic tests were performed on an individual
basis to determine etiology. Anticardiolipin IgG antibodies were
measured by enzyme-linked immunosorbent assay according to
international standardized methods. The results were expressed in GPL
units and considered positive if >20 U on at least on two occasions 3
months apart.
We used the following definitions for vascular risk factors.
Arterial hypertension was defined in three ways: (1) if the
patient was being treated with antihypertensive drugs or his/her
medical record gave such a diagnosis, (2) two blood pressure
recordings with both a systolic blood pressure
Five etiologic categories were considered: (1)
cardioembolism, (2) large-artery
atherosclerosis, (3) small-artery disease, (4) other
etiologies, and (5) undetermined etiology.
Cardioembolism
This category included patients with TIA or MIS likely caused by
an embolus arising in the heart. It was necessary to identify a
potential source of cardiac embolism. Cardiac sources were classified
as high risk or low risk. Large-artery disease had to be ruled out in
patients with low-risk sources. The following sources of cardiac emboli
were considered high-risk: atrial fibrillation, mitral
stenosis, recent myocardial infarct, atrial myxoma,
prosthetic valve, dilated cardiomyopathy,
akinetic left ventricular segment, infective endocarditis,
sick sinus syndrome, and left atrial thrombus. Mitral valve prolapse,
patent foramen ovale, and atrial septal aneurysm were
considered low-risk sources of cardiac emboli.
Large-Artery Atherosclerosis
This category required evidence by duplex imaging, MRA, or
angiography of a stenosis >50% in the appropriate
extracranial or intracranial artery.
Small-Artery Disease
The diagnosis of small-artery disease required all the following
criteria: (1) lacunar symptoms defined as unilateral dysfunction of at
least two of three body parts (face, arm, leg) in the absence of
clinical evidence of cerebral cortical dysfunction (visual field
defect, spatial neglect, disorder of language, writing, reading,
memory, or orientation); (2) absence of cardiac sources of embolism;
(3) absence of nonlacunar infarcts on CT/MRI; and (4) absence of
large-artery atherosclerosis.
Other Etiologies
This category included patients with nonatherosclerotic
vasculopathies and hematologic disorders (including hypercoagulable
states). We used the following definition for possible primary
antiphospholipid syndrome: (1) anticardiolipin antibodies >20 GPL
units on two occasions, determined at least 3 months apart, (2)
negative antinuclear antibodies, and (3) absence of
cardioembolism and large-artery
atherosclerosis.
Undetermined Etiology
This category included several possibilities: (1) no likely
etiology after a thorough evaluation, (2) no likely etiology but
evaluation was not complete, and (3) patients with two or more possible
causes, eg, a patient with atrial fibrillation and ipsilateral
significant carotid stenosis.
Continuous variables were compared with Student's unpaired
t test. Discrete variables were compared with Yates'
corrected
A cranial CT scan was obtained in all patients. Cranial MRI was
performed in 162 patients (69%). Brain imaging (CT/MRI) showed no
evidence of infarction in 70 patients (30%), and 9% of patients
harbored cerebral infarcts that were considered irrelevant.
The prevalence of vascular risk factors is shown in Table 1
Overall, vascular studies were obtained in 189 of the 235 patients
(80%). Carotid duplex ultrasound was performed in 78 patients (33%)
and MRA in 133 patients (57%); some patients underwent both
procedures. Noninvasive vascular studies (duplex ultrasound, MRA, or
both) were performed in 155 of 170 patients with carotid TIAs/MISs
(91%). Significant carotid stenosis was suspected by
noninvasive vascular studies in 25 patients (16%).
Intra-arterial angiography was performed in 2 patients
without previous noninvasive vascular studies. Of the 13 patients who
had no vascular studies performed, 10 had a high-risk cardiac disorder.
Intra-arterial angiography was performed in 15 of the 25
patients with suspected carotid stenosis, confirming the
presence of significant carotid stenosis in 11 patients. MRA
showed 50% to 69% stenosis of the ipsilateral internal
carotid artery in 4 patients, but this finding was not confirmed by
intra-arterial angiography (<50% stenosis).
Intra-arterial angiography was not performed in the other
10 patients because of the following reasons: unsuitable for surgery (6
patients), refusal of the patient (3 patients), and allergy to iodine
contrast (1 patient). One patient with bilateral internal carotid
artery occlusion was diagnosed with pseudoxanthoma
elasticum by skin biopsy. Symptomatic carotid
stenosis was finally diagnosed in 20 of the 157 patients with
carotid TIAs/MISs who had vascular studies performed (13%; 95% CI,
8% to 18%). Seven patients had occlusion of the ipsilateral internal
carotid artery (5 diagnosed by MRA and confirmed by angiography and 2
diagnosed by duplex and MRA), 7 patients had 70% to 99%
stenosis of the ipsilateral internal carotid artery (5
diagnosed by duplex and/or MRA and confirmed by angiography and 2
diagnosed by duplex and MRA), and 6 patients had 50% to 69%
stenosis of the ipsilateral internal carotid artery (5
diagnosed by duplex and/or MRA and 1 diagnosed by MRA and angiography).
MRA was performed in 32 of 62 patients with vertebrobasilar TIAs/MISs.
No significant stenosis of the carotid or vertebrobasilar
arteries was observed in 30 patients. MRA in the other 2 patients
disclosed stenosis of the basilar artery and occlusion of a
vertebral artery, respectively.
Transthoracic echocardiography was
performed in 84 patients (36%). Only 2 patients had a potential
cardiac source of emboli without any clinical evidence of cardiac
disease: a 50-year-old man with a mitral valve prolapse and a
62-year-old woman with a left atrial thrombus.
Transesophageal echocardiography
was performed in 13 patients (6%), detecting two cases of severe
aortic arch disease and one case of patent foramen ovale. None of these
patients had clinical evidence of cardiac disease. Holter ECG was
performed in 3 patients (1%) with negative results. Excluding patients
with known heart disease (ie, atrial fibrillation, sick sinus syndrome,
prosthetic cardiac valve), an echocardiogram was not obtained
in 117 patients (50%), although none of them had any clinical evidence
of heart disease.
The two most common etiologies were small-artery disease and
cardioembolism (Table 3
In the group of undetermined etiology, vascular studies were not
obtained in 17 patients and echocardiography was
not performed in 35 patients, although none of them had any clinical
evidence of heart disease. We did not find any patient with multiple
causes.
We considered five etiologic categories:
cardioembolism, large-artery
atherosclerosis, small-artery disease, other
etiologies, and undetermined etiology. Our etiologic classification is
similar to the Trial of Org 10172 in Acute Stroke Treatment (TOAST)
subtype classification system of acute ischemic stroke, which
includes five subtypes: large-artery atherosclerosis,
cardioembolism, small-artery occlusion (lacune), stroke
of other determined etiology, and stroke of undetermined
etiology.9 A more simple classification, based on clinical
findings, was developed by the Oxfordshire Community Stroke
Project10 for cerebral infarctions, but it is not
useful for TIAs and MISs. A clinical classification of TIAs with two
subtypes (lacunar versus nonlacunar or cortical) has been
proposed.11 12 13 This classification of TIAs has
pathogenetic and prognostic implications. Nonlacunar TIAs are
associated with cardiac and arterial sources of
thromboembolism and carry a better prognosis.13 However,
this classification of TIAs does not distinguish
cardioembolism from large-artery
atherosclerosis. A further problem is the different
definitions of lacunar syndromes that have been used in those studies,
although all of them required the absence of symptoms suggestive of
cortical dysfunction for the diagnosis.
Diagnostic difficulties arise when the neurologist tries to
classify TIAs as carotid or vertebrobasilar. The most common symptoms
in patients with carotid TIAs are contralateral weakness and/or sensory
disturbance. Although these "hemiphenomena" are usually
regarded as carotid distribution, vascular territory may be either
carotid or vertebrobasilar. In the absence of localizing symptoms such
as dysphasia (carotid) or diplopia (vertebrobasilar), it is difficult
to be sure of the site of the ischemia unless there is CT or
MRI evidence of recent infarction. However, in many patients (30% in
our series) there is no evidence of infarction, and when there is, it
may be irrelevant to the presenting complaint.
The diagnosis of small-artery disease is particularly difficult in the
setting of TIAs. The absence of clinical evidence of cortical
dysfunction on history does not eliminate the possibility that this
feature was present since it is seldom possible to examine the
patient during the attack. The definition of the lacunar syndrome has
not been the same in all studies. The study of Kapelle et
al12 required unilateral dysfunction of at least one of
three body parts (face, arm, leg). Landi et al13 required
involvement of at least two of the three body parts, partially or
completely. Hankey and Warlow11 adopted stricter criteria
since they required complete involvement of at least two of the three
body parts. We used restrictive criteria for the diagnosis of
small-artery disease since we required the presence of the lacunar
syndrome, absence of a cardiac source of embolism and large-artery
disease, and absence of a nonlacunar infarct on CT/MRI. Again, brain
imaging is slightly helpful since no lesions are detected on CT/MRI in
a substantial proportion of patients.
Our etiologic classification of TIAs and MISs seems feasible and has
the advantage of being applicable to TIAs and ischemic strokes.
It has the potential problem of requiring a rather large number of
diagnostic studies. However, appropriate
diagnostic evaluation is essential to identify specific
pathogenetic subtypes of TIAs and MISs. Neuroimaging studies are useful
to rule out nonischemic causes14 and to assist
clinicians in localizing the vascular territory
involved.15 16 Duplex scan and MRA provide noninvasive
imaging of the extracranial and intracranial vasculature, which is
essential to distinguish large-artery atherosclerosis
from small-artery disease, although MRA tends to overestimate the
degree of stenosis.17 The yield of
transthoracic echocardiography is low
in patients without clinical, ECG, or chest x-ray evidence of heart
disease.18 However, it is a noninvasive method that can
change the management of some patients. Transthoracic
echocardiography identified a potential source of
embolism in two patients in our series who had no evidence of heart
disease, resulting in change of therapy in one.
Transesophageal echocardiography
increases the detection of potential sources of embolism but has the
disadvantage of its invasive nature.19 Anticardiolipin
antibodies have been reported to be an independent risk factor for
ischemic stroke in a case-control study,20 but it
has been suggested that these antibodies may be a nonspecific
accompaniment of vascular disease.21 Furthermore,
anticardiolipin antibodies are not associated with an increased risk of
thrombo-occlusive events or death.22 Routine testing for
anticardiolipin antibodies does not seem justified.
The two most common etiologies of TIAs and MISs in our study were
small-artery disease and cardioembolism, which
accounted for over half of the patients. We found a low prevalence of
large-artery atherosclerosis in Spanish patients with
TIAs and MISs. Overall, large-artery atherosclerosis
was diagnosed in 11% of the patients. Only 13% of the patients with
carotid territory events had
If extracranial carotid atherosclerosis is less
frequent in Mediterranean countries than in the United States and
northern Europe, what are the reasons for that difference? The most
significant risk factors for extracranial carotid
atherosclerosis in the Framingham Study were age,
cigarette smoking, systolic blood pressure, and
cholesterol.30 It is difficult to compare the
prevalence of vascular risk factors among studies because of the
different definitions that have been used. The prevalence values of
arterial hypertension and current smokers in Oxfordshire
and in our study were similar (49% versus 50% and 27% versus 26%,
respectively). However, we found a striking difference in
cholesterol levels between both studies. Mean
cholesterol levels were 5.4 mmol/L (208 mg/dL) in our
study compared with 6.9 mmol/L in Oxfordshire.7
Hypercholesterolemia (fasting plasma
cholesterol
The prevalence of vascular risk factors and the distribution of
etiologic categories were similar in TIAs and MISs. Another
community-based study found no significant differences between both
groups in the prevalence of vascular risk factors except for
cholesterol levels that were higher in the TIA
group.7 Mean cholesterol levels were also
higher in the TIA patients in our study, although the difference was
not statistically significant. This difference may be explained by the
transient fall in cholesterol levels observed after a
stroke.34 We found a higher prevalence of
arterial hypertension and diabetes in women. Women also
suffered from arterial hypertension more frequently than
men in one Italian study4 ; this could be explained by the
older age of women in both studies. The lower prevalence of
ischemic heart disease in women could be explained, at least in
part, by the different smoking habits.
Treatment of patients with TIA must be tailored to the underlying
stroke mechanism.35 As Caplan said, we need to know what is
wrong with Mr Jones before we begin to think about
treatment.36 Clinical research on TIAs should focus on the
role of etiologic categories in their prognosis and treatment.
Received July 28, 1997;
revision received October 20, 1997;
accepted October 20, 1997.
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© 1998 American Heart Association, Inc.
Original Contributions
Etiopathogenesis of Transient Ischemic Attacks and Minor Ischemic Strokes
A Community-Based Study in Segovia, Spain
Abstract
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Background and Purpose—We sought to
analyze the etiology and underlying vascular risk factors of
transient ischemic attacks (TIAs) and minor ischemic
strokes (MISs). 
50%) was
present in 13% of patients with carotid territory events. No cause
could be found or it was uncertain in almost one third of the patients.
The distribution of etiologic categories was similar in TIAs and MISs.
The most prevalent vascular risk factors were as follows:
arterial hypertension (50%), smoking (26%), atrial
fibrillation (20%), hypercholesterolemia
(17%), diabetes (15%), ischemic heart disease (12%), and
peripheral vascular disease (3%). Carotid bruits were
detected in 3% of the patients.
Key Words: atherosclerosis • carotid arteries • cerebral ischemia, transient • etiology • risk factors
Introduction
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
It is considered that
anything that causes a TIA may cause an ischemic stroke. Based
on this assumption, the causes of TIAs have been inferred from the
causes of cerebral infarction.1 Although several
community-based studies have addressed the
epidemiology2 3 4 5 and
prognosis6 of TIAs, they have not analyzed the
pathogenetic mechanisms involved in them. On the other hand, there is
little reason to distinguish TIAs from MISs since both groups are very
similar in terms of age,7 8 sex,7 8 and
vascular risk factors.7
Subjects and Methods
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
This study formed part of a larger community-based study of TIAs
and MISs described elsewhere.8 The study was performed in
the province of Segovia, which is a rural area located in the center of
Spain with a population of 146 716 (1991 census). General
practitioners and hospital emergency departments were
mainly responsible for referral of the patients. General
practitioners were asked to notify the neurology unit as
soon as possible of all patients with a suspected TIA or nondisabling
stroke. A direct telephone line to the neurology clinic was available
for all general practitioners at their health centers.
Patients could also be referred immediately and directly to the
neurology clinic without previous appointment. All patients with
suspected cerebrovascular disease attending the emergency department of
our hospital were referred directly to the neurology unit, admitted to
the hospital, or evaluated in the emergency department by the
neurologist on call. 50% stenosis is >95%. Stenosis
of the internal carotid artery <50% was considered nonsignificant,
and stenosis 50% was considered significant. The initial
choice between the two techniques depended on the cooperation of the
patient or the presence of contraindications to MRI. The ultrasound
criteria for the diagnosis of 50% stenosis was a peak
systolic velocity in the internal carotid artery >120 cm/s.
MRA consisted of two-dimensional TOF examination of the carotid
bifurcation and three-dimensional TOF sequences. The degree of
stenosis was evaluated by a neuroradiologist who was blinded to
clinical data, although the neuroradiologist knew that the patient
suffered from cerebrovascular disease. If duplex ultrasound or MRA
showed 50% stenosis of the ipsilateral internal carotid
artery, digital subtraction angiography was performed if the patient
was considered suitable for carotid surgery and accepted the
possibility of surgical treatment. 50%. The carotid bifurcation was also examined by means of
two-dimensional TOF sequences in patients with vertebrobasilar
events. 140 mm Hg and a diastolic blood pressure 90
mm Hg, and (3) two blood pressure recordings with a
systolic blood pressure 160 mm Hg and a
diastolic blood pressure <90 mm Hg (isolated
systolic hypertension). A patient was defined as a smoker if
he/she was a current smoker in the last 12 months.
Peripheral vascular disease was defined in two ways: (1)
intermittent claudication and (2) previous peripheral
vascular surgery. Atrial fibrillation was present if confirmed by
ECG at presentation. Ischemic heart disease was
defined by a history of angina or myocardial infarction. Diabetes
mellitus was defined in two ways: (1) by history if the patient had
this diagnosis and (2) if there were at least two fasting glucose
concentrations >7.8 mmol/L (140 mg/dL).
Hypercholesterolemia was diagnosed if the
patient had this diagnosis and was on treatment or if a fasting
cholesterol level was >6.2 mmol/L (240 mg/dL). 
2 test and odds ratios with 95% CIs.
Statistical significance was set at P<.05. All
probabilities are two-tailed values.
Results
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
During the study period, 235 incident cases were included: 103
TIAs and 132 MISs. The mean age of the whole group was 70.8 years; 92
were women and 143 were men. The mean age of patients with TIAs (71.8
years) and MISs (70.1 years) did not differ significantly
(P=.231). The proportion of men in both groups also did not
differ (61 of 103 with TIA [59%], 82 of 132 with MIS [62%];
P=.65). According to clinical features, approximately 78%
of TIAs and MISs were in the carotid distribution, 19% were
vertebrobasilar, and 3% were considered of uncertain vascular
distribution. Neuroimaging studies changed this classification in 17
patients (7%). After CT/MRI, 170 (72.1%) of TIAs and MISs were
classified as carotid, 62 (26.4%) were classified as vertebrobasilar,
and 3 (1.5%) were considered of uncertain vascular distribution. 
. There were no significant differences
between patients with TIAs and MISs. Mean fasting
cholesterol concentration was 5.4 mmol/L (208 mg/dL)
(95% CI, 5.25 to 5.51 mmol/L). Mean cholesterol
levels were nonsignificantly higher in the TIA patients than in those
with MIS (5.51 mmol/L and 5.28 mmol/L, respectively;
P>.10). Women were older than men (73.3 and 69.3 years,
respectively; 95% CI, 1.2 to 6.9 years) and had a higher prevalence of
arterial hypertension and diabetes (Table 2). Men smoked more often and had a
higher prevalence of ischemic heart disease.
View this table:
[in a new window]
Table 1. Prevalence of Vascular Risk Factors in Patients
With TIAs and MISs
View this table:
[in a new window]
Table 2. Sex-Specific Prevalence of Vascular Risk Factors in
Patients With TIAs and MISs ).
Small-artery disease was the etiology responsible for TIAs and MISs in
41% of women and 24% of men, and cardioembolism was
diagnosed in 27% of women and 25% of men. The distribution of
etiologic categories was similar in TIAs and MISs. Large-artery
atherosclerosis was detected in 11% of the patients
(12% of men and 9% of women). Within the cardioembolic category, the
most common cardiac disorder was nonvalvular atrial
fibrillation (67%) followed by mitral stenosis (8%),
prosthetic cardiac valve (5%),
cardiomyopathy (5%), sick sinus syndrome (5%),
akinetic left ventricular segment (3%), left atrial
thrombus (3%), patent foramen ovale (1.6%), and mitral valve prolapse
(1.6%). Unusual etiologies were discovered in 7 patients, which
represents 3% of the whole group: fibromuscular dysplasia (1),
essential thrombocythemia (1), migraine (1),
pseudoxanthoma elasticum (1), herpes zoster vasculitis
(1), hereditary protein C deficiency (1), and disseminated
intravascular coagulation (1). Eight patients were diagnosed of
possible primary antiphospholipid syndrome.
View this table:
[in a new window]
Table 3. TIAs and MISs: Etiologic Categories
Discussion
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Our study is the first community-based series that
analyzes the etiology of TIAs and MISs. Community-based studies
have more difficulty in obtaining diagnostic tests such as
neuroimaging, vascular studies, and
echocardiography than hospital-based studies. Many
patients are not admitted to the hospital, and some of them, especially
among the elderly, refuse to undergo further studies. We do not know
how many patients with a TIA were seen by general
practitioners and not referred to the neurology unit. To
estimate the number of cases not ascertained, we assessed the
possibility of a preceding TIA in all patients with a stroke who were
admitted to the hospital. During the study period we found two patients
who had not been referred to the neurology unit by their general
practitioners and had later suffered a stroke. A more
important problem is that many patients do not seek medical attention.
We succeeded in obtaining a high rate of brain imaging and vascular
tests, although vascular evaluation was not performed in half of the
patients with vertebrobasilar events. Investigation of cardioembolic
disorders was also limited; transthoracic and
transesophageal echocardiography
were performed in 36% and 6% of the patients, respectively. 50% stenosis of the
symptomatic internal carotid artery. Previous Spanish
hospital-based studies have also shown a similar low prevalence of
carotid atheromatosis.23 24 25 An Italian
community-based study detected 50% stenosis of the carotid
artery in 14% of the patients with a TIA in the carotid distribution
who underwent duplex scanning of cervical vessels.5 The
prevalence of severe carotid atheromatosis seems to be
higher in northern Europe and the United States than in Mediterranean
countries like Spain and Italy. In a British hospital-based study, 39%
of carotid TIAs had 50% stenosis of the
symptomatic internal carotid artery.26 In
hospital series from the United States, severe extracranial carotid
stenosis has been found in 40% to 60% of patients with
carotid TIAs.27 28 Vascular studies have not been routinely
performed in community-based studies. However, we can use the
prevalence of carotid bruits as a rough measure of the prevalence of
carotid stenosis. In the TIA series from Oxfordshire, carotid
bruits were detected in 21% of the patients,7 compared
with only 3% of patients with carotid bruits in our study. The
prevalence of carotid bruits in hospital-based studies of TIAs and MISs
in Spain ranged between 1% and 4%.23 24 25 We also found a
low prevalence (6%) of large-artery stenosis in
vertebrobasilar events. We are unaware of any prospective series of MRA
in vertebrobasilar TIAs. A prospective study of 70 patients from
Switzerland with infarcts in the posterior circulation disclosed a high
frequency of severe intracranial large-artery
disease.29 7 mmol/L or treated
hypercholesterolemia) was diagnosed in 52% of
TIA patients in Oxfordshire,31 while only 17% of the
patients were diagnosed with
hypercholesterolemia in our study (fasting
plasma cholesterol 6.2 mmol/L or treated
hypercholesterolemia). Mediterranean diet has
been related to lower total cholesterol
values.32 Hispanic Americans have lower levels of serum
cholesterol than non-Hispanic whites.33 Higher
HDL-cholesterol and lower triglyceride serum
levels, as well as dietary factors, may also play an important role in
the protection against severe extracranial carotid
atheromatosis.25
Selected Abbreviations and Acronyms
CI
=
confidence interval
GPL
=
IgG phospholipid
MIS
=
minor ischemic stroke
MRA
=
magnetic resonance angiography
TIA
=
transient ischemic attack
TOF
=
time of flight
Acknowledgments
This study was supported by a grant from Spain's Fondo de
Investigaciones Sanitarias (FIS-Health Research Fund) 97/1253. The
authors thank Dr L. Calandre for helpful comments.
References
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
1.
Hankey GJ, Warlow CP. Transient Ischaemic
Attacks of the Brain and Eye: Major Problems in Neurology. London,
England: WB Saunders; 1994:vol 27.
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