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Anew technique to stratify stroke risk in transient ischemic attack patients.

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EDITORIAL
A New Technique to Stratify Stroke
Risk in Transient Ischemic Attack
Patients?
T
ransient ischemic attack (TIA) presents a golden opportunity to prevent strokes. Many studies in recent
years have demonstrated that 10 to 20% of patients will
go on to an ischemic stroke, acute coronary event, or
death in the ensuing days and weeks.1–3 Of all vascular
outcomes that occur in the ensuing high-risk 90-day period, about half will occur in the first 2 days. In addition,
it is clear that various features of the TIA itself are predictors of risk, so we can identify those patients at low
versus high risk and base evaluation and treatment recommendations and urgency on this. The ADCD2 score has
emerged as a useful predictor for early stroke,4 as have
certain magnetic resonance imaging features.5–7 Patients
with a very high ABCD2 score may have a 90-day stroke
rate as high as 20 to 25%, whereas those with a very low
score may have a rate of 0 to 3%.
Clearly, a major goal of stratifying risk for vascular
events in patients in the short term after TIA is to assess
the need for urgency in identifying cause and the need for
carotid endarterectomy or stenting, anticoagulation to
prevent cardioembolism, or antiplatelet therapy.
It is commonly believed that 5 to 10% of ischemic
strokes in whites, and more in blacks, Asians, and Hispanics, are caused by intracranial atherosclerosis marked
by stenoses of ⬎50% or occlusions. Early studies have
suggested both extracranial and intracranial stenoses are
predictors of stroke.8,9 Amarenco and his colleagues studied a large cohort of patients presenting to their SOS-TIA
clinic. They hypothesized that intracranial arterial stenoses
and occlusions would be independent predictors of early
stroke after TIA. In this issue, these investigators report
the results of their study of transcranial Doppler (TCD)
results to determine if TCD offers additional independent
predicting information regarding future stroke.10
This study has several strengths. It is a large study
conducted in a major center for acute assessment of TIA
and was conducted over 5 years. TCD is an attractive
technique that avoids the well-known risks and limitations of computed tomography and magnetic resonance
angiography. Consequently, the conclusion that “Immediate TCD examination upon arrival at the TIA clinic is
feasible and could help to identify patients at high risk of
vascular events recurrence. This study supports a systematic intracranial vascular examination in the initial management of TIA” may be true. It is an appealing one.
However, the study has limitations that prevent establishing this technique as routine.
The origin of the diagnostic TCD criteria for stenosis/occlusion is not described. Were these criteria ever validated? What do the data regarding confirmatory testing
with magnetic resonance angiography (MRA)/computed
tomography angiography (CTA) reveal? Was MRA/CTA
performance and interpretation blinded and standardized?
These issues are important to clarify whether the approach used in this study—ultra early TCD to stratify the
long-term risks in TIA patients—is to be generalized to
other populations.
For example, should other ultrasound laboratories
use these TCD criteria or their own?
Without data on confirmatory imaging, do we assume that all the TCD findings are accurate? Concluding
that a lesion here was “symptomatic” required a correlation between lesion site and the vascular territory of
symptoms, and confirmation by a second imaging test.
The authors report that half of the intracranial lesions
were deemed symptomatic. Did TCD fail to correlate
with other imaging half of the time, or was this conclusion reached based on the vascular territory criterion? If
TCD and other imaging failed to correlate a substantial
portion of the time, how are we to interpret the overall
finding that TCD abnormalities identify a TIA patient at
high long-term risk? The accuracy of the TCD is important not only for identifying the high-risk patient but for
pointing to specific needs for further evaluation and management.
Data regarding the confirmatory imaging tests may
provide further insight into the risk stratification of these
patients. It is reported that 1,353 confirmatory imaging
© 2010 American Neurological Association
1
ANNALS
of Neurology
tests were performed. These were performed when symptomatic TCD abnormalities were suspected. Given that
only 8.8% of all patients had TCD lesions, and not all of
these were symptomatic, how often was confirmatory imaging performed for other reasons? If MRA and CTA
were often performed even if TCD was normal, how often were MRA and CTA independently abnormal, and
what was the long-term prognosis in those patients?
In the statistical analysis, outcome was assessed in all
patients with TCD abnormalities, not just those with
symptomatic abnormalities. The authors were exploring
the relationship of TCD abnormalities to outcome regardless of TIA mechanism. This is a study of how any
intracranial atherosclerosis or occlusion affects long-term
risk after TIA. The issue raised by these data, that early
TCD abnormalities are important in TIA patients, may
be extended. What are the risks for patients with symptomatic TCD abnormalities? Does stenosis versus embolism/occlusion make a difference in risk? Do simultaneous
carotid or cardiac sources add to the risk?
In conclusion, the authors have identified a potential role for an easily performed, noninvasive test, TCD,
to aid in the risk stratification of the TIA patient. Given
the clinical importance of such a role, further studies that
address the issues cited above would be welcome.
Potential Conflicts of Interest
Edward Feldmann, MD
Department of Neurology
Rhode Island Hospital and Alpert Medical School of Brown
University
Providence, RI
References
1.
Johnston SC, Gress DR, Browner WS, Sidney S. Short-term prognosis after emergency department diagnosis of TIA. JAMA 2000;
284:2901–2906.
2.
Rothwell PM, Warlow CP. Timing of TIAs preceding stroke: time
window for prevention is very short. Neurology 2005;64:
817– 820.
3.
Giles MF, Rothwell PM. Risk of stroke early after transient ischaemic attack: a systematic review and meta-analysis. Lancet Neurol 2007;6:1063–1072.
4.
Johnston SC, Rothwell PM, Nguyen-Huynh MN, et al. Validation
and refinement of scores to predict very early stroke risk after
transient ischaemic attack. Lancet 2007;369:283–292.
5.
Ay H, Arsava EM, Johnston SC, et al. Clinical- and imagingbased prediction of stroke risk after transient ischemic attack: the
CIP model. Stroke 2009;40:181–186.
6.
Calvet D, Touze E, Oppenheim C, et al. DWI lesions and TIA
etiology improve the prediction of stroke after TIA. Stroke 2009;
40:187–192.
7.
Coutts SB, Eliasziw M, Hill MD, et al. An improved scoring system for identifying patients at high early risk of stroke and functional impairment after an acute transient ischemic attack or minor stroke. Int J Stroke 2008;3:3–10.
8.
Purroy F, Montaner J, Delgado P, et al. Usefulness of urgent
combined carotid/transcranial ultrasound testing in early prognosis of TIA patients. Med Clin (Barc) 2006;126:647– 650.
9.
Purroy F, Montaner J, Molina CA, et al. Patterns and predictors
of early risk of recurrence after transient ischemic attack with
respect to etiologic subtypes. Stroke 2007;38:3225–3229.
10.
Meseguer E, Lavallée PC, Mazighi M, et al. Yield of systematic
transcranial Doppler in patients with transient ischemic attack.
Ann Neurol 2010;68:xx–xx.
Nothing to report.
J. Donald Easton, MD
Department of Neurology
University of California-San Francisco
San Francisco, CA
2
DOI: 10.1002/ana.22039
Volume 68, No. 1
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