Response to Letter by Poppe et al

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cohort would be needed to better explore TIA subgroups,
especially lacunar and undetermined TIAs. Therefore, an ideal
multicenter study that should include DWI and should consider
etiology and clinical risk scores would be of great interest.
Until such a study is conducted we believe that the risk of
recurrent stroke after TIA could be established after an
etiologic study that included carotid and transcranial ultrasound testing.1,12 Clinical scales alone seemed not to be enough
to predict new cerebral ischemic events.1,13 Therefore, future
TIA scores could be improved, adding vessel and parenchymal
imaging information.
Response to Letter by Poppe et al
Response:
Downloaded from http://stroke.ahajournals.org/ by guest on November 20, 2016
We appreciate the comment by Dr Poppe et al on our recent
article regarding the patterns and predictors of early risk of
recurrence among the different etiologic subtypes of transient
ischemic attacks (TIA). They raise 2 interesting points: the
additional benefits of using diffusion-weighted imaging (DWI)
in those studies and the prognostic significance of TIA clusters.
We definitively agree that DWI-MRI results could further
improve not only the etiologic diagnosis but also the prognosis of
TIA patients. As we mentioned in our study,1 TOAST criteria
were meant to be applied to cerebral ischemic infarction and not
to TIA. Therefore, performing DWI-MRI could alter the attending physician’s opinion regarding vascular localization and the
TIA mechanism in almost 35% of patients with DWI abnormalities.2 In a recent study, small-vessel disease subtype was higher
in the TIA patients with acute ischemic lesion (13%) or in minor
stroke patient (14%) than in TIA patients without DWI abnormalities (6%).3 Moreover, DWI could add prognostic information to clinical stroke risk scales. Latest studies have shown that
TIA patients with acute ischemic lesions on DWI have a higher
risk of vascular episodes, both in the short and medium term
follow-up.4 –9
Regarding multiple TIAs, among our patients there was only a
trend (P⫽0.18) of association of that TIA presentation with
stroke recurrence at 7 days follow-up: 17 patients among 295
without cluster TIA (5.8%) versus 9 patients among 93 with
initial cluster TIA (9.7%) had recurrent strokes. Moreover, we
found an association with clustering of TIAs within 1 week of the
index event and large-artery atherosclerosis. Those patients with
cluster TIA and atherotrombotic etiology seemed to be at higher
risk of early stroke recurrence within the first 7 days after
symptoms onset: hazard ratio 2.14 (95% CI: 0.89 to 5.16;
P⫽0.089). However TIA clustering was a covariable of atherotrombotic etiology, and the combination of cluster TIA and this
etiologic subtype was not an independent predictor when the
variable atherotrombotic etiology was included in the multivariable study. Theoretically, repeated transient brain ischemia
would cause cumulative damage that would be expected to result
in a higher probability of brain infarct; however, an alternative
hypothesis might be that the absence of high stroke recurrence
after multiple TIAs could be explained by the well-known
ischemic tolerance phenomena.10 A recent study has shown that
the detectability of DWI lesions after TIA was 12% in the
large-artery atherosclerosis group, 57% in the cardioembolism
group and 8% in the small-artery occlusion group, raising the
possibility of different susceptibility to transient ischemia among
etiologic subtypes.11
Among small-vessel subtypes it would be interesting to
differentiate between patients with persistent symptoms (definite
capsular warning syndrome) after 24-hour follow-up and lacunar
TIA (transient capsular warning syndrome). However, we might
have lost patients that arrive with an established stroke after a
capsular warning syndrome. Therefore, we believe that a larger
Disclosures
None.
Francisco Purroy, MD, PhD
Stroke Unit
Department of Neurology
Universitat de Lleida
Hospital Universitari Arnau de Vilanova de Lleida
Lleida, Spain
Joan Montaner, MD, PhD
Carlos A. Molina, MD, PhD
Pilar Delgado, MD, PhD
Marc Ribo, MD, PhD
José Álvarez-Sabı́n, MD, PhD
Neurovascular Unit
Department of Neurology
Universitat Autònoma de Barcelona
Hospital Universitari de la Vall d’Hebron
Barcelona, Spain
1. Purroy F, Montaner J, Molina CA, Delgado P, Ribo M, Alvarez-Sabin J.
Patterns and predictors of early risk of recurrence after transient ischemic
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2. Kidwell CS, Alger JR, Di Salle F, Starkman S, Villablanca P, Bentson J,
Saver JL. Diffusion MRI in patients with transient ischemic attacks.
Stroke. 1999;30:1174 –1180.
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PG, Lesèche G, Labreuche J, Touboul PJ, Amarenco P. A transient
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(Stroke. 2008;39:e109-e110.)
© 2008 American Heart Association, Inc.
Stroke is available at http://stroke.ahajournals.org
DOI: 10.1161/STROKEAHA.108.515676
e109
e110
Letters to the Editor
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AM.Diffusion-weighted imaging-negative patients with transient ischemic
attack are at risk of recurrent transient events. Stroke. 2007;38:2367–2369.
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E, Quintana M, Alvarez-Sabı́n J. Usefulness of urgent combined carotid/
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ABCD score in the early risk of stroke of transient ischemic attack patients.
Stroke. 2007;38:855–856.
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Response to Letter by Poppe et al
Francisco Purroy, Joan Montaner, Carlos A. Molina, Pilar Delgado, Marc Ribo and José
Álvarez-Sabín
Downloaded from http://stroke.ahajournals.org/ by guest on November 20, 2016
Stroke. 2008;39:e109-e110; originally published online May 8, 2008;
doi: 10.1161/STROKEAHA.108.515676
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