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(Stroke. 2008;39:e109.)
© 2008 American Heart Association, Inc.
Letters to the Editor |
Stroke Unit, Department of Neurology, Universitat de Lleida, Hospital Universitari Arnau de Vilanova de Lleida, Lleida, Spain
Neurovascular Unit, Department of Neurology, Universitat Autònoma de Barcelona, Hospital Universitari de la Vall d'Hebron, Barcelona, Spain
Response:
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 physicians 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 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.
Acknowledgments
Disclosures
None.
References
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