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Stroke. 2008;39:e109-e110
Published online before print May 8, 2008, doi: 10.1161/STROKEAHA.108.515676
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(Stroke. 2008;39:e109.)
© 2008 American Heart Association, Inc.


Letters to the Editor

Response to Letter by Poppe et al

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-Sabín, MD, PhD

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 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 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

  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 attack with respect to etiologic subtypes. Stroke. 2007; 38: 3225–3229.[Abstract/Free Full Text]
  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.[Abstract/Free Full Text]
  3. Lavallee PC, Meseguer E, Abboud H, Cabrejo L, Olivot JM, Simon O, Mazighi M, Nifle C, Niclot P, Lapergue B, Klein IF, Brochet E, Steg PG, Lesèche G, Labreuche J, Touboul PJ, Amarenco P. A transient ischaemic attack clinic with round-the-clock access (SOS-TIA): feasibility and effects. Lancet Neurol. 2007; 6: 953–960.[CrossRef][Medline] [Order article via Infotrieve]
  4. Purroy F, Montaner J, Rovira A, Delgado P, Quintana M, Alvarez-Sabín J. Higher risk of further vascular events among transient ischemic attack patients with diffusion-weighted imaging acute ischemic lesions. Stroke. 2004; 35: 2313–2319.[Abstract/Free Full Text]
  5. Ay H, Koroshetz WJ, Benner T, Vangel MG, Wu O, Schwamm LH, Sorensen AG. Transient ischemic attack with infarction: A unique syndrome? Ann Neurol. 2005; 57: 679–686.[CrossRef][Medline] [Order article via Infotrieve]
  6. Coutts SB, Simon JE, Eliasziw M, Sohn CH, Hill MD, Barber PA, Palumbo V, Kennedy J, Roy J, Gagnon A, Scott JN, Buchan AM, Demchuk AM. Triaging transient ischemic attack and minor stroke patients using acute magnetic resonance imaging. Ann Neurol. 2005; 57: 848–854.[CrossRef][Medline] [Order article via Infotrieve]
  7. Boulanger J-M, Coutts SB, Eliasziw M, Subramaniam S, Scott J, Demchuk AM. Diffusion-weighted imaging-negative patients with transient ischemic attack are at risk of recurrent transient events. Stroke. 2007; 38: 2367–2369.[Abstract/Free Full Text]
  8. Calvet D, Lamy C, Touzé E, Oppenheim C, Meder JF, Mas JL. Management and outcome of patients with transient ischemic attack admitted to a stroke unit. Cerebrovasc Dis. 2007; 24: 80–85.[CrossRef][Medline] [Order article via Infotrieve]
  9. Prabhakaran S, Chong JY, Sacco RL. Impact of abnormal diffusion-weighted imaging results on short-term outcome following transient ischemic attack. Arch Neurol. 2007; 64: 1105–1109.[Abstract/Free Full Text]
  10. Kirino T. Ischemic tolerance. J Cereb Blood Flow Metab. 2002; 22: 1283–1296.[CrossRef][Medline] [Order article via Infotrieve]
  11. Uno H, Taguchi A, Oe H, Nagano K, Yamada N, Moriwaki H, Naritomi H. Relationship between detectability of ischemic lesions by diffusion-weighted imaging and embolic sources in transient ischemic attacks. Eur Neurol. 2008; 59: 38–43.[CrossRef][Medline] [Order article via Infotrieve]
  12. Purroy F, Montaner J, Delgado P, Arenillas JF, Molina CA, Santamarina E, Quintana M, Alvarez-Sabín J. Usefulness of urgent combined carotid/transcranial ultrasound testing in early prognosis of TIA patients. Med Clin (Barc). 2006; 126: 647–650.[CrossRef][Medline] [Order article via Infotrieve]
  13. Purroy F, Molina CA, Montaner J, Alvarez-Sabín J. Absence of usefulness of ABCD score in the early risk of stroke of transient ischemic attack patients. Stroke. 2007; 38: 855–856.[Free Full Text]




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