Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
Stroke. 2006;37:767
doi: 10.1161/01.STR.0000204060.73207.c5
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Imray, C. H.E.
Right arrow Articles by Pattinson, K. T.S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Imray, C. H.E.
Right arrow Articles by Pattinson, K. T.S.

(Stroke. 2006;37:767.)
© 2006 American Heart Association, Inc.


Letters to the Editor

Potential Role for TCD-Directed Antiplatelet Agents in Symptomatic Carotid Artery Dissection

Christopher H.E. Imray

Coventry and Warwickshire County Vascular Unit, Coventry and Warwickshire University Hospitals, Coventry, UK

Kyle T.S. Pattinson

Nuffield Department of Anaesthetics, University of Oxford, The John Radcliffe Hospital, Oxford, UK


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

To the Editor:

We read with interest the debate regarding the role of anticoagulation in extracranial arterial dissection.1–3 We agree with Norris1 that artery to artery embolism is the most likely cause of stroke, and also agree with Lyrer2 that there is no evidence supporting anticoagulation for extracranial internal carotid artery dissection (CAD). Donnan and Davis3 make a most important contribution when they differentiate between the use of antithrombotic agents and antiplatelet agents in CAD.

The commonest mechanism of stroke in carotid artery dissection is hypothesized to be artery to artery embolism.1 If this hypothesis is correct, then the situation would appear to be analogous to transient ischemic attacks arising from a critical internal carotid artery stenosis. Transcranial Doppler (TCD)-directed intravenous antiplatelet agents have been successful in treating these patients4,5,6 both before and after elective surgery. In further support of this hypothesis, we have recently reported a 45-year-old patient who was successfully treated with TCD-directed antiplatelet agents7 for recurrent focal deficits associated with an embolizing subintimal CAD.

Converging lines of evidence suggest that embolization from large arteries can cause focal cerebral symptoms and can be treated in the short-term with TCD-directed antiplatelet agents.4 TCD can rapidly and noninvasively assist both in identifying those patients at higher risk of a subsequent neurological event,8 and in assessing the efficacy of interventions.5 TCD emboli detection appears to offer an important advance, enabling the optimal integration of both medical therapy and the timing of any surgical intervention, in patients with symptomatic large-vessel disease. We . . . [Full Text of this Article]