Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
Stroke. 2006;37:2428-2429
Published online before print July 20, 2006, doi: 10.1161/01.STR.0000236037.87109.fc
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
37/9/2428    most recent
01.STR.0000236037.87109.fcv1
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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Fisher, M.
Right arrow Articles by Barnett, H. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fisher, M.
Right arrow Articles by Barnett, H. J.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Medline Plus Health Information
*Blood Thinners
Related Collections
Right arrow Antiplatelets

(Stroke. 2006;37:2428.)
© 2006 American Heart Association, Inc.


Emerging Therapies

CHARISMA

The Antiplatelet Saga Continues

Marc Fisher, MD; Kennedy Lees, MD, Section Editors:; John W. Norris, MD Henry J. Barnett, MD, CC

From the St Georges Medical School (J.W.N.), University of London, UK; and the Robarts Research Institute (H.J.B.), London, Ontario, Canada.

Correspondence to John W. Norris, MD, FRCP, Centre for Clinical Neuroscience, St Georges Medical School, University of London, London SW17 0RE, UK. E-mail carotid@btopenworld.com


Key Words: antiplatelet agents • antiplatelet drugs • clinical trials


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

Ever since the Antithrombotic Trialists reported a clear benefit from aspirin in the secondary prevention of vascular disease in patients with a variety of cardiovascular events,1 there has been a search for more effective antithrombotic agents. The first relatively nontoxic drug to undergo randomized clinical trial was clopidogrel in the CAPRIE study2 (Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events) where 3 groups of patients (myocardial ischemia (MI), ischemic stroke or peripheral arterial disease) were given either aspirin or the drug. The compound end point of MI, ischemic stroke and vascular death was significantly reduced by clopidogrel compared with patients taking aspirin. However, the substantial benefit on vascular outcome evident in the peripheral vascular group was not shared by either the stroke patients or those with MI.

Because aspirin and clopidogrel have different biochemical pathways inhibiting platelet adhesiveness, a combination of the 2 drugs might be even more effective in secondary prevention of vascular events. In CURE (Clopidogrel in Unstable Angina to Prevent Recurrent Events) the dual antiplatelet therapy was found even more beneficial than clopidogrel alone in reducing combined cardiac and cerebral ischemic end points, but a group with aspirin alone was not included.3 This was followed by CREDO (Clopidogrel for the Reduction of Events During Observation), and once again clopidogrel was found more effective than placebo in reducing the compound end points of death and myocardial and cerebral infarction in patients undergoing percutaneous coronary intervention.4

However, all these studies failed to show any significant prophylactic effect . . . [Full Text of this Article]




This article has been cited by other articles:


Home page
StrokeHome page
S. Sacco and A. Carolei
CHARISMA: The Antiplatelet Saga Continues
Stroke, March 1, 2007; 38(3): 854 - 854.
[Full Text] [PDF]