Secondary prevention of stroke and transient ischemic attack: is more platelet inhibition the answer?
BACKGROUND
Recurrent cerebrovascular events constitute an estimated 200,000 of the 700,000 strokes reported annually in the United States, which makes secondary stroke prevention an important goal in the management of disease among patients who have experienced stroke or transient ischemic attack.


RESULTS
Various pharmacological approaches have been advocated, but the relative efficacy and safety of these regimens has remained the subject of much debate. The results of recent clinical trials on the use of antiplatelet therapy suggest that patients with a history of stroke or transient ischemic attack may constitute a population distinct from patients with coronary or peripheral vascular disease. This may be caused, in part, by the differing etiologies of stroke and the increased vulnerability of cerebral vessels to bleeding. Indeed, dual antiplatelet therapy, which has been found to be beneficial for the treatment of acute coronary syndromes and percutaneous coronary interventions, does not confer secondary stroke protection. The emerging paradigm is that some level of platelet inhibition is required for secondary stroke protection; a level beyond which increased risk of bleeding arises.


CONCLUSIONS
Because the vast majority of patients with ischemic stroke have recurrent stroke or transient ischemic attack, rather than myocardial infarction, as their next event, antiplatelet therapies for these patients should be administered according to what has been shown to be efficacious for secondary stroke protection rather than for myocardial protection. Combination therapies, which provide optimal platelet inhibition as well as vascular protection, may offer the best strategy for secondary stroke protection.
Liao
James K
JK
Cardiovascular Division, Department of Medicine, Brigham & Women's Hospital, 65 Landsdowne St, Rm 275, Cambridge, MA 02139, USA. jliao@rics.bwh.harvard.edu
D001241:Aspirin / Q000494:pharmacology / Q000627:therapeutic use; D050197:Atherosclerosis / Q000150:complications / Q000453:epidemiology; D000077407:Cilostazol; D002986:Clinical Trials as Topic; D000077144:Clopidogrel; D003327:Coronary Disease / Q000453:epidemiology / Q000209:etiology / Q000517:prevention & control; D004176:Dipyridamole / Q000494:pharmacology / Q000627:therapeutic use; D004198:Disease Susceptibility; D004347:Drug Interactions; D004359:Drug Therapy, Combination; D050171:Dyslipidemias / Q000453:epidemiology; D006470:Hemorrhage / Q000139:chemically induced / Q000517:prevention & control; D006801:Humans; D002546:Ischemic Attack, Transient / Q000209:etiology / Q000517:prevention & control*; D015337:Multicenter Studies as Topic; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D016032:Randomized Controlled Trials as Topic; D012008:Recurrence; D020521:Stroke / Q000453:epidemiology / Q000209:etiology / Q000517:prevention & control*; D013777:Tetrazoles / Q000494:pharmacology / Q000627:therapeutic use; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000494:pharmacology / Q000627:therapeutic use; D016896:Treatment Outcome; D014665:Vasodilator Agents / Q000494:pharmacology / Q000627:therapeutic use
D010975:Platelet Aggregation Inhibitors; D013777:Tetrazoles; D014665:Vasodilator Agents; D004176:Dipyridamole; D000077144:Clopidogrel; D000077407:Cilostazol; D013988:Ticlopidine; D001241:Aspirin