Antithrombotic Therapy for Cerebrovascular Disorders: Nonembouc Stroke

Nonembouc Stroke
Atherosclerotic cerebrovascular disease accounts for the bulk of ischemic strokes. Patients with HA, reversible ischemic neurologic deficit (RIND), progressing stroke and completed stroke have been managed variably with platelet antiaggregating agents, anticoagulants, and surgery.
Anticoagulation Therapy
Although anticoagulant therapy has been widely used in the treatment of cerebrovascular disease, its value remains controversial.
Transient Ischemic Attack and Minor Stroke
Only level III and II studies with insufficient numbers of patients are available to evaluate the effectiveness of anticoagulation in preventing stroke following HA. The doses of warfarin used in those studies was somewhat higher than is customarily used today, and there was a tendency toward increased mortality in the anticoagulant-treated patients.
Progressing Stroke
Initial level II studies showed a trend for lower mortality in patients with progressing stroke who received anticoagulants. In a randomized, doubleblind comparison of heparin and placebo for 7 days following partial stroke, stroke progression was almost identical, 17% in the heparin and 19.5% in the untreated patients. This difference was not statistically significant. Link

Completed Stroke
Level II trials have shown anticoagulation to be potentially dangerous or without value in patients with completed stroke not due to cardiogenic embolism. There is a consensus that longterm anticoagulant treatment of completed stroke patients is not indicated.
Platelet Antiaggregation Agents
Transient ischemic attack and minor stroke: There have been over 20 trials of antiplatelet therapy for patients with a history of TIA, minor stroke, unstable angina, or MI involving some 25,000 patients. A metaanalysis of this data reveals that antiplatelet therapy makes no difference in nonvascular mortality but reduces that due to vascular events by about 15 ± 4% (p = 0.003). Nonfatal events such as MI and stroke are reduced by 22 ±3%. Individual trial results vary from being individually “negative” to showing a 50% reduction, but these values do not differ significantly from 22%, and there is no reason to suppose that the difference between trials is any more than the play of chance.