The available evidence , predominantly from secondary -prevention observational studies , supports that dosages greater than 75 to 81 mg/d do not enhance efficacy , whereas larger dosages are associated with an increased incidence of bleeding events , primarily related to gastrointestinal tract toxicity .
CONCLUSIONS Currently available clinical data do not support the routine , long-term use of aspirin dosages greater than 75 to 81 mg/d in the setting of cardiovascular disease prevention .
Higher dosages , which may be commonly prescribed , do not better prevent events but are associated with increased risks of gastrointestinal bleeding
CONTEXT More than 50 million US adults take aspirin regularly for long-term prevention of cardiovascular disease , typically either 81 mg/d or 325 mg/d .
Controversy remains regarding the most appropriate long-term daily dose .
OBJECTIVE To review the mechanism of action of aspirin and the clinical literature for relationships among  aspirin dosage , efficacy , and safety .
EVIDENCE SYNTHESIS Although pharmacodynamic data demonstrate that long-term aspirin dosages as low as 30 mg/d are adequate to fully inhibit platelet thromboxane production , dosages as high as 1300 mg/d are approved for use .
A comparison of two doses of aspirin (30 mg vs. 283 mg a day) in patients after a transient ischemic attack or minor ischemic stroke.
BACKGROUND Aspirin is known to improve the outcome of patients who have had a cerebral transient ischemic attack , but the optimal dose of aspirin remains uncertain . Experimental evidence indicates that 30 mg of aspirin daily alters platelet aggregation more favorably than the 300-mg dose currently used in patients after transient ischemic attack or minor ischemic stroke . METHODS We assessed the effects of two doses of a water-soluble preparation of acetylsalicylic acid , or aspirin ( 30 mg vs. 283 mg a day ) , on the occurrence of death from all vascular causes , nonfatal stroke , or nonfatal myocardial infa rct ion in a double-blind , r and omized , controlled clinical trial in patients who had had a transient ischemic attack or minor stroke . A total of 3131 patients participated in the study . The mean follow-up was 2.6 years . RESULTS In the group assigned to receive 30 mg of aspirin , the frequency of death from vascular causes , nonfatal stroke , or nonfatal myocardial infa rct ion was 228 of 1555 ( 14.7 percent ) , as compared with 240 of 1576 ( 15.2 percent ) in the group assigned to receive 283 mg . The age- and sex-adjusted hazard ratio for the group receiving the lower dose was 0.91 ( 95 percent confidence interval , 0.76 to 1.09 ) . There were slightly fewer major bleeding complications in the 30-mg group than in the 283-mg group ( 40 vs. 53 ) , and significantly fewer reports of minor bleeding ( 49 vs. 84 ) . Fewer patients receiving 30 mg of aspirin reported gastrointestinal symptoms ( 164 vs. 179 ) and other adverse effects ( 73 vs. 90 ) . CONCLUSIONS Our data indicate that 30 mg of aspirin daily is no less effective in the prevention of vascular events than a 283-mg dose in patients with a transient ischemic attack or minor stroke , and has fewer adverse effects
The available evidence , predominantly from secondary -prevention observational studies , supports that dosages greater than 75 to 81 mg/d do not enhance efficacy , whereas larger dosages are associated with an increased incidence of bleeding events , primarily related to gastrointestinal tract toxicity .
CONCLUSIONS Currently available clinical data do not support the routine , long-term use of aspirin dosages greater than 75 to 81 mg/d in the setting of cardiovascular disease prevention .
Higher dosages , which may be commonly prescribed , do not better prevent events but are associated with increased risks of gastrointestinal bleeding
CONTEXT More than 50 million US adults take aspirin regularly for long-term prevention of cardiovascular disease , typically either 81 mg/d or 325 mg/d .
Controversy remains regarding the most appropriate long-term daily dose .
OBJECTIVE To review the mechanism of action of aspirin and the clinical literature for relationships among  aspirin dosage , efficacy , and safety .
EVIDENCE SYNTHESIS Although pharmacodynamic data demonstrate that long-term aspirin dosages as low as 30 mg/d are adequate to fully inhibit platelet thromboxane production , dosages as high as 1300 mg/d are approved for use .