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 .
Two year Cottbus reinfarction study with 30 mg aspirin per day.
All 701 heart infa rct ion patients admitted to 15 hospitals in the district of Cottbus between 1981 and 1983 were r and omly administered 30 , 60 or 1000 mg aspirin daily according to the territorial affiliation of their local hospitals . The physical and drug therapy during the 2 years follow-up was highly st and ardized ; deviations -- as far as they occurred -- were documented . Lower all-cause mortality was statistically demonstrated in patients over 60 and a lower fatal reinfa rct ion rate in patients over 50 as well as in men .  Deaths and fatal reinfa rct ions were significantly lower among patients with a history of angina pectoris , marked ST-depression , with an infa rct ion location except for the posterior wall and among hypercholesterolemic patients . The preventive effect of 60 mg aspirin daily was less than that of 30 mg in comparison to the 1000 mg group . Side effects were seen in 4 and 8 % ( first and second year ) , respectively , of the patients administered 30 mg aspirin as opposed to 22 and 17 % in patients allocated 1000 mg . We conclude that the optimum dose of aspirin for preventing reinfa rct ions could be as low as 30 mg daily
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 .