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 .
Aspirin dose and six-month outcome after an acute coronary syndrome.
OBJECTIVES This study was design ed to compare the efficacy of low and intermediate aspirin doses in acute coronary syndromes . BACKGROUND Little is known of the comparative efficacy of low and intermediate aspirin doses in this setting . METHODS We compared six-month death , myocardial infa rct ion ( MI ) , and stroke in patients with unstable angina or acute MI discharged while receiving low ( < 150 mg ) or intermediate ( > or = 150 mg ) aspirin therapy in the GUSTO IIb and PURSUIT trials ( n = 20,521 ) . We used multivariable analysis and performed a propensity analysis in order to adjust for baseline imbalances between the groups . RESULTS Aspirin doses < 150 mg were prescribed to 29.9 % ( 6,128 ) of patients . By six months , 6.4 % of the patients ( 1,310 of 20,521 ) had a primary event , 6.2 % of the patients receiving < 150 mg and 6.6 % of the patients receiving aspirin doses > or = 150 mg ( hazard ratio [ HR ] 1.06 [ 95 % confidence interval ( CI ) 0.94 to 1.19 ] , p = 0.35 ) . After adjusting for baseline imbalances and the propensity score for discharge aspirin dose , there was no effect of aspirin dose on the composite end point at six months ( HR 0.92 [ 95 % CI 0.79 to 1.07 ] , p = 0.28 ) . However , the higher aspirin dose was associated with a reduction in six-month MI ( HR 0.79 [ 95 % CI 0.64 to 0.98 ] , p = 0.03 ) . The outcome was similar when patients were matched on the basis of the propensity score for aspirin dose ( HR for death/MI/stroke 0.94 [ 95 % CI 0.80 to 1.12 ] , p = 0.51 ) , although stroke occurred significantly more frequently among patients receiving the higher aspirin dose ( HR 1.74 [ 95 % CI 1.01 to 3.02 ] p = 0.05 ) and the effect on MI was no longer apparent . CONCLUSIONS Although these data are non-r and omized , they suggest that the aspirin dose upon discharge may influence the clinical course after unstable angina or acute MI
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 .