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 .
Secondary prevention of ischemic stroke with low dose acetylsalicylic acid.
In order to evaluate the efficacy of low dose acetylsalicylic acid ( ASA ) for the secondary prevention of ischemic stroke , this cooperative multicenter clinical trial was conducted on a non-blind basis . Patients having a first transient ischemic attack ( TIA ) , reversible ischemic neurological deficit ( RIND ) or completed ischemic stroke were eligible for this trial . A total of 590 patients including 47 cases of TIA , 23 cases of RIND and 520 cases of completed stroke entered this study . These patients were allocated by the time of admission to one of the following 5 trial regimens : ( 1 ) vasodilators having no known inhibitory effect on platelet function ( control group ) , ( 2 ) dipyridamole ( DP ) 50 mg 3 times a day ( DP group ) , ( 3 ) ASA 300 mg once a day ( ASA 300 mg group ) , ( 4 ) ASA 300 mg once in combination with DP 50 mg 3 times a day ( ASADP group ) , and ( 5 ) ASA 100 mg once a day ( ASA1 group ) . No difference in effect between the control and DP groups was observed , nor between the ASA 300 mg and ASADP groups . Therefore , we combined the control and DP groups to make a non-ASA group , and joined the ASA 300 mg and ASADP groups to make an ASA3 group . The differences in the cumulative event-free rate appeared to be significant between the non-ASA group and the ASA3 group and also between the non-ASA group and the ASA1 group . But the frequency distribution of age , territory of stroke , diabetes mellitus , cardiac disease , hematological disease and hyperuricemia were significantly different among these 3 study groups . We thus included these covariates in the Cox 's proportional hazard model to control their possible confounding effects . ( ABSTRACT TRUNCATED AT 250 WORDS
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 .