Low-dose aspirin therapy has not been reported to affect renal function or BP control, which is consistent with its lack of effect on renal PGs that derive primarily from constitutively expressed COX-2 in the human kid-ney. Moreover, aspirin therapy, 75 mg daily, did not affect BP or the need for antihypertensive therapy in intensively treated hypertensive patients. The suggestion that the use of aspirin and other antiplatelet agents is associated with reduced benefit from therapy with enala-pril in patient
Thus, in summary, the inhibition of TXA 2 -dependent platelet function by aspirin may lead to the prevention of thrombosis as well as to excess bleeding. Assessing the net effect requires an estimation of the absolute thrombotic risk vs the hemorrhagic risk of the individual patient. In individuals who are at very low risk for vascular occlusion, a very small absolute benefit may be offset by the exposure of very large numbers of healthy subjects to undue bleeding complications. As the risk of experiencing
A general change to lower doses of aspirin (ie, 75 mg) would not eliminate risks but would reduce risk by about 40% compared with doses of 300 mg and by 30% compared with doses of 150 mg, if the assumptions from indirect comparisons are correct. Given that the mortality rate among patients who are hospitalized for NSAID-induced upper GI bleeding is about 5 to 10%, such a strategy could save a significant number of lives.