Mg / d produced lower gastrointestinal proteasome inhibitors bleeding in a dose of 300-325 mg / d, the incidence of other types of major bleeding was not different between the two groups. 48 In summary, supporting the lack of a dose-response relationship for the effi ciency of aspirin in clinical trials and dose- Dependence of gastrointestinal bleeding, the use of lower doses to be effective aspirin proved to be the most appropriate strategy to maximize the effi ciency and minimize toxicity t. Reactivity t 9High platelets in patients prescribed aspirin was associated with a increased Hten associated risk of thrombotic events. Therefore, this Ph Phenomenon as a defi nition of aspirin resistance has been used. Observational studies show that nearly a third of patients treated with aspirin inhibition of agonist-induced platelet aggregation less thanexpected and demonstrated increased Hte levels of urinary thromboxane. 10.8 Sch estimates Of Pr Prevalence of high Thrombozytenreaktivit t be on the treatment used by differences between studies in patient characteristics, concomitant medications, laboratory test to measure the antiplatelet effect of aspirin, the threshold used affected by defi ne the high reactivity t of treatment and patient compliance with aspirin therapy. Despite these differences, increased 25 High Thrombozytenreaktivit ht t prescribed aspirin in patients associated with a twofold increased Hten risk of myocardial infarction was associated quadrupled, stroke or death. If 9,10,26,27 thrombotic events were treated with aspirin in patients at high Thrombozytenreaktivit T to treatment were exclusively Lich to the lower reactivity t to aspirin, strategies to improve the response to be expected w Re to To reduce this risk. Observational studies suggest that aspirin platelet function and coagulation 68 72 73 79 a dose- Independent way inhibits fi RMED a configuration ends in a randomized dose comparison. 80 Thus, in a randomized double-blind crossover, which included 125 patients with stable coronary artery disease, demonstrated Gurbel and colleagues that inhibits 80 in doses of 81, 162 or 325 mg / d aspirin, adenosine diphosphate and platelet aggregation induced by collagen blocked sheardependent platelet aggregation by the PFA-100 device t is measured, and reduced urinary concentration of thromboxane in a dose-dependent ngigen way. Most patients had enrolled in this study almost completely Requests reference requests getting the inhibition of arachidonic Acid-induced platelet aggregation by 81 mg / dose aspirin, but the h Reduced higher doses of aspirin, the proportion of patients in whom the arachidonic Acid-induced aggregation exceeded a threshold of 20%. 80 However, the dose- Independent inhibition of platelet function and thromboxane production by aspirin in this study were not observed fi t with the results of the current OASIS 7 trial, the evidence failed to reduce risk of thrombotic events with h Higher doses of aspirin. How we may use the explained Ren, this apparent paradox The most likely explanation Tion is that the relationship between Thrombozytenreaktivit t and thrombotic risk due to comorbidities Everolimus 159351-69-6 such as smoking or diabetes, both platelet function and the kardiovaskul Is confused re influence risk. It is also Possible that the laboratory tests used to measure Thrombozytenreaktivit t k Can not contr L is the mechanism by which aspirin reduces the risk of thrombotic events. Many of these tests use nonphysiologi.