Some patients taking aspirin will develop thromboembolic disease. A subset of these patients are thought to have platelets that are resistant to the functional inhibition caused by aspirin. These patients may benefit from alternative therapeutic strategies.


The mechanism of aspirin's antiplatelet activity is acetylation of platelet cyclo-oxygenase, which causes irreversible inhibition of platelet-dependent thromboxane formation.


Features of aspirin resistance:

(1) presence of thrombotic event while on aspirin therapy

(2) no evidence of decreased platelet function in laboratory tests

(3) exclusion of alternative explanations


Laboratory tests:

(1) platelet aggregation studies (optical aggregometer)



(1) noncompliance

(2) inadequate dose

(3) hypercoagulable state

(4) nonthrombotic vascular disease

(5) drug interaction interfering with aspirin effect


If a patient is suspected of having aspirin resistance, a number of therapeutic options are available:

(1) clopidogrel

(2) dipyridamole plus aspirin

(3) warfarin plus aspirin


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