Aspirin is a well-established medication in the treatment of atherothrombotic vascular disease. However, despite aspirin treatment a substantial number of patients experience recurring ischaemic episodes. Aspirin resistance denotes those situations when it is unable to protect individuals from thrombotic complications, or when it fails to produce an anticipated effect in laboratory tests of platelet function. There are various laboratory techniques with which to evaluate the effectiveness of aspirin and other antiplatelet drugs. It has been estimated that in 5-60% of patients, aspirin does not achieve adequate efficacy in various measures of platelet activity. Some studies have revealed that vascular patients shown by laboratory tests to be aspirin-resistant are at an increased risk of major vascular events. The suggested mechanisms of aspirin resistance, among others, include genetic polymorphisms, alternate pathways of platelet activation, aspirin-insensitive thromboxane biosynthesis, drug interactions, or low aspirin dose. An increase in the dosage of aspirin or conversion to clopidogrel or clopidogrel plus aspirin might be beneficial in the management of those patients who are aspirin resistant. Additional work is required to improve and validate laboratory tests of platelet function, so that they may become useful tools for selecting the most appropriate antiplatelet therapy for an individual patient. Improvements in antiplatelet treatment strategies in the future should lead to a reduction in premature vascular events.