['Antiplatelet therapy has been proven to be effective for both primary and secondary prevention of myocardial infarction, stroke, and cardiovascular death. However, a significant proportion of patients treated with aspirin experience ischemic events. A number of prospective studies have demonstrated that decreased responsiveness to antiplatelet therapy as measured by various methods, is strongly associated with an increase in clinical events. Our objective was to characterize platelet function in patients presenting with chest pain using a point-of-care assay, PFA-100 and correlating results to traditional platelet aggregometry to determine if patients with aspirin non-responsiveness have increased clinical sequelae.', 'Platelet function was assessed using PFA-100, flow cytometry, and optical aggregometry in 94 patients presenting to the emergency department with chest pain. All patients were on aspirin 81-325 mg daily. Clinical events occurring during the index hospitalization were documented.', 'Forty-seven patients (50%) were defined as aspirin non-responders by PFA-100 (collagen-epinephrine closure time <or= 193). Compared to aspirin responders, aspirin non-responders had higher levels of mean platelet aggregation to adenosine diphosphate (ADP) (P = 0.004) and high dose epinephrine (P = 0.03). Furthermore, expression of PAC-1 was significantly increased in patients with aspirin nonresponse as compared to aspirin responders (P = 0.003 and P = 0.0006 respectively). No significant difference in clinical events during the index hospitalization was noted between aspirin non-responders and aspirin responders.'] Is abnormal PFA-100 closure time associated with increased platelet aggregation in patients presenting with chest pain?