nhibition of Platelet Aggregation y Aspirin Progressively ecreases in Long-Term Treated Patients
abio M. Pulcinelli
Abstract
abio M. Pulcinelli
Abstract
OBJECTIVES We sought to investigate, during a two-year follow-up period, the effects of aspirin on platelet aggregation. BACKGROUND The platelets of patients given aspirin may be less sensitive to antiplatelet treatment, although the extent of such phenomenon over long-term follow-up is unclear. METHODS Adenosine diphosphate (ADP) and collagen-induced platelet aggregation was periodically monitored before and after 2, 6, 12, and 24 months of treatment with aspirin (n 150) or ticlopidine (n 80) in patients matched for gender, age, and risk factors for atherothrombosis. RESULTS Compared with baseline values, two months of aspirin treatment significantly inhibited platelet aggregation; thereafter, this inhibitory effect progressively decreased. At 24-month follow-up, collagen-induced platelet aggregation was significantly higher than that observed at two months (p 0.05); a more pronounced difference was observed when collageninduced lag phase was considered (p 0.01). Restoration of platelet aggregation was less evident when ADP was used as an agonist. Conversely, the inhibition induced by ticlopidine was constant throughout follow-up with both agonists. CONCLUSIONS The study demonstrates that a long-term treatment with aspirin is associated with a progressive reduction in platelet sensitivity to this drug. (J Am Coll Cardiol 2004;43: 979–84) © 2004 by the American College of Cardiology Foundation
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OBJECTIVES We sought to investigate, during a two-year follow-up period, the effects of aspirin on platelet aggregation. BACKGROUND The platelets of patients given aspirin may be less sensitive to antiplatelet treatment, although the extent of such phenomenon over long-term follow-up is unclear. METHODS Adenosine diphosphate (ADP) and collagen-induced platelet aggregation was periodically monitored before and after 2, 6, 12, and 24 months of treatment with aspirin (n 150) or ticlopidine (n 80) in patients matched for gender, age, and risk factors for atherothrombosis. RESULTS Compared with baseline values, two months of aspirin treatment significantly inhibited platelet aggregation; thereafter, this inhibitory effect progressively decreased. At 24-month follow-up, collagen-induced platelet aggregation was significantly higher than that observed at two months (p 0.05); a more pronounced difference was observed when collageninduced lag phase was considered (p 0.01). Restoration of platelet aggregation was less evident when ADP was used as an agonist. Conversely, the inhibition induced by ticlopidine was constant throughout follow-up with both agonists. CONCLUSIONS The study demonstrates that a long-term treatment with aspirin is associated with a progressive reduction in platelet sensitivity to this drug. (J Am Coll Cardiol 2004;43: 979–84) © 2004 by the American College of Cardiology Foundation
Key concepts: Aspirin, Platelet, Ticlopidine, Adenosine diphosphate, Platelet aggregation, Agonist, Medicine, Antiplatelet drug