Current Oral Antiplatelets: Focus Update on Prasugrel
Current Oral Antiplatelets: Focus Update on Prasugrel
Platelet activation and aggregation plays an integral role in the pathogenesis of acute coronary syndrome (ACS). The mainstay of ACS treatment revolves around platelet inhibition. It is known that greater platelet inhibition results in better ischemic outcomes; hence, focus in drug development has been to create more potent inhibitors of platelet aggregation. Prasugrel, a potent, third-generation thienopyridine, was approved by the US Food and Drug Administration in July 2009 for its use in ACS and percutaneous coronary intervention. The addition of prasugrel to aspirin for dual antiplatelet therapy has been shown to reduce the ischemic outcomes compared with clopidogrel and aspirin in combination. However, being a more potent antiplatelet agent, prasugrel increases the risk of bleeding, especially in those patients who are at a higher risk of bleeding complications. Elderly patients ≥75 years, patients who weigh ≥60 kg, and patients with a history of stroke or transient ischemic attack are at a higher risk of bleeding complications when prasugrel is used in combination with aspirin. Newer antiplatelets currently are being clinically evaluated to assess their efficacy in reducing ischemic events without increasing the bleeding risk.
Chest pain and acute coronary syndrome (ACS) are major diagnoses for hospital admissions and as single diagnoses they remain major determinants of health care cost. It is important that the high incidence of ACS is also associated with high mortality. The American Heart Association reports that ACS affects one American every 25 seconds and of those, one person dies every minute. It is estimated that 785,000 people in United States will have a new coronary event in 2010. Hence, targeting strategies to improve the outcome related to this condition has been the primary focus in the last 20 to 30 years. Most of the developments in pharmacotherapy have been in targeting platelet inhibition because platelet aggregation and the resultant formation of platelet-rich thrombi are the primary events in the pathogenesis of ACS.
Abstract and Introduction
Abstract
Platelet activation and aggregation plays an integral role in the pathogenesis of acute coronary syndrome (ACS). The mainstay of ACS treatment revolves around platelet inhibition. It is known that greater platelet inhibition results in better ischemic outcomes; hence, focus in drug development has been to create more potent inhibitors of platelet aggregation. Prasugrel, a potent, third-generation thienopyridine, was approved by the US Food and Drug Administration in July 2009 for its use in ACS and percutaneous coronary intervention. The addition of prasugrel to aspirin for dual antiplatelet therapy has been shown to reduce the ischemic outcomes compared with clopidogrel and aspirin in combination. However, being a more potent antiplatelet agent, prasugrel increases the risk of bleeding, especially in those patients who are at a higher risk of bleeding complications. Elderly patients ≥75 years, patients who weigh ≥60 kg, and patients with a history of stroke or transient ischemic attack are at a higher risk of bleeding complications when prasugrel is used in combination with aspirin. Newer antiplatelets currently are being clinically evaluated to assess their efficacy in reducing ischemic events without increasing the bleeding risk.
Introduction
Chest pain and acute coronary syndrome (ACS) are major diagnoses for hospital admissions and as single diagnoses they remain major determinants of health care cost. It is important that the high incidence of ACS is also associated with high mortality. The American Heart Association reports that ACS affects one American every 25 seconds and of those, one person dies every minute. It is estimated that 785,000 people in United States will have a new coronary event in 2010. Hence, targeting strategies to improve the outcome related to this condition has been the primary focus in the last 20 to 30 years. Most of the developments in pharmacotherapy have been in targeting platelet inhibition because platelet aggregation and the resultant formation of platelet-rich thrombi are the primary events in the pathogenesis of ACS.