Abstract
Anti-thrombotic drugs constitute the cornerstone of therapy in the management of acute coronary syndromes (ACS) and for patients undergoing percutaneous coronary intervention. Anti-thrombotic therapy during percutaneous coronary intervention for ACS has evolved substantially over the past 15 years. In the original 1996 ACC/AHA guidelines for the management of acute myocardial infarction (MI), only one antiplatelet agent (aspirin) and one anticoagulant (unfractionated heparin) were recommended as class I therapies. Much has since changed and the contemporary therapeutic armoury for the treatment of ACS reflects the pharmacological advances that have taken place. Recent developments in the medical management of ACS have been based around developing drugs with more predictable efficacy and at known drug targets. However there has also been considerable development of novel agents. New pharmacotherapies for ACS reflect efforts to improve efficacy and minimize complications by increasing target specificity and reducing inter-individual variation in therapeutic response.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.
Key issues
Patients suffering from acute coronary syndromes are in a prothrombotic state and benefit from both antiplatelets and anticoagulants, regardless of whether they progress to percutaneous coronary intervention.
The novel antiplatelet agents, prasugrel and ticagrelor, have been shown to offer more predictable antiplatelet activity and this has translated to improved outcomes in trials to date. Intravenous P2Y12 inhibitors such as cangrelor are on the horizon and may fill a role as a bridging strategy in patients awaiting surgery.
The use of glycoprotein IIb/IIIa inhibitors is declining as more potent oral antiplatelets are available and evidence shows bivalirudin alone may yield better outcomes due to decreased bleeding rates.
The protease-activated-receptor 1 blockers vorapaxar and atopaxar are new drugs, though the benefits when added to standard dual oral antiplatelet therapy appear modest at best.
Anticoagulation remains largely an acute practice. Newer agents such as bivalirudin focus on safer and more predictable anticoagulation and improved endpoints in trials are largely secondary to improved safety profiles rather than efficacy. However, a recent trial questions the efficacy of bivalirudin in the setting of PPCI for ST-elevation myocardial infarction.
Longer-term anticoagulation with new oral anticoagulants does indeed improve cardiovascular endpoints, but at the expense of large increases in bleeding.
Future medical management of acute coronary syndromes will likely focus on individualized care, where bleeding rates can be better estimated and a combination of drugs tailored to the patients; the ‘standard’ therapy including aspirin may become decreasingly ubiquitous.