Antiplatelet therapy in acute coronary syndromes

Abstract

Introduction: Coronary thrombosis is a frequent cause of death and myocardial infarction most often explained by superimposition of a platelet-rich thrombus on existing coronary artery disease. Therefore, antiplatelet drugs are essential in the treatment and secondary prevention of acute coronary syndromes (ACS) and during percutaneous coronary intervention. Several novel antiplatelet drugs are now available.

Areas covered: For several years, aspirin and clopidogrel remained the cornerstone of treatment for ACS. However, prasugrel and ticagrelor have a more consistent, faster-acting and more potent antiplatelet effect than clopidogrel, which translates into improved clinical outcomes, although at the expense of an increased bleeding risk. Importantly, some patients experience cardiovascular events despite current antiplatelet treatment, because platelet activation may occur via pathways not inhibited by these agents. Therefore, improved antiplatelet strategies are warranted.

Expert opinion: Despite undisputable benefits of current antiplatelet strategies, a considerable number of patients continue to experience adverse thrombotic events, although clinical outcomes have been improved with new oral P2Y₁₂ antagonists. New drugs have been developed, including intravenous P2Y₁₂ antagonists and oral antagonist targeting the protease-activated receptor-1 platelet activation pathway stimulated by thrombin. This review provides an overview of current and novel antiplatelet strategies and also discusses unmet needs related to antiplatelet therapy for ACS.

Keywords:

• acute coronary syndromes
• antiplatelet drugs
• aspirin
• clopidogrel
• glycoprotein IIb/IIIa inhibitors
• percutaneous coronary intervention
• prasugrel
• ticagrelor
• vorapaxar

Declaration of interests

EL Grove has received speaker honoraria from AstraZeneca, Bayer, Baxter Boehringer Ingelheim, Bristol-Myers Squibb and Pfizer and has participated in advisory board meetings for AstraZeneca, Bayer, Bristol-Myers Squibb and Boehringer Ingelheim. SD Kristensen has received speaker honorarium from Aspen, AstraZeneca and The Medicines Company and has participated in advisory board meetings for AstraZeneca. M Würtz has received financial support for scientific activities from Bristol-Myers Squibb. The authors have no other 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 apart from those disclosed.

Notes

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