The Challenge of Getting it Just Right Optimizing Long-Term Antithrombotic Therapy After Acute Coronary Syndrome ∗

Acute coronary syndrome (ACS) is associated with substantial morbidity and mortality (1,2). Initial treatment in the hospital consists of intensive antithrombotic therapy combining parenteral anticoagulation with antiplatelet therapy, whereas secondary prevention relies primarily on dual antiplatelet therapy (DAPT), most commonly aspirin and clopidogrel. However, patients with ACS remain at significant risk of recurrent adverse cardiovascular events (3). Mitigation of this risk requires a delicate balance between escalation of antithrombotic therapy to reduce ischemic events, while hoping the increase in bleeding is tolerable. This has been successful with regard to platelet inhibition, as substituting clopidogrel for the more potent P2Y12 receptor antagonists, prasugrel and ticagrelor, reduces cardiovascular death, myocardial infarction (MI), and stroke in patients with ACS, at the expense of increasing major spontaneous bleeding (4,5). Regardless of the DAPT regimen, there remains a 9% to 11% risk of an adverse cardiovascular event within 1 year of ACS (3–5). This forces a broader consideration of where to intervene in the complex hemostatic interplay between the vascular endothelium, platelets, and the coagulation cascade to improve outcomes in patients with ACS (6).
Source: Journal of the American College of Cardiology - Category: Cardiology Source Type: research