TY - JOUR T1 - Antithrombotic therapy for patients with chronic coronary syndromes JF - Heart JO - Heart SP - 925 LP - 933 DO - 10.1136/heartjnl-2020-316914 VL - 107 IS - 11 AU - William AE Parker AU - Robert F Storey Y1 - 2021/06/01 UR - http://heart.bmj.com/content/107/11/925.abstract N2 - Learning objectivesLearn the pathophysiology of atherothrombosis and mechanisms by which aspirin, P2Y12 inhibitors and anticoagulants exert antithrombotic effect.Describe key randomised clinical trials of antithrombotic therapy in patients with chronic coronary syndromes (CCS) that inform current practice.Use recommendations in the 2019 European Society of Cardiology CCS guidelines to make evidence-based decisions regarding choice and duration of antithrombotic agent for patients with CCS.Globally, much morbidity and premature mortality arises from coronary artery disease (CAD). Coronary artery atherothrombosis is the dominant cause of acute coronary syndromes (ACS), including spontaneous myocardial infarction (MI) and unstable angina. Those with chronic coronary syndromes (CCS), including stable CAD or an ACS event >1 year ago, are at ongoing atherothrombotic risk.1 Modifiable or partially modifiable risk factors such as hypercholesterolaemia, diabetes mellitus (DM), hypertension and smoking, and unmodifiable factors such as age and chronic kidney disease (CKD), can initiate and accelerate coronary atherosclerosis.2 Understanding the pathophysiology of atherothrombosis has helped to identify and exploit therapeutic targets.In 2019, the European Society of Cardiology (ESC) published new guidelines on the management of CCS, including antithrombotic therapy.3 In this review, we evaluate the pathophysiology and pharmacology of atherothrombosis, highlight up-to-date evidence from randomised controlled trials (RCTs), and discuss the content and application of the the ESC 2019 CCS guidelines.The thrombotic responseWhile atherosclerotic plaques are thrombogenic even when intact, thrombosis is typically triggered by plaque rupture/erosion, allowing blood constituents to make contact with prothrombotic factors such as collagen.4 Platelet activation is central to atherothrombosis (figure 1).5 Collagen activates platelets via glycoprotein VI receptors. Subsequently, arachidonic acid is converted to prostaglandin H2 by the enzyme cyclo-oxygenase (COX) 1, and then, by thromboxane A2 (TXA2) synthase, to TXA2, which further enhances platelet activation via thromboxane-receptor-α.6 Intracellular granules fuse with the … ER -