Anti-platelet agents. Anti-platelet agents act via a variety of mechanisms to inhibit platelet aggregation. They are the cornerstone of treatment in cardiovascular disease and are used prophylactically in patients with significant atherosclerosis who are at risk of thrombotic events. Anti-platelet agents, particularly aspirin, have been used for decades and the drug class continues to evolve as novel agents with increasingly efficacious anti-platelet actions are identified. The main risk associated with all forms of anti-platelet therapy is bleeding, and physicians need to carefully weigh the possible adverse effects against the benefits of prescribing these drugs to patients with cardiovascular disease. Aspirin, which has been recognised to have anti-thrombotic effects since the 1960s, continues to be prescribed almost ubiquitously for patients with acute coronary syndrome (ACS), and P2Y12 antagonists are now often added in; such dual anti-platelet therapy (DAPT) confers greater anti-thrombotic efficacy but at the risk of increased bleeding. Over recent years, it has become apparent that these drugs may also exert powerful anti-inflammatory effects that provide additional benefit in the management of ACS. Anti-platelet therapy may improve outcomes not only through anti-thrombotic properties but also via their anti-inflammatory effects, although their relative contribution in this context remains a subject of debate. What is clear, however, is that increased anti-thrombotic efficacy improves outcomes post-ACS, but carries the price of increased bleeding risk, so that at some point diminishing returns accrue from ever more efficacious anti-platelet therapy. The challenge for the future is to better predict the benefit / risk ratio in individual patients, so that the intensity of anti-platelet therapy can be optimised on a personalised basis. The following sections of this thesis will discuss anti-platelet agents that are currently used in clinical practice.
