Novel antiplatelet therapy in acute coronary syndromes: what is new in the pipeline?
Acute coronary syndromes (ACS) are triggered by enhanced platelet activation and aggregation. Hence, a cornerstone of successful secondary prevention in ACS is an effective platelet inhibition. Additionally, coronary interventions (PCI) lead to even increased artherothrombotic risks, another challenge in preventing recurrent events including stent thrombosis. Promising platelet targets were characterized and novel molecules were developed that are currently under investigation. Intensified antiplatelet therapy includes the risk of major bleeding which itself increases the mortality rate. Previous strategies of antiplatelet therapy were based on an "one-size fits all" concept. However, there has been evidence that variability of drug response exists and represents a clinically relevant issue. This observation is in line with results of randomized clinical trials that standard-of-care antiplatelet therapy is not sufficient to reduce cardiovascular (CV) risk in certain subgroups of ACS patients. In the last years, novel antiplatelet substances have entered the clinical arena and others are currently under investigation in phase II and III clinical trials. These include 3rd generation thienopyridine (prasugrel, elinogrel), ATP analogs (Ticagrelor, cangrelor), and non-ADP-receptor blocking antiplatelet substances like thrombin receptor antagonists. These agents have shown promising results in pilot studies and recent randomized trials. As the prevention of atherothrombotic risk is at the expense of bleeding risk, it will be a future task to clearly define patients' groups and subsets of ACS for the best net clinical benefit. This article focuses on the role of novel antiplatelet substances to reduce CV risk in ACS, discuss clinical implications and their potential future role.
Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Universitätsklinikum der Eberhard-Karls-Universität Tübingen, Tübingen, Germany.
Karin A L
KA
Müller
Tobias
T
Geisler
D054058:Acute Coronary Syndrome / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control; D001792:Blood Platelets / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000209:etiology / Q000517:prevention & control; D015195:Drug Design; D006470:Hemorrhage / Q000139:chemically induced; D006801:Humans; D015539:Platelet Activation / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D012307:Risk Factors; D055502:Secondary Prevention / Q000379:methods
D010975:Platelet Aggregation Inhibitors