Antithrombotic therapy and the transition to the catheterization laboratory in UA/NSTEMI.
The management of unstable angina/non ST elevation myocardial infarction (UA/NSTEMI) has evolved substantially in recent years. Multiple new antithrombotic options are available; in addition, the use of interventional strategies in patients with UA/NSTEMI has become the dominant strategy, particularly in tertiary centers. On the one hand, we are doing more percutaneous interventions more rapidly in ACS patients. On the other hand, we have an ever-expanding therapeutic armamentarium to apply in these complex clinical circumstances. Much of the controversy surrounding modern-day management is not so much about the specific the choice of agent or strategy, but rather how to use these agents most effectively in a clinical environment where patients may come forward to the catheterization laboratory, sometimes rapidly, and may require percutaneous or surgical revascularization. All available antithrombotic agents act on one (or more) of the four steps of coagulation: platelet activation, platelet aggregation, thrombin generation, and thrombin activity. The antiplatelet agents, aspirin, thieno-pyridines, and glycoprotein (GP) IIb/IIIa antagonists, target the early steps of platelet activation and aggregation. The antithrombin agents, unfractionated heparin, low molecular weight (LMW) heparin, Xa inhibitors, and direct thrombin antagonists, act specifically to target thrombin generation, thrombin activity, or both. We will review the major recent trials that comprise the current state of knowledge regarding these new antithrombotic agents in ACS, and discuss some of the near-future additions to our armamentarium, including prasugrel, Cangrelor, and AZD6140. The most recent ACC/AHA and ESC unstable angina guidelines have emphasized that multiple options are available, and no one agent can be recommended over the others in all cases. There is NOT one perfect antithrombotic regimen for all patients. Antithrombotic therapy needs to be individualized, and that so-called ''standard'' therapy may need to be supplemented (or even replaced) in specific circumstances. Ultimately, determining optimal therapy means understanding the physiology, understanding the therapeutic options - not just how they work, but how they may work together, and being able to interpret a never-ending supply of new clinical trial data that have to be applied in the ''real world''.
Ferguson
J J
JJ
Texas Heart Institute at St. Luke's Episcopal Hospital, Baylor College of Medicine, The University of Texas Health Science Center at Houston, Houston 77030, USA. jferguson@heart.thi.tmc.edu
Wilson
J M
JM
Diez
J
J
D000789:Angina, Unstable / Q000188:drug therapy*; D015906:Angioplasty, Balloon, Coronary; D001241:Aspirin / Q000627:therapeutic use; D000077144:Clopidogrel; D003328:Coronary Thrombosis / Q000517:prevention & control*; D004359:Drug Therapy, Combination; D004562:Electrocardiography; D019317:Evidence-Based Medicine; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006495:Heparin, Low-Molecular-Weight / Q000627:therapeutic use; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors; D017410:Practice Guidelines as Topic; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000627:therapeutic use; D016896:Treatment Outcome
D005343:Fibrinolytic Agents; D006495:Heparin, Low-Molecular-Weight; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin