Antiplatelet Therapy and Anticoagulation
Preoperative withdrawal of antiplatelet (AP) therapy in secondary prevention multiplies the risk of myocardial infarction, stent thrombosis, stroke, or death, by five to ten times. Aspirin is a lifelong therapy and should never be interrupted. Dual AP the
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Antiplatelet Therapy and Anticoagulation Pierre-Guy Chassot, Stefano Barelli, Sabine Blum, Anne Angelillo-Scherrer, and Carlo E. Marcucci
8.1
Antiplatelet agents
8.1.1
Introduction
Perioperative management of antiplatelet (AP) drugs is a major challenge. Dual AP therapy (aspirin plus clopidogrel, prasugrel, or ticagrelor) is the key to preventing myocardial infarction (MI) after acute coronary syndrome (ACS) or stent thrombosis (ST) following the implant of bare-metal (BMS) or drug-eluting stents (DES). In this population, platelet inhibition in the perioperative period is particularly important because of the increased platelet activity associated with the postoperative acute inflammatory response. Unfortunately, AP drugs also increase the risk of surgical bleeding. The key question is whether the risk of thrombosis when AP agents are withdrawn is higher than the risk of hemorrhage when they are maintained. Current recommendations are based on the results of highly reliable cardiologic trials (level of evidence A) and on large observational or prospective studies collected in surgery and anesthesiology (level of evidence B). Taken together, these data can be considered as adequate for defining the safest possible strategy.
P.-G. Chassot (*) • C.E. Marcucci Service of Anesthesiology, Lausanne University Hospital (CHUV), Lausanne CH-1011, Switzerland e-mail: [email protected]; [email protected] S. Barelli • S. Blum • A. Angelillo-Scherrer Service of Hematology, Lausanne University Hospital (CHUV), Lausanne CH-1011, Switzerland e-mail: [email protected]
C.E. Marcucci, P. Schoettker (eds.), Perioperative Hemostasis, DOI 10.1007/978-3-642-55004-1_8, © Springer-Verlag Berlin Heidelberg 2015
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Irreversible COX-1 inhib.: aspirin Reversible COX-1 inhib.: NSAID Thrombin
Irreversible ADP inhibitor: clopidogrel prasugrel
TXA2
ADP
α-granule
GP IIb/IIIa
Reversible ADP inhib.: ticagrelor cangrelor elinogrel
GP Ib/V/IX TXA2 ADP vWF
Fib
Reversible GP IIb/IIIa inhib.: abciximab eptifibatide tirofiban
Fig. 8.1 Classification of the different AP agents. Blockers of von Willebrand factor/adhesion molecules and thrombin receptor blockers are under investigation (Adapted with permission from www.pac4.ch). ADP adenosine diphosphate, cAMP cyclic adenosine monophosphate, COX-1 cyclooxygenase-1, Fib fibrinogen, inhib inhibitor, NSAID nonsteroidal anti-inflammatory drug, TXA2 thromboxane A2, vWF von Willebrand factor
8.1.2 Antiplatelet Therapy The different AP agents are classified according to the type of receptor they inhibit on the platelet (Fig. 8.1). Their pharmacology is described in Tables 8.1 and 8.2. At doses of 50–160 mg/day, aspirin completely inhibits the cyclooxygenase-1 (COX-1) enzyme which converts arachidonic acid to thromboxane A2 (TXA2), the ligand for the homonymous platelet receptor. However, 6–10 % of the population shows a low response to aspirin treatment, resulting in insufficient platelet inhibition. In some patients, this is due to insufficient
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