Introduction

Extract

Laboratory professionals who specialize in hemostasis have been preoccupied with the development and implementation of assays for the direct oral anticoagulants dabigatran, rivaroxaban, apixaban, and edoxaban since their release in 2010–14. Practitioners have also maintained and improved methods for monitoring Coumadin, unfractionated heparin, enoxaparin (low molecular weight heparin), and fondaparinux (synthetic pentasaccharide). Meanwhile, although antiplatelet therapy is more prevalent than anticoagulant therapy, laboratorians pay scant attention to monitoring antiplatelet drugs. Their lesser laboratory prominence may reflect our understanding that dose-response characteristics are reproducible, or that platelet function assays require specialized equipment, are highly complex, and require fresh blood and thus must be conducted near the patient.

The commonly employed antiplatelet drugs include aspirin, whose antiplatelet effect is delivered through acetylation of platelet cyclooxygenase, and the thienopyridines clopidogrel, prasugrel, and ticagrelor, which occupy and block platelet membrane ADP receptor site P2Y₁₂. Aspirin is often prescribed in combination with a thienopyridine to prevent secondary arterial thrombotic events subsequent to acute myocardial infarction (AMI). The aspirin-thienopyridine combination is termed dual antiplatelet therapy, and is a mainstay in post-infarction treatment. Because aspirin and clopidogrel low response (ALR and CLR) have been documented, several laboratory methods are devised to monitor these drugs' efficacy. These are detailed in the accompanying article, Managing Platelet Therapy. Nearly all methods are point of care (POC) modifications of platelet aggregometry. Prasugrel and ticagrelor escape laboratory monitoring, as they have proven to have predictable dose-response characteristics.

The accompanying article, Platelet Structure and Function, provides an overview of platelet physiology.¹ The reader…

ABBRVIATIONS: ACS-acute coronary syndrome; ADP-adenosine diphosphate; ALR-aspirin low response; CLR-clopidogrel low response; DOAC-direct oral anticoagulant; FDA-US Food and Drug Administration; GP-glycoprotein; GPI-glycoprotein inhibitor; IV-intravenous; PCI-percutaneous intervention; POC-point of care; RGD-arginine-glycine-aspartic acid sequence; TRAP-thrombin receptor activating peptide