Anticoagulant Therapy Overview

1. George A. Fritsma, MS MT (ASCP)[⇑][1] 1. The Fritsma Factor, Your Interactive Hemostasis ResourceSM, Fritsma & Fritsma LLC, Birmingham, AL 1. Address for Correspondence: George A. Fritsma MS MT (ASCP), The Fritsma Factor, Your Interactive Hemostasis ResourceSM, Fritsma & Fritsma LLC, 153 Redwood Drive, Birmingham, AL 35173, 205-655-0687, George{at}fritsmafactor.com. 1. Recount the history of heparin, Coumadin, and hirudin 2. Summarize the function of the anti-Xa drugs, vitamin K antagonists, and direct thrombin inhibitors. 3. List two oral anticoagulants that have been cleared by the US FDA since 2009. Anticoagulants do not thin the blood, even though we call them “blood thinners.”1 Blood viscosity is a function of hematocrit and, in leukemia, white blood cell burden, but not plasma protein concentration or enzyme activity. Although thrombolytic “clotbusters” like tissue plasminogen activator (TPA) or streptokinase can dissolve clots, anticoagulants cannot, another popular misconception. Anticoagulants can only prevent thrombus formation or extension by reducing plasma thrombin activity, the basis for their effectiveness. Though this may seem like a limitation, anticoagulants save many lives and promote recovery following a thrombotic (clotting) event.2 Anticoagulant treatment is either prophylactic or therapeutic. Prophylactic anticoagulation includes the prevention of ischemic stroke in people with chronic atrial fibrillation or artificial heart valves, or the prevention of venous thromboembolic (VTE) disease in the form of deep venous thrombosis (DVT, clots in major leg veins) or pulmonary emboli (PE, clots in lung vasculature), subsequent to orthopedic surgery, neurosurgery, or during a complicated pregnancy.3 Therapeutic anticoagulation, which usually implies higher doses than prophylactic anticoagulation, is used in patients with current VTE disease or those with coronary artery disease (CAD) complicated by cardiac insufficiency.4 Anticoagulants are a subset of a family of drugs called antithrombotics, which include the oral antiplatelet drugs such as aspirin and clopidogrel (Plavix); the intravenous antiplatelet membrane glycoprotein receptor drugs, abciximab, eptifibatide, and tirofiban; and the thrombolytics. This series does not address the antiplatelet drugs or the thrombolytics. In this series we first address the anti-Xa anticoagulants, heparin and its analogues; next, the historical mainstay Coumadin, our… ABBREVIATIONS: APTT or PTT-activated partial thromboplastin time; CAD - coronary artery disease; DTI - direct thrombin inhibitor; DVT - deep venous thrombosis; FDA - US Food and Drug Administration; HIT-heparin-induced thrombocytopenia with thrombosis; INR - international normalized ratio; LMWH - low molecular weight heparin; PE - pulmonary embolism; PT - prothrombin time; RI - reference interval; RUO - research use only; TPA - tissue plasminogen activator; UFH - unfractionated heparin; VKORC - vitamin K epoxide reductase; VKA - vitamin K antagonist; VTE - venous thromboembolism. 1. Recount the history of heparin, Coumadin, and hirudin 2. Summarize the function of the anti-Xa drugs, vitamin K antagonists, and direct thrombin inhibitors. 3. List two oral anticoagulants that have been cleared by the US FDA since 2009. [1]: #corresp-1