anticoagulant
An anticoagulant makes blood slower to clot, which is why people loosely call them blood thinners (though they do not actually thin the blood). Clotting is a chain reaction, like a row of dominoes that ends in a solid clot; an anticoagulant removes a domino so the chain cannot finish. This prevents harmful clots from forming in veins and in the chambers of a fibrillating heart.
Anticoagulants target the coagulation cascade, the sequence of clotting-factor reactions that builds fibrin. Warfarin blocks vitamin K, which the liver needs to make several clotting factors. Heparin and low-molecular-weight heparins boost the natural inhibitor antithrombin. Direct oral anticoagulants act on a single factor: dabigatran blocks thrombin (factor IIa), while apixaban, rivaroxaban and edoxaban block factor Xa. They are used to prevent and treat deep vein thrombosis, pulmonary embolism, and stroke in atrial fibrillation.
The central risk of every anticoagulant is bleeding, from minor bruising to life-threatening haemorrhage. Warfarin's effect is unpredictable, interacts with many foods and drugs, and requires regular blood-test (INR) monitoring, whereas direct oral anticoagulants give a more predictable response without routine monitoring. Specific reversal agents exist for some, such as vitamin K and prothrombin complex for warfarin, and idarucizumab for dabigatran.
A patient with atrial fibrillation is prescribed apixaban, a direct oral anticoagulant, to greatly reduce the risk of a clot forming in the heart and travelling to the brain as a stroke.
In atrial fibrillation, anticoagulation is the key intervention that prevents stroke.
Anticoagulants stop clots from forming or growing but do not dissolve a clot that already exists; breaking down an established clot is the job of a thrombolytic.