Anticoagulants and antiplatelet agents are medicines that reduce blood clotting in an artery, a vein or the heart. Blood clots can block the blood flow to your heart muscle and cause a heart attack. They can also block blood flow to your brain, causing a stroke.
Anticoagulants (or sometimes known as “blood thinners”) are medicines that delay the clotting of blood. Examples are heparin, warfarin, dabigitran, apixaban, and rivoraxaban. Anticoagulants make it harder for clots to form or keep existing clots from growing in your heart, veins or arteries. Treatment should be managed by your healthcare provider.
A Blood Clot Consists of platelets meshed into fibrin, a web-like accumulation of strands with RBCs. There are two major facets of the clotting mechanism – the platelets, and the thrombin system.
Platelets; Tiny cellular elements, made in the bone marrow, that travel in the bloodstream waiting for a bleeding problem to develop. When bleeding occurs, chemical reactions change the surface of the platelet to make it activated and become “sticky”. These activated platelets begin adhering to the wall of the blood vessel at the site of bleeding.
Thrombin System. Calcium ions must be present for the thrombin system to begin. The thrombin system consists of several blood proteins that activate when bleeding occurs. The activated clotting proteins engage in a cascade of chemical reactions that finally produce a substance called fibrin. Fibrin strands stick to the exposed vessel wall, clumping together and forming a web-like complex of strands. Red blood cells become caught up in the web, causing a clot.
Heparin is a naturally-occurring anticoagulant produced by basophils and mast cells to prevent formation and extension of blood clots. Heparin does not disintegrate clots that have already formed. It permits the body’s natural clot lysis mechanisms, i.e. fibrinolysis, to work normally to break down previously formed clots. As the thrombokinase is released, it neutralizes the action of heparin to allow clotting to occur.
Anticoagulant drugs help prevent the development of harmful clots in the blood vessels by lessening the blood’s ability to cluster together. The function of these drugs is often misunderstood because they are sometimes referred to as blood thinners; they do not in fact thin the blood. These drugs will not dissolve clots that already have formed, but it will stop an existing clot from becoming worse and prevent future clots.
Heparin and warfarin are the two traditional anticoagulants. Anticoagulants are used for acute coronary syndromes, deep-vein thrombosis (DVT), pulmonary embolism (PE), and heart surgery
Thrombus – A blood clot that forms abnormally within the blood vessels
Embolus – When a blood clot becomes dislodged from the vessel wall and travels through the bloodstream.
It is also given to certain people at risk for forming blood clots, such as those with artificial heart valves or who have atrial fibrillation (AF)
Warfarin is an oral medication. It is a synthetic derivative of coumarin, a chemical found naturally in many plants — it decreases blood coagulation by interfering with vitamin K metabolism. It stops the blood from clotting within the blood vessels and is used to stop existing clots from getting bigger (as in DVT) and to stop parts of clots breaking off and forming emboli (as in PE).
Warfarin: Mechanism of Action
Interferes with the cyclic interconversion of vitamin K and its 2,3epoxide (vitamin K epoxide). Vitamin K is an essential cofactor for post-translational carboxylation of glutamate residues on the N-terminus regions of vitamin K-dependent proteins to gamma-carboxy-glutamates
Descarboxyprothrombin is converted to prothrombin by carboxylation of glutamate residues to gamma-carboxyglutamate. By inhibiting vitamin K epoxide reductase and vitamin K reductase, warfarin leads to the accumulation of vitamin K epoxide in the liver and plasma and the depletion of reduced vitamin K (active form, KH2)
Reduced vitamin K is necessary for carboxylation of glutamate residues. Decrease in KH2 limits the gamma-carboxylation of vitamin K dependent coagulant proteins –
• Prothrombin (Factor II)
• Factors VII, IX, X
• Protein C and Protein S
It was developed by Boehringer Ingelheim. Dabigatran etexilate is a new oral direct thrombin inhibitor and the prodrug of dabigatran. Dabigatran is a small molecule that reversibly inhibits both free and clot-bound thrombin by binding to exosite 1 and/or the active site of thrombin.
Developed by Bayer. Rivaroxaban is an orally available, small-molecule, active site-directed factor Xa inhibitor. There are no significant interactions between food, antacids, digoxin, aspirin, naproxen and rivaroxaban have been noted suggesting that dose adjustment of rivaroxaban would not be required when these agents are concurrently administered
Anisindione (brand name Miradon) is a synthetic oral anticoagulant and an indanedione derivative. Reduces the prothrombin activity of the blood. It prevents the formation of active procoagulation factors II, VII, IX, and X, as well as the anticoagulant proteins C and S, in the liver by inhibiting the vitamin K–mediated gamma-carboxylation of precursor proteins.
It is a potent oral anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent clotting factors (prothrombin and factors VII, IX and X) in the liver; it is starting to largely replace warfarin. Dicumarol is produced naturally by conversion of nontoxic coumarin in moldy sweet clover hay, lespepeza hay or sweet vernal hay. It is used especially in preventing and treating thromboembolic disease. Formerly called bishydroxycoumarin
Low-molecular weight heparin
Low-molecular weight heparin is gradually replacing heparin for treatment of most patients with venous thromboembolism and acute coronary syndromes because it has more convenient and cost-effective. It has similar results to heparin. Administered by subcutaneous injection. LOVENOX® is an example
Fondaparinux is given via injection once daily. It is licensed for initial treatment of deep vein thrombosis (DVT) and pulmonary embolism (PE) and for venous thromboembolism prevention in patients undergoing surgery for hip fracture or hip/knee replacement