الفهرس 
Physiology of the Coagulation SystemOnly 14 pages are availabe for public view
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Abstract
Blood coagulation is a part of a series of haemostatic reactions, including plasma, platelets, and vascular components.
Platelets adhere to the damaged endothelium or to the sub-endothelium under the effect of adhesive proteins, and after being activated they aggregate and expose binding sites for the coagulation factors. Therefore, platelets help to concentrate and potentiate the coagulation reactions on damaged blood vessels.
Then a cascade of activation occurs to the coagulation protease zymogens. This results in the conversion of fibrinogen to fibrin and finally a platelet-fibrin plug. During healing process, fibrin deposition and removal is regulated by the fibrinolytic system.
Venous thromboembolism (VTE) is a disease that includes both deep vein thrombosis (DVT) and pulmonary embolism (PE). It is a common lethal disorder that affects hospitalized and non-hospitalized patients. Venous thromboembolism results from a combination of hereditary and acquired risk factors.
Venous thromboembolism is the third most common cardiovascular illness after acute coronary syndrome and stroke. Pulmonary embolism is the third most common cause of hospital-related death and the most common preventable cause of hospital-related death.
Anticoagulants are the cornerstone of VTE treatment. The goal of therapy is to prevent thrombus extension or embolization and to prevent new thrombi from forming, thus minimize resulting morbidities and long term complications as post-thrombotic syndrome (PTS) and chronic thromboembolic pulmonary hypertension (CTEPH).
Current guidelines recommend 3 months of anticoagulation with an episode of DVT or PE resulting from a transient cause. Long-term (indefinite) anticoagulation is recommended in patients with malignancy as long as the cancer remains active and in patients who have unexplained recurrent VTE.
Anticoagulants may be parenteral, such as unfractionated heparin (UFH), low molecular weight heparin (LMWH) or fondaparinux, or oral anticoagulants such as vitamin K antagonists (VKAs) or new oral anticoagulants (NOACs).
NOACs, also known as direct oral anticoagulants (DOACs), encompass two main classes: the oral direct thrombin inhibitors and oral direct factor Xa inhibitors. VKAs block the formation of multiple active vitamin K-dependent coagulation factors (factors II, VII, IX and X), where NOACs directly block the activity of a single step in the coagulation pathway, hence called ”direct” anticoagulants.
New oral anticoagulants such as rivaroxaban, apixaban, edoxaban and dabigatran are superior to VKAs in having more predictable anticoagulant response, thus can be administered in fixed doses (except when a patient has a functional disorder of the liver or kidney) and do not require routine monitoring. They also have fewer food and drug interactions compared with VKAs.
However, no antidotes are currently available for NOACs, and the international normalized ratio (INR) cannot be used to monitor the coagulation profile with the use of NOACs.
The present systematic review and meta-analyses yielded that the efficacy and safety of NOACs for VTE are comparable or superior to VKAs; NOACs and VKAs had no difference in risk reduction of VTE/fatal PE, but NOACs had a significant decrease in risk of major bleeding. Overall results did not show a significant difference between NOACs and VKAs for recurrent DVT, nonfatal PE, or all-cause mortality. NOACs also showed significant decrease in risk of GI bleeding and ICH.
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