Deep vein thrombosis: pathogenesis, diagnosis, and medical management

Abstract

Deep vein thrombosis (DVT) is a major preventable cause of morbidity and mortality worldwide. Venous thromboembolism (VTE), which includes DVT and pulmonary embolism (PE), affects an estimated 1 per 1,000 people and contributes to 60,000-100,000 deaths annually. Normal blood physiology hinges on a delicate balance between pro- and anti-coagulant factors. Virchow's Triad distills the multitude of risk factors for DVT into three basic elements favoring thrombus formation: venous stasis, vascular injury, and hypercoagulability. Clinical, biochemical, and radiological tests are used to increase the sensitivity and specificity for diagnosing DVT. Anticoagulation therapy is essential for the treatment of DVT. With few exceptions, the standard therapy for DVT has been vitamin K-antagonists (VKAs) such as warfarin with heparin or fractionated heparin bridging. More recently, a number of large-scale clinical trials have validated the use of direct oral anticoagulants (DOACs) in place of warfarin in select cases. In this review, we summarize the pathogenesis, diagnosis, and medical management of DVT, with particular emphasis on anticoagulation therapy and the role of DOACs in the current treatment algorithm.

Overexpressed microRNA‐103a‐3p inhibits acute lower‐extremity deep venous thrombosis via inhibition of CXCL12

“…Acute LEDVT happens when large veins are obstructed by thrombi and its clinical manifestations are swelling and pain that can cause morbidity and mortality without treatment . Venous stasis, vascular injury and hypercoagulability have been identified to be responsible for LEDVT . The ideal targets for LEDVT therapies are eliminating the embolic capacity of existing thrombi, reconstructing unobstructed blood flow, maintaining venous valve function, and preventing further thrombosis .…”

“…2 Venous stasis, vascular injury and hypercoagulability have been identified to be responsible for LEDVT. 3 The ideal targets for LEDVT therapies are eliminating the embolic capacity of existing thrombi, reconstructing unobstructed blood flow, maintaining venous valve function, and preventing further thrombosis. 4 However, the molecular mechanism of LEDVT remains unclear, which greatly limits the screening for LEDVT diagnostic markers.…”

A phenome-wide approach to identify causal risk factors for deep vein thrombosis

“…Under normal physiological circumstances, platelets and fibrin form clots to prevent blood loss at sites of vessel injury (1). Thrombosis is characterised as the abnormal formation of a clot within a blood vessel, which leads to reduced blood flow through the circulatory system (2,3). When these abnormal clots occur in the deep veins of the legs, groin or arms this is known as deep vein thrombosis (DVT), and when part of one of these clots breaks away and becomes lodged in the lungs this is known as pulmonary embolism.…”

“…Intravenous heparin and oral warfarin (a vitamin K antagonist) have been used in combination to treat DVT for over 50 years. Whilst new treatments (dabigatran, rivaroxaban) have shown increased anticoagulative activity relative to the traditional treatment, they do not target the main cause(s) of DVT (2,3). Hence, the identification of novel causal risk factors for DVT is desired, as this could aid in the development of an efficient prophylactic drug (3).…”

“…Whilst new treatments (dabigatran, rivaroxaban) have shown increased anticoagulative activity relative to the traditional treatment, they do not target the main cause(s) of DVT (2,3). Hence, the identification of novel causal risk factors for DVT is desired, as this could aid in the development of an efficient prophylactic drug (3). Current research has established several risk factors for DVT: these are genetic, such as deficiencies in anticoagulants antithrombin, protein C, and protein S or acquired, such as age, obesity, cancer, pregnancy, trauma, or smoking (2,5,6).…”