Disorders of the Veins and Arteries
Disorders of Arteries and Veins
Deep Vein Thrombosis
In the pathogenesis of deep vein thrombosis, three factors are known as Virchow’s triad. The first pathophysiological mechanism is venous stasis which commonly develops in immobilized and low-active patients. However, venous stasis alone cannot lead to significant impairment of coagulation and clot formation. The risk of venous stasis increases with the presence of other factors, namely surgery, obesity or pregnancy, compression of vein by tumor, and decline of blood flow due to congestive heart disease. Vascular injury develops in cases of surgical impairment of vessels, or due to natural reasons, as in the peripartum period. Additionally, in some anatomical formations as pockets near vein valves, blood flow is reduced. Vascular injury leads to the activation of mechanisms of clotting formation. Finally, hypercoagulation is the result of excessive expression of clot formation factors. Genetic factors that play role in the pathogenesis of deep vein thrombosis are levels of VII, VIII, von Villebrand factor, and antithrombin. Overexpression of genes that are responsible for the synthesis of these factors leads to a predisposition to DVT. Other genetically determined pathologies are issues with the anticoagulant system, namely, deficits of proteins C and S, thrombomodulin, heparin system, etc. Oppositely, a deficit of these factors leads to disease of the clotting system, the most famous of which is hemophilia. Incidence of deep vein thrombosis is remarkably higher in the African-American population in comparison to Caucasians and other races though precise genetic reasons for this are not discovered. However, in the Caucasian population, about 5 percent have a factor V impairment that makes it insensitive to anticoagulants (protein C). The lowest proportion of diagnosed cases is in the population of Pacific Islanders. Deep vein thrombosis develops if are present venous stasis, vascular injury, and hypercoagulation. These disease-predisposing factors are genetically determined while this pathology is the most spread in African American population.
Deep vein thrombosis differs in pathophysiology from arterial thrombosis as in arteries speed of blood flow is significantly higher than in veins and blood stasis as a factor of clot formation is insufficient. Arterial thrombosis is important atherosclerotic plaque development that results in a disturbance of blood flow and activation of the platelets adhesion process. Nevertheless, these conditions have common risk factors such as age, obesity, and impairment in a system of coagulation. In addition, recent studies demonstrate that atherosclerosis plays role in DVT as it can promote the development of thrombotic disorders and excessive coagulation (Prandoni, 2009). Though the pathophysiology of arterial thrombosis is atherosclerosis, this process can trigger coagulative disorders that can also initiate DVT mechanisms.
Treatment of deep vein thrombosis is more similar to arterial thrombosis than to vein insufficiency and consists of anticoagulants, cava filter placement, and thrombolysis. Anticoagulants in the initial phase of thrombosis are unfractionated heparin or heparin with low molecular weight, later patient is transited to direct oral anticoagulants or vitamin-K antagonists. A new generation of anticoagulants includes Xa factor inhibitor Rivaroxaban, an oral direct thrombin inhibitor Edoxaban (Stubbs & Thomas, 2018). A Cava filter is a preventive measure to avoid pulmonary embolism in patients that have contraindications to anticoagulant administration. Thrombolysis is the local injection of anticoagulants to dilute blood clots (Stone, 2017). DVT treatment targets the pathophysiological mechanism of hypercoagulation and aims to restore blood flow and prevent new thrombus formation.
Chronic Venous Insufficiency
In the pathogenesis of chronic venous insufficiency and varicose veins disease are two processes reflux of the vein blood, and obstruction of vessels. Primary vein weakness with insufficiency of valves is a primary theory that suggests that blood reflux in the lower segment leads to an increase of vein blood pressure in that part and respective changes in the leaflet and gradual dilatation of the vein. This mechanism is similar to the venous stasis mechanism for deep venous thrombosis. However, deep vein thrombosis differs a major role in its play impairment in the system of coagulation and injury of vessels, while for chronic vein insufficiency blood pressure in the vein segment and pre-existing vein wall leaflet are more important (Stone, et all, 2017). In addition, in both conditions obesity, pregnancy, sedentary lifestyle, or long hours of standing play important role in triggering pathological processes.
Predisposition to chronic venous insufficiency is genetically transited with the family history of the disease as one of the major risk factors, if both parents have this condition, the risk is about 90%. Genetic predisposition to CVI is a result of collagen synthesis impairment (production of collagen I instead of collagen III and fibronectin) that leads to weakness of valves annulus and blood reflux. Leaflets of vein walls are also often genetically determined which makes genetic factors one of the most important for the assessment of CVI risks. Similar to DVT, African American race is a predisposing factor to CVI since representatives of this ethnical group have both higher frequency, earlier onset of the disease, and ulceration. However, there is no racial difference between mortality and treatment outcomes between races (Santler & Goerge, 2017). Genetics and race are valuable risk factors for CVI.
Treatment of chronic vein disease consists of surgical and pharmacological components. Pharmacological treatment includes purified flavonoid fraction, calcium dobesilate, and horse chestnut extract that effectively reduce edema, pain, and itching by increasing venous tone (Wittens et all, 2015). One more effective treatment option is sclerotherapy which is a method of filling pathological veins with chemical agents (liquids or foams). Surgical treatment is phlebotomy which is the removal of superficial veins through small incisions (Santler & George, 2017). Surgical treatment is usually combined with pharmacological methods of ablation. Differences in the pathophysiological mechanisms of DVT and CVD explain their different treatment approaches. For the former condition, an anticoagulant is necessary to resolve hypercoagulation while for the latter it is important to relieve symptoms such as edema and to remove impaired veins.