A flight from Minnesota to Sydney lasts about 19,5 hours. When individuals travel by plane, especially during long periods, they remain relatively immobile, which is not the best state for those with CVS diseases. Stasis results in the accumulation of platelets and clotting factors. Moreover, immobility causes a decrease in chemical interactions with inhibitors of coagulation. These factors might lead to increased thrombus formation risk. Speaking about Leona’s case, there are several additional risks, including overweight, smoking, and atherosclerosis.
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There are diverse data regarding the impact of smoking on DVT. Some research shows that regardless of amount and duration, smoking is not a risk factor. In turn, other studies have proved that heavy cigarette smoking has a secure interconnection with this disease. Mi et al. (2016) conducted research demonstrating the positive correlation between DVT and smoking. Additionally, it is a substantial risk factor for the development of the atherosclerotic disease. There is a possible explanation of such controversies in research results. Some of them might not have used sufficiently detailed data, including previous versus current smoking status, lighter versus heavier smokers, and others. Nevertheless, there is no doubt that smoking increases hypercoagulability, simultaneously associated with increased blood viscosity, inflammation, and reduced fibrinolysis.
Additionally, Leona has atherosclerosis, which is another severe disease to be taken into account. Recent studies claim that DVT and atherosclerosis have common risk factors such as cigarette smoking, obesity, age, and metabolic syndrome. Moreover, atherosclerosis potentially might promote the thrombotic disorder’s development in a venous system. Nevertheless, according to Mi et al. (2016), the population studies conducted in the USA revealed that atherosclerosis itself is unlikely to be a risk factor for DVT.
Atherosclerosis is defined as a chronic inflammatory illness characterized by different complex processes that contribute to the atherosclerotic plaque’s development for decades and its pathophysiology. The blood flow is disturbed by atherosclerosis, and the vascular endothelium is damaged, and, hence, platelet adherence increases. Moreover, platelets gain increased sensitivity to factors causing aggregation and adhesiveness. The growth factors enhancing the proliferation of smooth muscle in the vessel wall are released by the adhering platelets. Therefore, platelet aggregation is likely to contribute both to atherosclerosis development and progression.
In terms of atherosclerosis, platelets are responsible for the early stages of this chronic pathology development, including endothelial dysfunction. Nevertheless, they also have an impact on its final consequences, like the vulnerable plaque’s rupture. For example, platelets take part in cell-cell direct interaction, oxLDL (oxidized low-density lipoprotein) surface association, atherogenesis through chemokine release, inflammatory mediators release, and microparticles release (Nording et al., 2015). Platelets might remain activated within the plaque of atherosclerotic nature for an extended time, hence providing for the production of proinflammatory IL-1β.
The primary function of platelets in terms of atherosclerosis is the leukocytes recruitment through the direct interactions between receptors and ligands. Additionally, it might be augmented through released factors like chemokines. Dendritic cells (DCs) play the role of a specific leukocyte subtype. DC is a classical antigen which presents the cells of individuals bodies. Platelets interact with DCs, which function in atherosclerosis development has recently been emphasized in numerous studies (Nording et al., 2015). In practice, the interaction between GPIb (glycoprotein Ib) and Mac-1 (macrophage-1 antigen) is currently viewed as a signaling mechanism in terms of DC- platelet crosstalk modulating atheroprogression (Nording et al., 2015). This factor’s particular importance is caused by the fact that DC is proposed to affect the different stages of atherosclerosis development significantly.
The impact of atherosclerosis and immobility is a little contradictory. Immobility causes increased pro-coagulation, therefore, contributing to hypercoagulability. In turn, atherosclerosis is able to improve the platelet function through the encouragement of adherence and aggregation. Atherosclerosis progression assumes the active participation of platelets attached to intact endothelium. Moreover, platelets are a vital factor of thrombus formation on atherosclerotic plaque rupture or erosion. The thrombogenic substrates’ exposure to circulating platelets challenges the recruitment of the last to the vessel’s injured wall in specific (both in place and time) series of events. They include the so-called “arrest” of platelet on the exposed subendothelium, the additional platelet’s recruitment and activation utilizing the local release of primary platelet agonists, and platelet aggregates stabilization. Therefore, at plaque rupture site, thrombus formation starts with the interaction of platelets with the exposure to blood ECM (extracellular matrix) components, including non-collagenic adhesion proteins (fibronectin, VWF (von-Willebrand-factor), and laminin) and fibrillar collagen. Such kinds of adhesive interactions are significantly influenced by the rheological conditions.
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In simple words, there is the so-called thrombogenic theory, assuming that the reason for atherogenesis is a local bleeding disorder, causing local thrombosis, followed by the formation of an atherosclerotic plaque. Response-to-injury theory, created in the 1970s, is also associated with it (“Pathogenesis,” n.d). According to this theory, atherosclerosis occurs due to local damage to cells of the inner surface of the vessel, the cause of which is unknown. Platelets begin to adhere to the damaged vascular wall, and this, in turn, can cause local thrombosis. In addition, during the formation of a thrombus, platelets eject substances into the blood plasma that cause the development of the whole complex of changes in the vessel wall distinctive for atherosclerosis.
Heparin is one of the most efficient treatments encouraging the clotting factors inactivation and, hence, fibrin formation inhibiting. Heparin is never absorbed by the gastrointestinal system; therefore, it is appropriate to administer it only by IV infusion or injection. There is a certain number of patients who might be treated at home. If Leona’s doctor insisted that she would stay at the hospital, obviously, she had an extensive blood clot and might have needed more treatment and invasive testing. More medication was likely to include heparin therapy and the elevation of the affected leg and wearing compression stockings. The primary goals of this therapy include the need to stop the growth of clot, prevention of the clot’s breaking off in the patient’s vein, and its movement to the lungs. Moreover, it is crucial to reduce the risk of other blood clots formation. The long-term complications from the clots (like chronic venous insufficiency) should be paid special attention.
Heparin is a blood thinner and one of the most commonly used anticoagulants in cases of DVT. It does not break up the existing clot, but it is efficient in preventing it from growing and reducing the risks of developing new blood clots. The best strategy for the treatment of DVT includes the use of injectable blood thinners for several days. After that, the patient can start pills such as dabigatran or warfarin (“Deep vein thrombosis,” n.d.). Once the patient’s blood is thinned by warfarin, the treatment by injectable blood thinner (particularly, heparin in Leona’s case) might be stopped. It is also noteworthy that bleeding is one of the most common side effects of any anticoagulant (“Deep vein thrombosis,” n.d.). Hence, the doctor might have preferred to keep the patient at the hospital for at least a few initial days of such therapy to ensure there is no threat to her life.
Deep vein thrombosis (DVT). (n.d.). Mayo Clinic. 2020, Web.
Mi, Y., Yan, S., Lu, Y., Liang, Y., & Li, C. (2016). “Venous thromboembolism has the same risk factors as atherosclerosis.” Medicine (Baltimore), 95(32), 44-95.
Nording, H. M., Seizer, P., & Langer, H. F. (2015). “Platelets in Inflammation and Atherogenesis.” Front Immunol., 6, 98.
Pathogenesis of atherosclerosis. (n.d.). 2020, Web.