1/2/2023 0 Comments Reddit half life 1 pc tipsAnticoagulants are therefore very effective for prevention and treatment of venous thromboembolism, and drugs that suppress platelet function are of less benefit. Activation of blood coagulation is the critical mechanism in pathogenesis of venous thromboembolism, whereas platelet activation is less important. They can produce long-term complications due to venous hypertension by damaging the venous valves. Venous thrombi usually occur in the lower limbs although often silent, they can produce acute symptoms due to inflammation of the vessel wall, obstruction of flow, or embolism into the pulmonary circulation. Therefore, both anticoagulants and drugs that suppress platelet function are potentially effective in the prevention and treatment of arterial thrombosis, and evidence from results of clinical trials indicates that both classes of drugs are effective. These 2 fundamental mechanisms of thrombogenesis are closely linked in vivo, because thrombin, a key clotting enzyme generated by blood coagulation, is a potent platelet activator, and activated platelets augment the coagulation process. Activation both of blood coagulation and of platelets is important in the pathogenesis of arterial thrombosis. Arterial thrombi usually occur in association with preexisting vascular disease, most commonly atherosclerosis they produce clinical tissue ischemia either by obstructing flow or by embolism into the distal microcirculation. 9 12 13 When flow is slow, the degree of stenosis is severe, or the thrombogenic stimulus is intense, the thrombi may become totally occlusive. 7 8 9 10 11 Nonocclusive thrombi may become incorporated into the vessel wall and can accelerate the growth of atherosclerotic plaques. The complications of thrombosis are caused either by the effects of local obstruction of the vessel, distant embolism of thrombotic material, or, less commonly, consumption of hemostatic elements.Īrterial thrombi usually form in regions of disturbed flow and at sites of rupture of an atherosclerotic plaque, which exposes the thrombogenic subendothelium to platelets and coagulation proteins plaque rupture may also produce further narrowing due to hemorrhage into the plaque. Eventually, the fibrin clot is digested by fibrinolytic enzymes released from endothelial cells and leukocytes. The aggregated platelets swell and disintegrate and are gradually replaced by fibrin. 6 Leukocytes are attracted by chemotactic factors released from aggregated platelets 2 or proteolytic fragments of plasma proteins and become incorporated into the thrombi. As thrombi age, they undergo progressive structural changes. 4 5 When a platelet-rich arterial thrombus becomes occlusive, stasis occurs, and the thrombus can propagate as a red stasis thrombus. Thrombi that form in regions of slow to moderate flow are composed of a mixture of red cells, platelets, and fibrin and are known as mixed platelet-fibrin thrombi. 3 4 5 In contrast, venous thrombi form in areas of stasis and are predominantly composed of red cells, with a large amount of interspersed fibrin and relatively few platelets. 1 2 Arterial thrombi form under conditions of high flow and are composed mainly of platelet aggregates bound together by thin fibrin strands. Because the relative proportion of cells and fibrin depends on hemodynamic factors, the proportions differ in arterial and venous thrombi. Thrombi are composed of fibrin and blood cells and may form in any part of the cardiovascular system, including veins, arteries, the heart, and the microcirculation. Customer Service and Ordering Information.Journal of the American Heart Association (JAHA).Stroke: Vascular and Interventional Neurology.Circ: Cardiovascular Quality & Outcomes.Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB).
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