Arterial thrombosis is a blood clot in an artery, which can be very serious because it can stop blood reaching important organs. 1999;353:1386–9. Much less attention has been given to the clinically more important problem of how clotting takes place inside blood-vessels, and what limits or favours the spread of these clots. For a mural thrombus (defined as a thrombus in a large vessel that restricts the blood flow but does not occlude completely), histological reorganisation of the thrombus does not occur via the classic wound healing mechanism. [Margaretten W, Csavossy I, McKay DG. Guias y Recomendaciones del Capitulo de Circulacion Pulmonar de la Sociedad Mexicana de Cardiologia. MARTIN MECHANISM SILBERBERG OF THROMBOSIS of Medicine, Department of Pathology, Washington University, Saint LOU&~, nf0. [3] It usually happens in the setting of another disease such as pancreatitis, cirrhosis, diverticulitis or cholangiocarcinoma. Guidelines on diagnosis and management of acute pulmonary embolism. 2002;160:227–36. Below is a timely collection of articles relating to the Coronavirus outbreak. Why so many COVID-19 patients get blood clots (thrombosis) remains uncertain. The diagnosis is usually made with a CT or MRI scan. Thrombosis is a condition of major concern worldwide as it is associated with life-threatening diseases related to the cardiovascular system. A blood clot does not usually have any symptoms until it blocks the flow of blood to part of the body. [22] Inflammatory and other stimuli (such as hypercholesterolemia) can lead to changes in gene expression in endothelium producing to a pro-thrombotic state. 1993;341:507–511. Mechanism of activation Arterial thrombosis results from clot formation in the setting of atherosclerotic plaque rupture, leading to platelet aggregation, thrombus formation, vessel occlusion and possible MI or ischemic stroke. An understanding of the complex interplay between these … Antithrombotic therapy in the elderly. The mechanism of thrombosis triggered by cardiovascular grafts. Gorog DA. [24] The end result is a sustained activation of thrombin and reduced production of protein C and tissue factor inhibitor, which furthers the pro-thrombotic state. Thrombosis triggered by systemic hypoxemia is mediated by tissue factor induction in macrophages following activation of the transcription factor early growth response-1 gene. Obesity has become a worldwide epidemic that is driving increased morbidity and mortality from thrombotic disorders such as myocardial infarction, stroke, and venous thromboembolism. [38], With reperfusion comes ischemia/reperfusion (IR) injury (IRI), which paradoxically causes cell death in reperfused tissue[39] and contributes significantly to post-reperfusion mortality and morbidity. 2004;74 Suppl 3:S547–85. Antiplatelet and anticoagulant agents in heart failure. Finally, pathologic evidence shows left and right myocarditis associated with endocardium thrombosis in patients who died secondary to pulmonary embolism. [citation needed], Alternatively, arterial occlusion occurs as a consequence of embolism of blood clots originating from the heart ("cardiogenic" emboli). Author information: ... and venous thrombosis. 1964;145:1310-1312 . Riveiro A, Lindmarker P, Johnson H, Juhlin-Dannfelt A, Jorfeldt L. Pulmonary embolism: one-year follow-up with echocardiography Doppler and five-year survival analysis. [8] Some of these risk factors are related to inflammation. Gouni-Berthold I, Berthold HK. Thrombosis occurs more … Forensic Sci Int. Deep vein thrombosis (DVT) can lead to chronic venous hypertension because of persistent venous obstruction and valvular reflux. Bench to bedside: new developments in our understanding of the pathophysiology of thrombosis. 2011;8:443–55. Cite as. 2010;56:1–7. Hence, protective therapies are required to attenuate IRI alongside reperfusion in acute ischemic conditions to improve clinical outcomes. [citation needed], Renal vein thrombosis is the obstruction of the renal vein by a thrombus. Treatment varies between therapy and surgical intervention by the use of shunts. Venous thromboembolism and atherotrombosis. 2010;31:777–83. Instead, the platelet-derived growth factor degranulated by the clotted platelets will attract a layer of smooth muscle cells to cover the clot, and this layer of mural smooth muscle will be vascularised by the blood inside the vessel lumen rather than by the vasa vasorum. Also, atrial fibrillation, causes stagnant blood in the left atrium (LA), or left atrial appendage (LAA), and can lead to a thromboembolism. Significant in vitro and in vivo studies confirm that aPL are pathogenic [49-51]. Vascular inflammation and repair. Rev Esp Cardiol. This is a preview of subscription content. 2005;26:1–2. Prospective with seven-year follow-up trial. 2002;347:1025–6. Sotiriou SN, Orlova VV, Al-Fakhri N, Ihanus E, Economopoulou M, Isermann B, Bdeir K, Nawroth PP, Preissner KT, Gahmberg CG, Koschinsky ML, Chavakis T. Lipoprotein (a) in atherosclerotic plaques recruits inflammatory cells through interaction with Mac-1 integrin. Review: Viral infections and mechanisms of thrombosis and bleeding J Med Virol. Given the complexity of the hemostatic mechanism, paradigms developed from biochemical and cell biological approaches have been revisited by studying thrombus formation in a live animal by intravital microscopy. A thrombus may become detached and enter circulation as an embolus, finally lodging in and completely obstructing a blood vessel, which unless treated very quickly will lead to tissue necrosis (an infarction) in the area past the occlusion. A piece of either an arterial or a venous thrombus can break off as an embolus which can travel through the circulation and lodge somewhere else as an embolism. 2005;26:77–83. Hyperhomocysteinemia is now recognized as a common risk factor for thrombotic vascular events such as stroke, myocardial infarction, and venous thrombosis. Portal vein thrombosis (PVT) is a blood clot that causes irregular blood flow to the liver. The tissue can become irreversibly damaged, a process known as necrosis. 2008;94:450–6. As a consequence, thrombosis and disseminated intravascular coagulation, hemorrhage, or both, may occur. Thrombosis describes the formation of a clot within a blood vessel that reduces blood flow and may cause infarction of tissues supplied by that vessel. Even when a blood vessel is not injured, blood clots may form in the body under certain conditions. J Thromb Thrombolysis. The treatment for thrombosis depends on whether it is in a vein or an artery, the impact on the person, and the risk of complications from treatment. 2008;19:369–77. The Task Force on the diagnosis and management of acute pulmonary embolism of the European Cardiology Society. Curr Opin Hematol. Venous thrombosis is a leading cause of morbidity and mortality in industrialized countries, especially in the elderly. Schreiner PJ, Morrisett JD, Sharrett AR, Patsch W, Tyroler HA, Wu K, Heiss G. Lipoprotein(a) as a risk factor for preclinical atherosclerosis. 2011;32:1968–76. This process is complex and involves the action of blood cells called platelets that recognise and respond to tissue injury, along with an array of factors present in the blood and released at sites of injury. The blood clotting process may not always proceed smoothly, as in the case of deep vein thrombosis. Heparin binds to AT through a high-affinity pentasaccharide, which is present on about a third of heparin molecules. Reitsma PH, Rosendaal FR. Post-thrombotic syndrome occurs as a result of venous hypertension. Learn about the symptoms and treatment of this condition. [23] When this occurs, endothelial cells downregulate substances such as thrombomodulin, which is a key modulator of thrombin activity. Eur Heart J. [43] Of these, RIC has the most robust clinical evidence, especially in the context of STEMI, but also emerging for other indications such as acute ischemic stroke and aneurysmal subarachnoid hemorrhage. Thus, arterial thrombi are treated with therapies that target platelet activation and aggregation (Figure 1). Jerjes-Sanchez C, Ramirez-Rivera A, Garcia ML, Arriaga-Nava R, Valencia-Sanchez S, Rosado-Buzzo A, Pierzo JA, Rosas ME. Thrombosis and Bleeding M. Goeijenbier,1* M. van Wissen,2 C. van de Weg,1 E. Jong,2 V.E.A. The effects are related to dose of estrogen and type of progestin. Under normal circumstances, intact endothelial cells and their surface protective agents keep circulating platelets at rest. AHA Scientific Statement from American Heart Association. [36] Other medications such as direct thrombin inhibitors and direct Xa inhibitors are increasingly being used instead of warfarin. Currently, with the combination of improved models of venous thromboembolism and high-resolution microscopy techniques, new evidence linking molecular, cellular mechanisms, platelets and innate immune cells with venous thrombosis have been identified. Deep Vein Thrombosis or DVT is caused when the blood clot takes place in … 1995;130:1276–82. 2006;367:1075–9. Lentz SR(1). Schermuly RT, Ghofrani HA, Wilkins MR, Grimminger F. Mechanisms of disease: pulmonary arterial hypertension. Smoking also increases the risk of developing clots because it reduces oxygen levels in the blood stream. Capodanno D, Angiolillo DJ. Thrombosis triggered by systemic hypoxemia is mediated by tissue factor induction in macrophages following activation of the transcription factor early growth response-1 gene. These include briefly: the activation of cellular components (endothelial cells, platelets and monocytes), activation of the coagulation cascade, … Arterial thrombosis Mechanism of activation. Furie F, Furie BC. This transcription factor with hypoxia inducible factor-1 is also an important transcription factor mediating adaptive responses to hypoxia in endothelium; in vitro, these responses include proinflammatory and pro-adhesive changes. Lualdi JC, Goldhaber SZ. Thrombosis triggered by systemic hypoxemia is mediated by tissue factor induction in macrophages following activation of the transcription factor early growth response-1 gene. 2003;24:1447–54. Davie EW, Ratnoff OD. Jerjes-Sanchez C. Venous and arterial thrombosis. 1993;3:826–33. Dahlback B. Nat Rev Cardiol. Such a process must be activatable within seconds of injury. Learn about the symptoms and treatment of this condition. Right ventricular damage due to pulmonary embolism: examination of the number of infiltrating macrophages. © 2020 Springer Nature Switzerland AG. 2001;116:189–95. [22] Cancers or malignancies such as leukemia may cause increased risk of thrombosis by possible activation of the coagulation system by cancer cells or secretion of procoagulant substances (paraneoplastic syndrome), by external compression on a blood vessel when a solid tumor is present, or (more rarely) extension into the vasculature (for example, renal cell cancers extending into the renal veins). 2014;2:1–14. Recent studies indicate that white blood cells play a pivotal role in deep vein thrombosis, mediating numerous pro-thrombotic actions. Pathogenic Mechanisms of Thrombosis in Antiphospholipid Syndrome (APS) 165 The literature on the clinical manifestations of APS, although extensive, mostly includes a large number of case reports. Blood coagulation. This type of embolism is known as a thromboembolism. There … Cancer-associated thrombosis is a leading cause of non-cancer death in cancer patients and is comprised of both arterial and venous thromboembolism. N Engl J Med. This animation illustrates thrombosis caused by the rupture of plaque buildup on the arterial wall. Lawson CA, Yan SD, Yan SF, Liao H, Zhou YS, Sobel J, Kisiel W, Stern DM, Pinsky DJ. All aspects of the coagulation cascade, primary hemostasis, coagulation, and fibrinolysis, can be affected. J Am Coll Cardiol. [26] Also, there are several predictive scores for thromboembolic events, such as Padua,[27] Khorana,[28][29] and ThroLy score.[30]. Kaplan MJ, Radic M. Neutrophil extracellular traps: double-edged swords of innate immunity. Heparin is a sulfated polysaccharide with a molecular weight range of 3000 to 30 000 Da (mean, 15 000 Da). The mortality rate is 4.3%. Gerdes,2,3 J.C.M. Organisation: following the thrombotic event, residual vascular thrombus will be re-organised histologically with several possible outcomes. [citation needed]. As a consequence, thrombosis and disseminated intravascular coagulation, hemorrhage, or both, may occur. But scientists have now identified a mechanism they believe to … Lancet. Thrombosis (from Ancient Greek θρόμβωσις thrómbōsis "clotting”) is the formation of a blood clot inside a blood vessel, obstructing the flow of blood through the circulatory system. Jerjes-Sanchez C, Elizalde GJ, Sandoval JZ, Gutierrez-Fajardo P, Seoane DLM, Ramirez-Rivera A, Pulido T, Beltran M, Santos E, Bautista E, Ibarra-Perez C, Arriaga-Nava R. Diagnostico, estratificacion y tratamiento de la tromboembolia pulmonar aguda. Portal vein thrombosis (PVT) is a blood clot that causes irregular blood flow to the liver. The latter can affect smaller vessels such as the branches of the circle of Willis. 2007;5 Suppl 1:264–9. Curr Opin Hematol. Classical signs of DVT include swelling, pain and redness of the affected area. The main mechanism is exposure of tissue factor to the blood coagulation system. In patients admitted for surgery, graded compression stockings are widely used, and in severe illness, prolonged immobility and in all orthopedic surgery, professional guidelines recommend low molecular weight heparin (LMWH) administration, mechanical calf compression or (if all else is contraindicated and the patient has recently suffered deep vein thrombosis) the insertion of a vena cava filter. Steffel J, Braunwald E. Novel oral anticoagulants: focus on stroke prevention and treatment of venous thrombo-embolism. The influence of viral infections on atherosclerosis and atherothrombosis is not discussed. Mechanisms of thrombosis related to hormone therapy Combined oral contraceptives and combined oral postmenopausal hormone therapy are associated with a weak, but clinically significant risk of arterial and venous thrombosis (VT). This can affect any organ; for instance, arterial embolism of the brain is one of the cause of stroke. Many of these paradigms have proven accurate, but others need to be reconsidered given the results of whole animal experiments. [5], Cavernous sinus thrombosis is a specialised form of cerebral venous sinus thrombosis, where there is thrombosis of the cavernous sinus of the basal skull dura, due to the retrograde spread of infection and endothelial damage from the danger triangle of the face. Goldhaber ZS. [22] There are scores that correlate different aspects of patient data (comorbidities, vital signs, and others) to risk of thrombosis, such as the POMPE-C, which stratifies risk of mortality due to pulmonary embolism in patients with cancer, who typically have higher rates of thrombosis. [Margaretten W, Csavossy I, McKay DG. Lastly, people who regularly get dehydrated are also at risk. Part of Springer Nature. Dubois C, Panicot-Dubois L, Gainor JF, Furie BC, Furie B. Thrombin-initiated platelet activation in vivo is vWF independent during thrombus formation in a laser injury model. 1997;99:1729–38. Begieneman MVP, Van de Goot FRW, Van der Bilt IAC, Vonk Noordegraaf C, Spreeuwenberg MD, Paulus WJ, Van Hinsbergh VWM, Visser FC, Niessen HWM. Nature. Prognostic value of plasma fibrinolysis activation markers in cardiovascular disease. Under normal conditions, endothelial cells sustain a vasodilatory and local fibrinolytic state in which coagulation, platelet adhesion, and activation, as well as inflammation and leukocyte activation, are suppressed. Monocytes and tissue factor promote thrombosis in a murine model of oxygen deprivation. Circulation. [37], Arterial thrombosis is platelet-rich, and inhibition of platelet aggregation with antiplatelet drugs such as aspirin may reduce the risk of recurrence or progression. The main causes of thrombosis are given in Virchow's triad which lists thrombophilia, endothelial cell injury, and disturbed blood flow. See the collection of COVID-19 articles in RPTH. You can get DVT if you have certain medical conditions that affect how your blood clots. The elegant studies of Urso et al 10 do not allow evaluation of the possibility that mechanisms in addition to the UP pathway may contribute to the effects of statins on skeletal muscle metabolism. Kroce K, Libby P. Intertwining of thrombosis and inflammation in atherosclerosis. November 23, 2020. Smeeth L, Cook C, Thomas S, Hall AJ, Hubbard R, Vallance P. Risk of deep vein thrombosis and pulmonary embolism after acute infection in a community setting. Forensic Sci Int. 2010;121:2146–50. Platelet adhesion-activation-aggregation. 51 Although a detailed discussion is outside the scope of this article, it seems likely that the TF/factor VIIa pathway is a principal initiator of fibrin formation in cancer patients. J Clin Invest. Lancet. Marcus AJ, Broekman MJ, Pinsky DJ. The hemostatic process is a host defense mechanism—nature’s effort to preserve the integrity of the closed high pressure circulatory system. Nevertheless, non-ischemic venous thrombosis may still be problematic, due to the swelling caused by blockage to venous drainage. J Am Coll Cardiol. In Germany, about 20% of patients were self-managed while only 1% of U.S. patients did home self-testing (according to one 2012 study). [citation needed], Portal vein thrombosis affects the hepatic portal vein, which can lead to portal hypertension and reduction of the blood supply to the liver. McKay DG. Three factors are important in the formation of a blood clot within a deep vein—these are the rate of blood flow, the thickness of the blood and qualities of the vessel wall. 2012;189:2689–95. 2007;117:953–60. 2009;27:154–62. The vessel may be any vein or artery as, for example, in a deep vein thrombosis or a coronary (artery) thrombosis. Myocardial infarction (MI) or heart attack, is caused by ischemia, (restriction in the blood supply), often due to the obstruction of a coronary artery by a thrombus. Eur Heart J. Deep Vein Thrombosis. Manly DA, Boles J, Mackman N. Role of tissue factor in venous thrombosis. 2003;348:1435–41. Considering all evidence linking inflammation with pulmonary embolism, it is possible that new elements have to be included in a contemporary viewpoint of Virchow’s triad and that unprovoked or idiopathic pulmonary embolism term has to be redefined. Mechanisms of thrombosis in hyperhomocysteinemia. Key NS. Alteplase versus heparin in acute pulmonary embolism; randomized trial assessing right-ventricular function and pulmonary perfusion. It most commonly affects leg veins, such as the femoral vein. Thrombotic stroke can be divided into two categories—large vessel disease and small vessel disease. Till such a higher quality of evidence appears, observational studies and expert opinion can serve … 2008;29:2276–315. [33][34] In patients with medical rather than surgical illness, LMWH too is known to prevent thrombosis,[34][35] and in the United Kingdom the Chief Medical Officer has issued guidance to the effect that preventative measures should be used in medical patients, in anticipation of formal guidelines.[32]. Curr Vasc Pharmacol. 1969; 36:67–81. 2. J Am Coll Cardiol. Lentz SR(1). Not logged in Knowledge of molecular and immunologic mechanisms for venous thrombosis and its resolution should allow for the future development of targeted therapies. 2009;54:2129–38. Tsimikas S, Witztum JL. Through its ability to express procoagulants and anticoagulants, vasoconstrictors, and vasodilators, as well as key cell adhesion molecules and cytokines, the endothelium has emerged as one of the pivotal regulators of hemostasis. 2010;56:1683–92. Venous thrombosis leads to congestion of the affected part of the body, while arterial thrombosis (and rarely severe venous thrombosis) affects the blood supply and leads to damage of the tissue supplied by that artery (ischemia and necrosis). Where a more effective response is required, heparin can be given (by injection) concomitantly. [40][41] For example, in a feline model of intestinal ischemia, four hours of ischemia resulted in less injury than three hours of ischemia followed by one hour of reperfusion. mechanism, and its function as a biological amplifier. Jonathan W. Yau, Jonathan W. Yau 1 School of Biomedical Engineering, and . Tissue damage in disseminated intravascular coagulation--mechanisms of localization of thrombi in the microcirculation. 2010;55:2701–9. 2009;114:1276–9. pp 1-17 | A venous thrombus may or may not be ischemic, since veins distribute deoxygenated blood that is less vital for cellular metabolism. 2002;347:1143–50. Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower. [32] Hence thromboprophylaxis (prevention of thrombosis) is increasingly emphasized. Rautou PE, Mackman N. Microvesicles as risk markers for venous thrombosis. Men are affected more than women. 2013;35:342–5. This can be due to ischemia, thrombus, embolus (a lodged particle) or hemorrhage (a bleed). Investigation of coagulation disorders as a consequence of different viral infections … 2011;73:515–25. Not affiliated 1999;99:1325–30. Annu Rev Physiol. Venous thrombosis can lead to pulmonary embolism when the migrated embolus becomes lodged in the lung. Circulation. Ichikawa T, Unoki H, Sun H, Shimoyamada H, Marcovina S, Shikama H, Watanabe T, Fan J. Lipoprotein (a) promotes smooth muscle cell proliferation and dedifferentiation in atherosclerotic lesions of human apo (a) transgenic rabbits. [citation needed], Arterial embolism can lead to obstruction of blood flow through the blood vessel that is obstructed by it, and lack of oxygen and nutrients (ischemia) of the downstream tissue. Tissue damage in disseminated intravascular coagulation--mechanisms of localization of thrombi in the microcirculation. The facial veins in this area anastomose with the superior and inferior ophthalmic veins of the orbit, which drain directly posteriorly into the cavernous sinus through the superior orbital fissure. Symptoms may include headache, abnormal vision, any of the symptoms of stroke such as weakness of the face and limbs on one side of the body and seizures. Some people have a higher risk of developing thrombosis and its possible development into thromboembolism. 2. J Am Coll Cardiol. Narrowing of channel leads to TURBULENCE which precipitates clot formation. The majority of persons affected make a full recovery. But scientists at Uppsala University and the University Hospital have now identified a mechanism … Jugular vein thrombosis can have a varying list of complications, including: systemic sepsis, pulmonary embolism, and papilledema. This is a key reason for the continued high mortality and morbidity in these conditions, despite endovascular reperfusion treatments and continuous efforts to improve timeliness and access to these treatments. Inflammation, a well-established pathway driven by interleukin-expression, could induce endothelial veins activity and vascular disease. 1995;2:67–9. COVID-19 in Journal of Thrombosis and Haemostasis. Arteries are blood vessels that carry blood from the heart to the rest of the body and the heart muscle. Fibrinolysis is the physiological breakdown of blood clots by enzymes such as plasmin. [42] Therapeutic strategies that have potential to improve clinical outcomes in reperfused STEMI patients include remote ischemic conditioning (RIC), exenatide, and metoprolol. [citation needed], Budd-Chiari syndrome is the blockage of a hepatic vein or of the hepatic part of the inferior vena cava. Over 10 million scientific documents at your fingertips. October 29, 2020. Purpose of review . A stroke is the rapid decline of brain function due to a disturbance in the supply of blood to the brain. Arterioscler Thromb. 2. Tang et al reported 11.5% mortality in patients with COVID‐19 pneumonia and noted that 71.4% of these deaths had abnormal coagulation profiles consistent with disseminated intravascular coagulation (DIC) based on criteria from the International Society on Thrombosis and Haemostasis (ISTH). The exact mechanism by which these antibodies participate in the prothrombotic tendency of APS, remain to be clearly defined. Libby P, Simon DI. Cancer tissue is in a state of coagulopathy, inflammation, and hypoxia, and various substances are produced by the induction of cancer proliferation genes, resulting in the formation of thrombi. DVT is the primary cause of pulmonary embolism. Indeed, the small number of subjects and high stringency applied to changes in gene expression may have underpowered the potential to detect modulation of key biological pathways. Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications. This transcription factor with hypoxia inducible factor-1 is also an important transcription factor mediating adaptive responses to hypoxia in endothelium; in vitro, these responses include proinflammatory and pro-adhesive changes. J Am Coll Cardiol. Topics: fibrin, hemorrhage, hemostatic … The main causes of thrombosis are given in Virchow's triad which lists thrombophilia, endothelial cell injury, and disturbed blood flow. Ischemia/infarction: if an arterial thrombus cannot be lysed by the body and it does not embolise, and if the thrombus is large enough to impair or occlude blood flow in the involved artery, then local ischemia or infarction will result. July 15, 2020. These have emerged amongst a multitude of cardioprotective interventions investigated with largely neutral clinical data. In the era of translational medicine, clinical and molecular evidence provide several links between inflammation and pulmonary embolism suggesting a close relationship among atherothrombosis risk factors and venous thrombosis. Curr Opin Lipidol. This service is more advanced with JavaScript available, Thrombolysis in Pulmonary Embolism An association between moderate hyperhomocysteinemia and vascular dysfunction was confirmed in recent studies in animals and humans. 1969; 36:67–81. 1987;84:9265–9. Circulation. [31] In people admitted to hospital, thrombosis is a major cause for complications and occasionally death. [citation needed], Arterial thrombosis is the formation of a thrombus within an artery. mechanism, and its function as a biological amplifier. Thrombosis is the homeostatic mechanism whereby blood coagulates or clots, a process crucial to the establishment of hemostasis after a wound. Symptoms and risks of arterial thrombosis. We also review the facets of this topic for which there is no consensus among experts in the field, for instance, the relative importance of various mechanisms in the precipitation of thrombosis. Management of massive and submassive pulmonary embolism, ileofemoral deep venous thrombosis and chronic thromboembolic pulmonary hypertension. Though characterized by a sharp pain at the site of the vein, it can prove difficult to diagnose, because it can occur at random. An arterial embolus may travel further down the affected blood vessel where it can lodge as an embolism. Science. ... primary hemostasis, coagulation, and fibrinolysis, can be affected. 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