Arterial and Venous Thrombosis: Similarities and Differences
Pathophysiology
There are clinically relevant similarities — and differences — in the pathophysiology of thrombi that form in different parts of the circulatory system. Regardless of whether a blood clot forms in a vein, an artery or the heart, the coagulation cascade generates fibrin, which comprises the main structural scaffolding of the thrombus. However, arterial and venous thrombi contain different proportions of fibrin and platelets.235
Blood clot composition: red clots versus white clots
Venous thrombi are rich in fibrin and trapped red blood cells and are therefore referred to as “red clots”. In contrast, arterial thrombi have a higher concentration of platelets and a lower concentration of red blood cells and are referred to as “white clots”.235
Currently, venous thrombosis generally is prevented with medications that interrupt the clotting cascade, while the prevention of arterial thrombi rests more heavily on the use of drugs that block platelet activation.235 However, because thrombin is a potent activator of platelets, and because arterial clots contain fibrin, anticoagulant drugs also have a proven role in the prevention and treatment of arterial thrombosis.235
Hypercoagulability
Hypercoagulability — whether inherited or acquired — increases the risk of thrombosis.237 Hypercoagulable states are primarily associated with venous thrombosis, but increasing evidence implicates abnormalities of clotting factors, such as high fibrinogen levels and elevated Factor VII activity, in some patients with arterial thrombosis. Measurement of these and other haematologic markers may eventually prove useful in the assessment and treatment of coronary heart disease.237 However, because of conflicting findings on the specific value of each of these markers, ongoing research is needed.241, 260
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Yahoo! My Web- 235 - Mackman N, Becker RC. DVT: a new era in anticoagulant therapy. Arterioscler Thromb Vasc Biol. 2010;30(3);369-371.
- 237 - Mahé I, Drouet L, Simoneau G, Minh-Muzeaux S, Caulin C, Bergmann JF. D-dimer can predict survival in patients with chronic atrial fibrillation. Blood Coagul Fibrinolysis. 2004;15(5):413-417.
- 241 - Miller GJ, Ireland HA, Cooper JA, et al. Relationship between markers of activated coagulation, their correlation with inflammation, and association with coronary heart disease (NPHSII). J Thromb Haemost. 2008;6(2):259-267.
- 260 - Scarabin PY, Arveiler D, Amouyel P, et al; Prospective Epidemiological Study of Myocardial Infarction. Plasma fibrinogen explains much of the difference in risk of coronary heart disease between France and Northern Ireland. The PRIME study. Atherosclerosis. 2003;166(1):103-109.
- Coagulation cascade
- Series of reactions by which a small stimulus is amplified to produce rapid coagulation.
- Fibrin
- The primary end product of the coagulation cascade. Fibrin links itself into strands to form a net. This net traps blood cells and tightens itself through cross-linkages, resulting in a dense blood clot.
- Platelet
- (Thrombocyte) Cell circulating in the blood that is involved in the cellular mechanisms of primary haemostasis leading to the formation of blood clots. When a blood vessel is injured, platelets gather at the site of injury and stick together to form a plug, thereby preventing blood loss.
- Thrombin
- Also called Factor IIa, thrombin performs two functions in the coagulation cascade: activating platelets, and catalysing the conversion of soluble fibrinogen into insoluble fibrin. It is formed from prothrombin by a reaction that is catalysed by Factor Xa.
- Hypercoagulability
- A potentially dangerous state of an increased tendency for blood to coagulate, even within blood vessels. Hypercoagulability can be an inherited condition (e.g., Factor V Leiden mutation) or acquired through circumstance (e.g., cancer).
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