Arterial Thrombosis

Arterial thrombosis is a blood clot in an artery, which can be very serious because it can either slow or stop blood reaching important organs. Arteries are blood vessels that carry blood from the heart to the body and the heart muscle. Blood clots do not usually cause symptoms until they blocks the flow of blood to part of the body. This can cause several serious medical issues, including:

• heart attack, when blood flow to the heart muscle is suddenly blocked, causing chest pain, shortness of breath and dizziness

• stroke, when blood flow to the brain is cut off; the main symptoms are one side of the face dropping, weakness in one side of the body and slurred speech

• transient ischaemic attack (TIA) or "mini-stroke", when blood flow to the brain is temporarily blocked, causing short-lived stroke symptoms

• critical limb ischaemia (a complication of peripheral arterial disease), when the blood supply to a limb is blocked, causing it to become painful, discoloured (either pale or blue) and cold

 

Arterial thrombosis typically affects people with atherosclerotic plaques (fatty deposits) in their arteries. These deposits cause the arteries to harden and narrow over time and can rupture and increase the risk of blood clots (thrombi). Myocardial infarction and stroke, the most common causes of morbidity and mortality in middle-aged Americans, are consequences of arterial thrombosis. The clinical manifestation of myocardial infarction and strokes are different, but they are the result of the same pathogenic process, formation of a thrombus over an atherosclerotic plaque in the environment of high flow and high shear arterial circulation. The thrombus typically overlies a ruptured plaque or an intact plaque with surface endothelial erosion. Plaque composition rather than plaque size or severity of stenosis dictates plaque rupture and subsequent thrombosis. Exposure of blood cells to the procoagulant materials in the ruptured plaque promotes thrombosis. Catalytically active tissue factor is present in the atherosclerotic plaque and seems to play a major role in the triggering of thrombosis following rupture. Under shear stresses in the artery, only platelets are capable of adhesion to the damaged vessel wall. Several adhesion molecules and platelet activators are present in the plaque such as collagen, and oxidized lipids. In contrast to venous thrombosis, activation of coagulation factors does not appear to play a major role in arterial thrombosis as these factors are likely to be removed by the high flow in the arterial system. Vessel wall damage due to atherosclerosis, hypertension, or vascular anomalies is a major risk factor for arterial thrombosis, by inducing turbulence and altered blood flow, which allows platelet adhesion. Consequently, hyperactivity of platelets also plays a role in the pathogenesis. Antiplatelet therapy such as aspirin is used to prevent vascular events in arterial thrombosis while they are of limited value in preventing venous thrombosis (adapted from https://www.ncbi.nlm.nih.gov/books/NBK53453/). Additional information on Thrombosis can be found from the NHS (https://www.nhs.uk/conditions/arterial-thrombosis/).