The aorta is typically about 1mm thick. Atherosclerosis causes intimal media thickening of the arteriales due to an accumulation of lipid-rich foam cells and smooth muscle cells, which migrated from the media arteriosclerosis can also cause ulceration, a fibrous cap, and calcification.
Severe mortality and morbidity are associated with thoracic aortic atherosclerosis. For patients receiving cardiopulmonary bypass, thoracic aortic atherosclerosis significantly increase the risk of complications, including stroke.
Usually, if you have thoracic aortic atherosclerosis, you may also have generalized atherosclerosis, including aneurysms and carotid, coronary, and peripheral arterial disease.
Smoking and hypercholesterolemia are two vascular risk factors associated with severe plaque building in the aortic arch.
The extent and severity of aortic atherosclerotic lesions is related to homocysteine and plasma fibrinogen concentrations.
Homocysteine is a common amino acid found in our blood.
It is mostly found in meat and, in high levels, is a risk factor for heart disease and atherosclerosis.
Homocysteine can cause endothelial dysfunction that causes the progression of atheroma. This can cause thrombi to attach to the atheromatous plaque.
Identifying these arterothrombi could be vital when treating patients with ischemic stroke.
There is not adequate research on the best therapeutic approach to use on individuals with aortic atheromas; however, warfarin may be indicated as the thrombi on the aortic plaques could mobilize.
Warfarin is used to prevent blood clots from being created or growing larger.
Cholesterol-lowering medication, such as statins, can reduce the risk of stroke. Statins make aortic plaques non thrombogenic, or stable, by decreasing the lipid plaques in patients with aortic atheromas.
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