Clinical significance the inflammatory biomarkers of atherosclerosis in carotid disease

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Atherosclerotic disease of the carotid arteries is major cause of ischemic stroke. The degree of carotid stenosis is the main marker for assessing the risk of stroke in "carotid disease", however, the degree of stenosis alone cannot accurately predict future stroke. Asymptomatic carotid artery stenosis is a well-recognized risk factor for ischemic stroke. Non-stenotic atherosclerotic carotid artery plaques can also cause atheroembolism in the presence of ulceration and rupture of the plaque. Atherosclerosis is a dynamic process involving inflammatory and thrombotic mechanisms with progressive degree of stenosis. The ability to predict the progression of atherosclerotic stenosis can be useful for clinical practice in assessing the risk of stroke development and its prevention. To identify subgroup of patients at higher risk for ipsilateral stroke is important aim. Inflammatory activity is an integral indicator of the development of atherosclerosis and its complications and plays a key role in the pathogenesis, progression, rupture of atherosclerotic plaque and the development of clinical manifestations in patients with atherosclerotic carotid stenosis. Several serum inflammatory markers such as C-reactive protein, interleukin-6, pentraxin 3, lipoprotein-associated phospholipase A2, adhesion molecules ICAM-1and selectins and matrix metalloproteinases proposed as tool for risk assessment in patients with carotid atherosclerosis. Even though there are some cardiovascular biomarkers identified, they have only modest predictive value. Some well-established biomarkers for coronary disease are not relevant to carotid atherosclerosis. Future research may clarify the clinical significance of serum inflammatory biomarker in carotid atherosclerosis.

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Dubenko O. Clinical significance the inflammatory biomarkers of atherosclerosis in carotid disease [Electronic resource] / O. Dubenko // Journal of brain and neuroscience research. ─ 2021. ─ Volume 5, issue 1. ─ 014.

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