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Endothelial dysfunction may be involved in the development of atherosclerosis [5] [6] [7] and may predate vascular pathology. [ 5 ] [ 8 ] Endothelial dysfunction may also lead to increased adherence of monocytes and macrophages , as well as promoting infiltration of low-density lipoprotein (LDL) in the vessel wall. [ 9 ]
Endothelial dysfunction has also been shown to be predictive of future adverse cardiovascular events including stroke, heart disease, and is also present in inflammatory disease such as rheumatoid arthritis, diabetes, and systemic lupus erythematosus. [18] [19] Endothelial dysfunction is a result of changes in endothelial function.
Endothelial activation is a proinflammatory and procoagulant state of the endothelial cells lining the lumen of blood vessels. [1] It is most characterized by an increase in interactions with white blood cells (leukocytes), and it is associated with the early states of atherosclerosis and sepsis , among others. [ 2 ]
The chronic endothelial injury hypothesis is one of two major mechanisms postulated to explain the underlying cause of atherosclerosis and coronary heart disease (CHD), the other being the lipid hypothesis. Although an ongoing debate involving connection between dietary lipids and CHD sometimes portrays the two hypotheses as being opposed, they ...
Endothelium dysfunction is a prototypical characteristic of vascular disease, which is common in patients with autoimmune diseases such as systemic lupus erythematosus. [20] Further, there is an inverse relationship between age and levels of EPCs. Inverse of endothelial dysfunction also occurs when other risk factors are treated. [21]
FMD is a noninvasive measure of blood vessel health (endothelial dysfunction [5] [6]) which (when low) is at least as predictive of cardiovascular disease as traditional risk factors. [4] [7] [8] Major cardiovascular disease associated with low FMD include cardiac death, myocardial infarction, and stroke. [8]
Endothelial injury/dysfunction; It is named after the renowned German physician Rudolf Virchow (1821–1902). However, the elements comprising Virchow's triad were not proposed by Virchow. Neither did he ever suggest a triad to describe the pathogenesis of venous thrombosis.
This condition is typically characterized by a series of structural and functional changes within the heart's microcirculation, such as endothelial dysfunction (which affects the inner lining of blood vessels), microvascular arteriolar remodeling (changes in the vessel structure) such as intimal thickening, smooth muscle cell proliferation ...