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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 ]
In women who develop preeclampsia, the sFlt-1 to PlGF ratio is higher than in normal pregnancy. [4] [14] [6] sFlt-1 produced in the placenta is thought to circulate in the maternal bloodstream to act on distant tissues, explaining the multi-system endothelial dysfunction observed in women with preeclampsia. [5]
The review suggests that magnesium deficiency may also contribute to endothelial dysfunction and changes in electrolyte metabolism. ... a number of the discussed studies focused on postmenopausal ...
Atherosclerosis generally starts when a person is young and worsens with age. Women are 78% at higher risk level than men [2] Almost all people are affected to some degree by the age of 65. [7] It is the number one cause of death and disability in developed countries.
Abnormal development of the placenta leads to poor placental perfusion. The placenta of women with pre-eclampsia is abnormal and characterized by poor trophoblastic invasion. [26] It is thought that this results in oxidative stress, hypoxia, and the release of factors that promote endothelial dysfunction, inflammation, and other possible reactions.
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 ...
Type I is also known as allergic vasospastic angina due to endothelial dysfunction. It occurs in people without underlying coronary artery disease or predisposing factors who have allergic ACS secondary to coronary artery spasm. Inflammatory mediators during an allergic reaction can cause arterial spasms with normal troponins.
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 ]