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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 ]
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.
The discovery that endothelial cell injury underlies this broad spectrum of TMA disorders has come into focus during the last two decades. In the 1980s, Mohamed Karmali (1945–2016) was the first to make the association between Stx, diarrheal E. coli infection and the idiopathic hemolytic uremic syndrome of infancy and childhood.
Multisystem inflammatory syndrome in children (MIS-C), or paediatric inflammatory multisystem syndrome (PIMS / PIMS-TS), or systemic inflammatory syndrome in COVID-19 (SISCoV), is a rare systemic illness involving persistent fever and extreme inflammation following exposure to SARS-CoV-2, the virus responsible for COVID-19. [7]
It consists of aggregates of foam cells, which are lipoprotein-loaded macrophages, [1] located in the intima, the innermost layer of the artery, beneath the endothelial cells that layer the lumina through which blood flows. Fatty streaks may also include T cells, aggregated platelets, and smooth muscle cells.
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.
Cutis marmorata telangiectatica congenita (CMTC) is a rare congenital vascular disorder that usually manifests in affecting the blood vessels of the skin. The condition was first recognized and described in 1922 by Cato van Lohuizen, [2] a Dutch pediatrician whose name was later adopted in the other common name used to describe the condition – Van Lohuizen syndrome.
Soluble fms-like tyrosine kinase-1 (sFlt-1 or sVEGFR-1) is a tyrosine kinase protein with antiangiogenic properties. A non-membrane associated splice variant of VEGF receptor 1 (Flt-1), sFlt-1 binds the angiogenic factors VEGF (vascular endothelial growth factor) and PlGF (placental growth factor), reducing blood vessel growth through reduction of free VEGF and PlGF concentrations. [1]