Endothelial dysfunction

In vascular diseases, endothelial dysfunction is a systemic pathological state of the endothelium (the inner lining of blood vessels) and can be broadly defined as an imbalance between vasodilating and vasoconstricting substances produced by (or acting on) the endothelium. Normal functions of endothelial cells include mediation of coagulation, platelet adhesion, immune function and control of volume and electrolyte content of the intravascular and extravascular spaces.

Endothelial dysfunction can result from and/or contribute to several disease processes, as occurs in hypertension, hypercholesterolaemia, diabetes, septic shock, and Behcet's disease, and it can also result from environmental factors, such as from smoking tobacco products and exposure to air pollution. Endothelial dysfunction is more prevalent in shift workers, a group known to have a higher risk for cardiovascular diseases. Most of these studies on human participants have involved the percentage flow-mediated dilation (%FMD) index as the study outcome, which must have proper statistical consideration to be interpreted correctly. Endothelial dysfunction is a major physiopathological mechanism that leads towards coronary artery disease, and other atherosclerotic diseases.

The epidemiology of endothelial dysfunction is unknown, as %FMD varies with baseline artery diameter. This can make cross-sectional comparisons of %FMD difficult. Endothelial dysfunction was found in approximately half of women with chest pain, in the absence of overt blockages in large coronary arteries. This endothelial dysfunction cannot be predicted by typical risk factors for atherosclerosis (e.g., obesity, cholesterol, smoking) and hormones.

Endothelial dysfunction is thought to be a key event in the development of atherosclerosis and has been reported to predate clinically obvious vascular pathology by many years. However, the problem with this assertion in terms of the flow-mediated response indicator of endothelial dysfunction is that a morphological characteristic of atherosclerosis (baseline artery size) is inherent in the calculation of percentage flow-mediated dilation. Endothelial dysfunction is associated with reduced anticoagulant properties as well as increased adhesion molecule expression, chemokine and other cytokine release, as well as reactive oxygen species production from the endothelium. This leads to inflammation and myofibroblast migration and proliferation inside the vessel all of which play important roles in the development of atherosclerosis.

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