Endothelial Dysfunction and Its Clinical Implications

Endothelial dysfunction (ED) plays a substantial role in the pathogenesis of atherosclerosis and some other vascular diseases. ED has been demonstrated in patients with hypercholesterolemia, diabetes, smoking, hypertension, and in patients with atherosclerotic disease. Besides classical risk factors, ED is affected by chronic inflammatory diseases and acute infections, particularly viral diseases. Causes of ED include oxidative stress, inflammation, and shear stress, which decrease the bioavailability of nitric oxide. Markers of ED have been sought, particularly circulating markers. Using these tests, it is possible to evaluate the response to harmful effects of risk factors and the effects of treatment on vessel wall function. Endothelial dysfunction is significantly and directly correlated with the occurrence of cardiac events and the risk of cardiac events increase as ED worsens. Because endothelial function plays a central role in atherogenesis it became a therapeutic target. Endothelial dysfunction is reversible and its improvement may be achieved by elimination of risk factors, inhibitors of endothelium-derived contracting factors (angiotensin-converting enzyme), smoking cessation, lipid-lowering drugs, diet, and physical exercise. By reversing ED, it is possible to restore vascular function.

Automated summary

Endothelial dysfunction is a significant factor in the pathogenesis of atherosclerosis and vascular diseases, influenced by various factors including oxidative stress and inflammation. By identifying markers of ED, the risk of disease and effectiveness of treatment can be assessed. Improvement of endothelial function can be achieved through lifestyle changes, medication, and exercise.