Abstract
The involvement of inflammation is described in all stages of atherosclerosis as well as in dyslipidemias, particularly in lipoproteins (especially oxidized LDL), coronary syndromes, hypertension, diabetes, infections, obesity, and also in the use of sexual replacement hormones. From the first steps of leukocyte recruitment in the nascent atheromatic lesion to the development of atheroma plaque, culminating in its rupture and thrombosis in the acute coronary event, we found a constant release of inflammatory mediators, soluble in plasma, from macrophages, T lymphocytes, endothelial cells and smooth muscle vessels of the vessels, hepatocytes, and adipocytes. The greatest evidence relating inflammation to the future development of cardiovascular events has been verified in large-scale population studies. High concentrations of inflammatory markers such as TNF-α, IL-6, ICAM-1, P-selectin, E-selectin, C Reactive Protein, fibrinogen, and amyloid serum A, in apparently healthy individuals, have shown predictive value for future vascular events. Considering the multifactorial etiology of coronary artery disease and its inflammatory nature, it was possible to find an association between the presence of risk factors and the increase in the concentration of biomarkers of inflammation. TNF-α is a multifunctional cytokine derived from smooth endothelial and muscle cells, as well as macrophages present in the coronary atheroma. It is involved in a number of cardiovascular processes, being increased in congestive heart failure.
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