Abstract
AbstractAtherosclerosis is initiated by the subendothelial accumulation of low density lipoproteins (LDL), which after oxidation trigger a local inflammatory reaction involving mainly monocytes/macrophages and T and B lymphocytes. Vascular smooth muscle cells differentiate into myofibroblasts to secrete collagen fibers, constituents of the fibrous cap that stabilizes the plaque. Beyond classic cardiovascular risk factors, clonal hematopoiesis is emerging as a new risk factor for atherosclerosis. A therapeutic arsenal targeting the main risk factors, including cholesterol and hypertension, is now available with real clinical benefit. But new treatments targeting inflammation more specifically are beginning to show their effectiveness.
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