Abstract

The growing interest in the mechanisms involved in atherogenesis is justifiable when it is verified that most of the deaths that occurred in the Western world are due to ischemic syndromes related to atherosclerotic disease, that is, coronary insufficiency, cerebral vascular and peripheral vascular. We can consider atherogenesis as a protective inflammatory response to injury of the endothelium and smooth muscle layer of the vessel, secondary to genetic, metabolic and hemodynamic influences, promoting the formation of a fibrofatty or fibrous plaque as a repair response of the arterial wall. Oxidized LDL has properties that alone can trigger and perpetuate atherogenesis, regardless of other agents that promote endothelial injury. Remaining lipoproteins rich in triglycerides and high-density lipoproteins: circulating lipoproteins rich in triglycerides at high levels may also be an endothelial injury factor, since intact vascular endothelium is a catabolism site of these lipoproteins. A great step was taken in this sense, with the use of lipid-lowering drugs in the control of dyslipidemias. Significant reductions in the overall mortality rate have been confirmed in prospective epidemiological studies, both in primary prevention and in the secondary prevention of coronary atherosclerotic disease. The intervention on complex mechanisms that promote atherogenesis, among others: preventing the modification of lipoproteins, blocking macrophages and hindering the formation of foamy cells, preventing cell proliferation and the deposition of immunocomplexes in the vascular wall opens a new horizon with drugs such as statins and Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) inhibitors.