The theme of inflammation in the atherosclerotic process has been the subject of numerous researches for years. Atherosclerosis is an inflammatory disease since the accumulation of leukocytes in the subendothelium is one of the first processes in plaque formation. Subsequently, other inflammatory cells (monocytes, macrophages, dendritic cells, lymphocytes and mast cells) participate continuously from forming the “fatty groove” until the occurrence of the acute coronary event. ^–

The orchestrated action of all the pro-inflammatory signals in the plaque increases inflammation and directly affects the structural elements that support its mechanical stability. Various pro-inflammatory messengers are released by immune and vascular endothelial cells, activating cytokines, chemokines, bioactive lipid compounds and adhesion molecules that maintain and accelerate inflammation and the local development of atherosclerotic lesions. ^,

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