[Immune cell activation in cardiovascular disease: new pathophysiological mechanisms explained]

Abstract

Optimal treatment of classical risk factors, such as dyslipidemia, cannot completely prevent atherosclerotic cardiovascular disease, which is called residual cardiovascular risk. The anti-inflammatory drugs colchicine and canakinumab can lower this residual risk, illustrating the importance of inflammation in the pathophysiology of cardiovascular disease. Circulating granulocytes and activated monocytes are associated with atherosclerotic cardiovascular disease in observational studies. In the past few years, two mechanisms have been discovered that contribute to monocyte and neutrophil activation in the context of atherosclerosis, namely trained immunity and clonal hematopoiesis. In this Perspective, we discuss these mechanisms, since we foresee that in the near future knowledge of these mechanisms could improve cardiovascular risk prediction and provide targets for novel drugs to prevent or treat cardiovascular diseases.