Monocyte‐to‐HDL‐cholesterol ratio as a prognostic marker in cardiovascular diseases

Inflammation and lipid accumulation are two basic hallmarks of atherosclerosis as a chronic disease. Inflammation not only is a local response but can also be considered as a systemic process followed by an elevation of inflammatory mediators. Monocytes are a major source of proinflammatory species during atherogenesis. In atherosclerosis, modified low‐density lipoproteins (LDLs) are removed by macrophages; these are recruited in the vessel wall, inducing the release of inflammatory cytokines in inflamed tissue. Hence, inflammatory cholesterol ester‐loaded plaque is generated. High‐density lipoprotein‐cholesterol (HDL‐C) exhibits antiatherosclerotic effects by neutralizing the proinflammatory and pro‐oxidant effects of monocytes via inhibiting the migration of macrophages and LDL oxidation in addition to the efflux of cholesterol from these cells. Furthermore, HDL plays a role in suppressing the activation of monocytes and proliferation–differentiation of monocyte progenitor cells. Thus, accumulation of monocytes and reduction of HDL‐C may participate in atherosclerosis and cardiovascular diseases (CVD). Given that the relationship between the high number of monocytes and low HDL‐C levels has been reported in inflammatory disorders, this review focused on understanding whether the monocyte‐to‐HDL ratio could be a convenient marker to predict atherosclerosis development and progression, hallmarks of CV events, instead of the individual monocyte count or HDL‐C level. Monocytes are a major source of proinflammatory species during atherogenesis; in atherosclerosis, modified low‐density lipoproteins (LDLs) are removed by macrophages and these are recruited in the vessel wall, inducing the release of inflammatory cytokines in inflamed tissue generating inflammatory cholesterol ester‐loaded plaque. High‐density lipoprotein‐cholesterol (HDL‐C) exhibits antiatherosclerotic effects by neutralizing the proinflammatory and pro‐oxidant effects of monocytes via inhibiting the migration of macrophages and LDL oxidation in addition to the efflux of cholesterol from these cells; furthermore, HDL plays a role in suppressing the activation of monocytes and proliferation–differentiation of monocyte progenitor cells. Thus, accumulation of monocytes and reduction of HDL‐C may participate in atherosclerosis and cardiovascular diseases (CVD); given that the relationship between the high number of monocytes and low HDL‐C levels has been reported in inflammatory disorders, this rev