Kitty Inzunza-Esparza, Artemio García-Escobar
Coronary heart disease represents a great economic expense, especially coronary artery calcification (CAC), which is associated with worse clinical outcomes and increased technical complexity of percutaneous coronary intervention. Red cell distribution width (RDW) is a marker of dysregulated erythropoiesis associated with inflammation and iron accumulation in macrophages that is mediated by hepcidin. Research has indicated that higher RDW levels are linked to an increased risk of adverse cardiovascular events, and some studies have shown an association with CAC. This narrative review aims to summarize the current evidence on the mechanisms responsible for elevated RDW and its relationship with inflammation and CAC. Systemic inflammation induces the expression of hepcidin, which alters iron levels; macrophages, depending on iron levels, can help to resolve inflammation or trigger inflammation in atherosclerotic cardiovascular disease (ASCVD) and can induce vascular calcification. This is known as macrophage polarization. Evidence from large-scale clinical trials has established the involvement of immune-mediated inflammation in the pathogenesis of ASCVD. Thus, systemic inflammation is a novel cardiovascular risk factor that can be treated with anti-cytokine therapy. RDW could be a useful marker of inflammation associated with CAC and a risk marker for experiencing adverse cardiovascular events.