A new risk factor associated with cardiovascular disease: clonal hematopoiesis of indeterminate potential.

Clonal hematopoiesis is a prevalent disease associated with all-cause death. Not only because it can be a precancerous lesion of blood system diseases but also has a strong association with cardiovascular disease. A narrow term, clonal hematopoiesis of indeterminate potential (CHIP), was proposed by Steensma et al. [1] to describe individuals with detectable somatic clonal mutations in their genes in blood or bone marrow but without a diagnosis of hematological disease or unexplained cytopenia. Recently, studies have suggested that CHIP is associated with adverse cardiovascular disease progression, particularly in patients with ten-eleven translocation 2 (TET2) mutations or DNA methyltransferase 3 alpha (DNMT3A) mutations. Age is the most crucial factor which is associated with increased CHIP prevalence. The underlying mechanisms appear to be related to inflammatory status. However, new evidence suggests that genetic factors, lifestyle and environmental factors such as smoking, obesity, and diet also play essential roles in developing CHIP. More research needs to be done on the potential genetic mechanisms driving CHIP and the environmental factors that modulate CHIP risk. This review summarizes the latest research on CHIP, discusses in detail the strong association between clonal hematopoiesis and accelerated cardiovascular disease, and rationalizes the intervention of CHIP in combination with existing evidence, which may be beneficial for future treatment.