Clonal hematopoiesis and atherosclerotic cardiovascular disease: A primer

Despite current standards of care, a considerable risk of atherosclerotic cardio-vascular disease remains in both primary and secondary prevention. In this setting, clonal hematopoiesis driven by somatic mutations has recently emerged as a relatively common, potent and independent risk factor for atherosclerotic cardiovascular disease and other car-diovascular conditions. Experimental studies in mice suggest that mutations in TET2 and JAK2, which are among the most common in clonal hematopoiesis, increase inflammation and are causally connected to accelerated atherosclerosis development, which may explain the link between clonal hematopoiesis and increased cardiovascular risk. In this review, we provide an overview of our current understanding of this emerging cardiovascular risk factor.(c) 2021 Sociedad Espan tilde ola de Arteriosclerosis. Published by Elsevier Espan tilde a, S.L.U. All rights reserved.

Automated summary

Despite current standards of care, there is still a significant risk of atherosclerotic cardiovascular disease in both primary and secondary prevention. Clonal hematopoiesis driven by somatic mutations has recently been identified as a common and independent risk factor for cardiovascular diseases. Experimental studies suggest that certain mutations in TET2 and JAK2 genes, which are frequently found in clonal hematopoiesis, contribute to inflammation and accelerated atherosclerosis development, providing a possible explanation for the increased cardiovascular risk. This review aims to provide an overview of our current understanding of this emerging cardiovascular risk factor.