Despite major progress in the pharmacological management of traditional cardiovascular risk factors, cardiovascular disease (CVD) remains the leading cause of mortality worldwide. There is increasing evidence that a substantial residual risk of atherosclerotic cardiovascular disease (ASCVD) persists even in patients who have achieved an apparently optimal control of conventional modifiable risk factors.[1] Moreover, noninvasive imaging studies suggest that more than one-third of asymptomatic middle-aged individuals with a very low cardiovascular risk profile may exhibit significant atherosclerosis,[2] the underlying cause of the most frequent cardiovascular and cerebrovascular disorders. Therefore, although targeting well-established cardiovascular risk factors is still crucial, it is also evident that identifying and characterizing new nonconventional risk factors for atherosclerosis is essential to improve the prevention of CVD. In this regard, clonal hematopoiesis is emerging as a new and quite common risk factor for ASCVD.[3]This condition occurs when a substantial proportion of an individual's blood cells is derived from a single hematopoietic stem cell clone. It is most frequently driven by the random acquisition of somatic mutations that provide a selective advantage to the mutant hematopoietic stem cell, allowing for the mutant cells to expand throughout the hematopoietic system and its progeny, including immune cells. Thus, individuals with clonal hematopoiesis carry a substantial proportion of immune cells that harbor the acquired mutation, which evidently has a high potential of affecting the inflammatory responses that are at the center of CVD.
Tuesday, January 9, 2024
