Clonal hematopoiesis describes a condition where specific blood-forming stem cells in the bone marrow or bloodstream acquire genetic mutations, leading to their excessive proliferation. These mutations, occurring in somatic cells (non-reproductive cells), can increase the risk of blood cancers and other disorders. Often, clonal hematopoiesis is discovered incidentally in older adults and may not cause immediate issues. However, recent research has revealed a new dimension to this condition: its link to increased cardiovascular risk.
A study published in *Nature Medicine* in August 2024 has identified clonal hematopoiesis as a novel risk factor for atherosclerosis, a condition characterized by plaque buildup in the arteries. This discovery adds to the list of well-known cardiovascular risk factors such as high blood pressure, high cholesterol, diabetes, obesity, smoking, and physical inactivity. The study highlights that individuals with clonal hematopoiesis are at a higher risk for developing atherosclerosis, further emphasizing the need to recognize this condition as a significant cardiovascular risk factor.
Another study, featured in the *European Heart Journal* in August 2024, suggests that colchicine, a medication long used for other conditions, might be valuable in personalized treatment plans for individuals with clonal hematopoiesis, especially those with mutations in the TET2 gene. José J. Fuster, PhD, the lead author of both studies, explained that their research clarifies the relationship between clonal hematopoiesis and atherosclerosis. Previously, some studies proposed that clonal hematopoiesis might accelerate atherosclerosis, while others suggested the opposite. The *Nature Medicine* study, through longitudinal analysis, shows that clonal hematopoiesis contributes to atherosclerosis development rather than the other way around.
Cheng-Han Chen, MD, highlighted that the study demonstrates increased clonal hematopoiesis correlates with greater atherosclerosis, pointing to causality. The mechanism by which clonal hematopoiesis increases the risk of arterial plaques is still under investigation, with some researchers hypothesizing that it might involve increased inflammatory mediators produced by the mutated blood cells.
Raj Dasgupta, MD, noted that the study challenges the notion that clonal hematopoiesis mutations are relevant only in older adults and suggests they could influence the development of diseases like heart disease earlier in life. As clonal hematopoiesis becomes recognized as a significant cardiovascular risk factor, some hospitals are even establishing specialized clinics to monitor individuals with this condition. However, current guidelines do not yet recommend screening for clonal hematopoiesis as a preventive measure for cardiovascular disease due to the lack of evidence-based interventions.
Future research aims to develop personalized treatment strategies to mitigate the cardiovascular risks associated with clonal hematopoiesis. Chen and Dasgupta agree that while we are in the early stages of understanding this relationship, the potential for new therapeutic approaches and screening methods to assess long-term health risks is promising.
