Researchers from the Centro Nacional de Investigaciones Cardiovasculares (CNIC) in Spain have uncovered new information about clonal hematopoiesis and its link to atherosclerosis, the underlying cause of most cardiovascular diseases. Clonal hematopoiesis occurs when blood-forming stem cells acquire genetic mutations and multiply more than usual. This condition is often discovered incidentally in older adults and can increase the risk of blood cancers. The researchers found that individuals with mutations linked to clonal hematopoiesis are more likely to develop atherosclerosis, suggesting a causal relationship between the two.
One study published in Nature Medicine identified clonal hematopoiesis as a new risk factor for atherosclerosis. The findings were based on longitudinal analysis of DNA sequencing and imaging data from a group of healthy middle-aged individuals. Participants with mutations linked to clonal hematopoiesis at the beginning of the study were more likely to develop atherosclerosis over time. The study also highlighted that atherosclerosis did not influence the expansion of mutated blood cells, indicating that clonal hematopoiesis contributes to the development of atherosclerosis, not the other way around.
Another study published in the European Heart Journal suggested that the anti-inflammatory drug colchicine could play a key role in personalized treatment plans for individuals with clonal hematopoiesis linked to mutations in the TET2 gene. Colchicine could potentially block the effects of these mutations and help prevent cardiovascular disease. While identifying the presence of clonal hematopoiesis is not yet recommended for the prevention of cardiovascular disease, ongoing research is focused on developing personalized treatment strategies tailored to carriers of specific mutations linked to this condition.
The research challenges the notion that clonal hematopoiesis mutations are only relevant in older adults and suggests they could play a role in the development of heart disease and cancers earlier in life. Screening for these mutations could potentially assess a person’s long-term health risks and lead to early interventions to prevent disease. The findings have prompted some hospitals to develop clonal hematopoiesis clinics to monitor the health status of individuals with the condition. Further research is needed to better understand how clonal hematopoiesis is related to atherosclerosis and clinical heart disease, and to explore potential therapeutic interventions to decrease the risk of cardiovascular disease in affected individuals.
Jose J. Fuster, PhD, lead author of the studies, emphasized the importance of clarifying that clonal hematopoiesis mutations are a cause of atherosclerosis, not a consequence. This understanding could guide the development of personalized strategies to block the effects of these mutations and prevent cardiovascular disease. While more research is required to uncover the mechanisms linking clonal hematopoiesis to atherosclerosis, the field holds promise for identifying new therapeutic avenues for reducing cardiovascular risk in individuals with this condition. Early screening for genetic risks associated with clonal hematopoiesis could empower individuals to take proactive steps to safeguard their long-term health.
