Researchers from CNIC in Spain have discovered that clonal hematopoiesis is a risk factor for atherosclerosis, leading to the development of potential personalized treatments for patients. Clonal hematopoiesis involves certain blood-forming stem cells acquiring genetic mutations and growing more than usual in the body. These acquired changes can increase the risk of blood cancers and other disorders. Mutations in the TET2 gene have been linked to clonal hematopoiesis, which was found to be associated with an increased cardiovascular risk.
In a study published in Nature Medicine, researchers clarified the relationship between clonal hematopoiesis and atherosclerosis by analyzing data from a population of healthy middle-aged individuals over several years. They found that participants with mutations linked to clonal hematopoiesis were more likely to develop atherosclerosis, suggesting that clonal hematopoiesis contributes to the development of this condition. A board-certified interventional cardiologist, Cheng-Han Chen, noted that increased clonal hematopoiesis resulted in greater atherosclerosis, indicating a causal relationship between the two.
Despite the findings, more research is needed to understand how clonal hematopoiesis leads to atherosclerosis. It is hypothesized that mutated blood cells produce inflammatory mediators that promote the buildup of arterial plaques. The increased understanding of clonal hematopoiesis mutations in younger, healthier individuals challenges previous assumptions that these mutations only affect older adults. Hospitals have established clonal hematopoiesis clinics to monitor individuals with this condition, but the identification of the condition for cardiovascular disease prevention is not yet recommended.
Future treatments for clonal hematopoiesis could involve personalized strategies tailored to specific mutations linked to the condition. By blocking the effects of these mutations, researchers hope to prevent cardiovascular disease in carriers of clonal hematopoiesis. Screening for these mutations could potentially assess long-term health risks and lead to earlier interventions, such as lifestyle changes or specific treatments, especially for those with high-risk mutations. The development of personalized treatments for clonal hematopoiesis could open up new avenues for decreasing the risk of cardiovascular disease in affected individuals.
