Researchers at the Centro Nacional de Investigaciones Cardiovasculares (CNIC) in Spain have discovered that clonal hematopoiesis—a condition where blood-forming stem cells acquire mutations and multiply excessively—can significantly increase the risk of atherosclerosis, a leading cause of cardiovascular diseases. These findings could pave the way for personalized treatments in the future. report from Medical News Today.
Clonal hematopoiesis involves genetic mutations in hematopoietic stem cells, causing them to proliferate and produce blood cells with the same mutations. This condition, often detected in older adults, has been linked to higher risks of blood cancers and now, cardiovascular issues, particularly atherosclerosis.
In a study published in Nature Medicine in August 2024, researchers identified clonal hematopoiesis as a new risk factor for atherosclerosis, alongside traditional factors like high blood pressure, high cholesterol, and smoking. The study used DNA sequencing and imaging data from a longitudinal analysis of healthy middle-aged individuals, demonstrating that those with clonal hematopoiesis mutations at the start were more likely to develop atherosclerosis over time.
A second study, published in the European Heart Journal, explored the potential of colchicine, a long-used anti-inflammatory medication, in personalized treatment plans for individuals with clonal hematopoiesis linked to TET2 gene mutations. Lead author Dr. José J. Fuster explained that the research clarifies the causal link between clonal hematopoiesis and atherosclerosis, establishing that the mutations drive the development of atherosclerosis, not the reverse. told by NIH.
Cardiologist Dr. Cheng-Han Chen, who was not involved in the research, emphasized that the studies confirm clonal hematopoiesis increases atherosclerosis risk by promoting inflammation, potentially leading to arterial plaque buildup. However, he noted that more research is needed to fully understand the mechanisms involved.
Dr. Raj Dasgupta, also not involved in the studies, highlighted the broader implications, suggesting that these mutations may be more common and significant than previously thought, even in younger individuals. He believes that understanding these genetic risks could lead to earlier interventions, such as lifestyle changes or targeted treatments, to prevent cardiovascular diseases.
While clonal hematopoiesis is increasingly recognized as a cardiovascular risk factor, there are no established guidelines for its monitoring or treatment. Dr. Fuster suggests that identifying and targeting these mutations could eventually help prevent cardiovascular disease, marking a step toward personalized medical strategies. As research progresses, screening for clonal hematopoiesis could become a crucial tool in assessing long-term health risks and guiding preventive measures.
