A recent study has resolved a long-standing debate in the medical field by confirming that mutations linked to clonal hematopoiesis increase the risk of atherosclerosis in those affected. Atherosclerosis, which involves the buildup of plaques in the arteries, is a major factor in cardiovascular disease.
While traditional risk factors for heart disease—such as high blood pressure, high cholesterol, diabetes, obesity, smoking, and inactivity—are well known, clonal hematopoiesis has now been added to the list. This condition, caused by mutations in blood stem cells, was previously connected to a higher risk of cardiovascular events. However, it remained unclear whether clonal hematopoiesis was a cause or a result of heart disease.
Published in Nature Medicine, a new study from researchers at the Centro Nacional de Investigaciones Cardiovasculares (CNIC) settles this question. It identifies clonal hematopoiesis as a direct risk factor for atherosclerosis, the underlying cause of many cardiovascular conditions.
In a related study, published in the European Heart Journal, the same research team suggests that colchicine, an ancient anti-inflammatory drug, could be a key component in personalized treatments targeting mutations in the TET2 gene, which are linked to clonal hematopoiesis. These findings will be presented at the European Society of Cardiology meeting in London.
