Reacción a "CNIC team proposes a new cardiovascular risk factor and a drug to reduce its effects"

Research in recent years has shown that clonal hematopoiesis, the result of acquired somatic mutations, is not only a frequent age-related process and a premalignant state, but a condition that predisposes to the development of cardiovascular disease.

The vast majority of mutations in clonal hemopoiesis affect genes involved in epigenetic regulation, such as TET-2. Experimental models with mutation for this gene are associated with increased atherosclerosis. Two recent studies led by Dr. José Javier Fuster of the CNIC, one clinical and the other experimental, demonstrate that clonal hematopoiesis emerges as a new risk factor for atherosclerotic disease, responsible for very relevant clinical pictures such as acute myocardial infarction and stroke, so its detection may have important therapeutic implications.

The clinical study included a PESA study population of more than 4,000 healthy middle-aged individuals, in whom the detection of clonal hematopoiesis was associated with the development of atherosclerosis over time and preceded its onset. Although the mechanisms involved are not precisely known, inflammation seems to play a relevant role. The experimental study in mice with TET-2 mutations showed an increase in atherosclerotic lesions and the most interesting finding was that the administration of colchicine, an anti-inflammatory drug, reduced the size of the lesions. Both studies are of great interest because of the demonstration of the role of clonal hematopoiesis as a new factor in the development of atherosclerosis and the role of anti-inflammatory strategies for the prevention of cardiovascular disease.