A new study has identified clonal hematopoiesis, a condition caused by mutations in blood stem cells, as a significant risk factor for cardiovascular disease.
Traditionally, factors like high blood pressure, high cholesterol, diabetes, obesity, smoking, and lack of physical activity have been known to contribute to heart disease.
Now, clonal hematopoiesis has been added to this list, offering fresh insights into the causes of conditions like atherosclerosis, which involves the buildup of fatty deposits in the arteries.
Clonal hematopoiesis occurs when mutations accumulate in blood stem cells, leading to the growth of genetically distinct groups of blood cells. While most of these mutations are harmless, some give the affected cells an advantage, allowing them to multiply faster than normal cells.
This leads to clonal populations of mutated blood cells in the bloodstream. Until now, scientists were unsure whether these mutations were a cause or a consequence of cardiovascular disease.
Researchers at the Centro Nacional de Investigaciones Cardiovasculares (CNIC) in Spain recently resolved this question through a study published in Nature Medicine.
Their work established that clonal hematopoiesis is indeed a cause of atherosclerosis, a condition that underlies many cardiovascular diseases by creating lesions in the arterial walls.
To reach this conclusion, the CNIC researchers analyzed data from the PESA-CNIC-Santander study, a long-term research project involving over 4,000 middle-aged participants.
These individuals, who appeared healthy, have been undergoing regular check-ups since 2010, using advanced imaging technology to monitor the development of atherosclerosis.
The researchers used highly sensitive DNA sequencing to detect mutations in blood samples and then assessed the presence and progression of atherosclerosis in these participants.
The study found that people who had mutations linked to clonal hematopoiesis at the beginning of the study were more likely to develop atherosclerosis in the following years.
Importantly, the presence of atherosclerosis did not seem to influence the growth of these mutated blood cells, indicating that the mutations are likely contributing to the disease, rather than resulting from it.
This discovery marks a significant shift in understanding how cardiovascular diseases develop and points to clonal hematopoiesis as a risk factor entirely separate from the traditional ones.
In a related study published in the European Heart Journal, the CNIC team explored potential treatments for those with clonal hematopoiesis, particularly focusing on mutations in the TET2 gene, one of the most common mutations associated with this condition.
They collaborated with researchers from the Broad Institute in Boston to investigate the effects of colchicine, an ancient anti-inflammatory drug still used today to treat conditions like gout.
The researchers found that administering colchicine to animals with TET2 mutations slowed the development of atherosclerosis to a rate similar to that in animals without these mutations.
Additionally, the study showed that people with TET2 mutations who were treated with colchicine for other conditions had a lower risk of heart attacks compared to those who were not treated with the drug.
Colchicine has a long history of use in traditional medicine, and it’s widely available and inexpensive. It is already approved by major health agencies like the European Medicines Agency and the FDA for preventing cardiovascular disease.
This makes it a promising candidate for treating individuals with clonal hematopoiesis and TET2 mutations.
However, the study’s authors emphasize that while colchicine shows potential, it is not a one-size-fits-all solution.
Each mutated gene involved in clonal hematopoiesis acts through different mechanisms, which means that specific interventions may be needed for each type of mutation.
The researchers hope that future clinical trials will confirm colchicine’s effectiveness in preventing cardiovascular disease in people with TET2 mutations.
In summary, the discovery that clonal hematopoiesis can directly contribute to atherosclerosis introduces a new perspective on the causes of cardiovascular disease. It also opens the door to personalized treatments that target the specific genetic mutations involved in this condition.
The use of colchicine as a treatment for those with certain mutations could mark a significant advancement in the prevention and management of heart disease.
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The research findings can be found in Nature Medicine.
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