A significant discovery has emerged in the field of cardiovascular health. Researchers have identified a new risk factor for heart disease that could reshape how we understand and treat atherosclerosis, the build-up of plaques in arteries. This discovery centers on a condition called clonal hematopoiesis, which occurs when certain blood-forming stem cells acquire genetic mutations, leading to their rapid proliferation. Although clonal hematopoiesis has long been associated with blood cancers, it is now being recognized as a key contributor to cardiovascular risk.
What is Clonal Hematopoiesis?
Clonal hematopoiesis refers to the process by which specific blood-forming stem cells acquire mutations in their DNA and begin to multiply at an abnormal rate. These mutated cells, originating in the bone marrow or bloodstream, are not passed down genetically but occur in somatic cells, meaning they arise spontaneously during an individual’s lifetime. As people age, especially in older adults, these mutations can accumulate, and clonal hematopoiesis is often discovered incidentally during routine medical examinations.
In many cases, clonal hematopoiesis does not lead to immediate health problems. However, it has been linked to an increased risk of blood-related disorders, such as leukaemia. Now, researchers are uncovering how this condition also contributes to cardiovascular disease.
Linking Clonal Hematopoiesis to Atherosclerosis
A study published in Nature Medicine in August 2024 revealed clonal hematopoiesis as a new risk factor for atherosclerosis. Atherosclerosis is a condition where plaques build up inside the arteries, leading to blockages that can cause heart attacks and strokes. Traditionally, well-known risk factors for atherosclerosis have included high cholesterol, high blood pressure, diabetes, obesity, smoking, and lack of physical activity. However, this new research shows that clonal hematopoiesis, particularly when associated with mutations in genes like TET2, plays a crucial role in the development of this condition.
Dr José J. Fuster, a leading researcher at the Spanish National Center for Cardiovascular Research, was at the forefront of this study. He explained how clonal hematopoiesis creates a unique population of blood cells with a different genetic makeup from the rest of the body’s blood cells. This altered genetic profile can impair the function of the blood cells, increasing the risk of cardiovascular problems such as heart attacks.
Also Read: Too Much Screen Time Can Make Your Kid Struggle With Language, Says Study
The Direction of Causality: Clonal Hematopoiesis First
Earlier research had raised questions about whether clonal hematopoiesis directly contributed to atherosclerosis or if the reverse was true—that atherosclerosis led to clonal hematopoiesis. However, the Nature Medicine study used longitudinal data from healthy middle-aged individuals to clarify this relationship. According to Dr. Fuster, the findings confirmed that clonal hematopoiesis is a driver of atherosclerosis rather than a consequence of it. Those participants who had mutations linked to clonal hematopoiesis at the beginning of the study were more likely to develop atherosclerosis over time.
Dr Cheng-Han Chen, a cardiologist not involved in the study, reinforced these conclusions. He pointed out that the research shows clonal hematopoiesis increases the risk of atherosclerosis, but the reverse does not hold true. However, he emphasized that further research is necessary to fully understand the mechanisms behind this link.
New Treatment Possibilities with Colchicine
In addition to identifying clonal hematopoiesis as a risk factor for cardiovascular disease, a second study published in the European Heart Journal offered potential treatment strategies for individuals with this condition. This research highlighted the drug colchicine, a medication traditionally used to treat gout and inflammation, as a promising option for people with clonal hematopoiesis who carry mutations in the TET2 gene.
Colchicine is known for its anti-inflammatory properties, which have been harnessed to manage conditions like pericarditis and gout. Researchers now suggest that it could be included in personalized treatment plans to reduce cardiovascular risk in patients with clonal hematopoiesis. Given the role of inflammation in the progression of atherosclerosis, colchicine’s ability to dampen the body’s inflammatory response might slow down or even prevent the development of plaques in arteries.
Also Read: Late Sleepers Face Higher Type-2 Diabetes Risk Regardless Of Lifestyle Factors: Study
A New Era in Cardiovascular Care
This discovery of clonal hematopoiesis as a cardiovascular risk factor is a breakthrough that opens up new avenues for both diagnosis and treatment. It also underscores the complex relationship between genetics and cardiovascular disease. While traditional risk factors such as lifestyle choices and metabolic conditions remain critical, understanding genetic mutations like those seen in clonal hematopoiesis could lead to more targeted therapies and earlier interventions.
With further research, clinicians may be able to identify individuals at high risk for atherosclerosis based on the presence of these genetic mutations and tailor treatment plans accordingly. The potential use of colchicine as a preventive measure marks an exciting step forward in addressing this newly recognized cardiovascular risk factor.
In the future, genetic screening for clonal hematopoiesis might become a routine part of cardiovascular risk assessments, helping to prevent heart attacks and strokes in individuals who would otherwise go undiagnosed until it's too late.