New research from Boston University School of Medicine (BUSM) provides evidence on the links between common mutations in blood cells and atherosclerosis in elderly patients.

The findings help shed light on why 60 percent of patients with atherosclerotic cardiovascular disease show no conventional risk factors, or have just one. Furthermore, the findings suggest that aging could just be one risk factor.

"Our studies show that mutations in our white blood cells, which we acquire as we age, may cause cardiovascular disease,” said study author Kenneth Walsh, PhD, a professor of medicine at BUSM, in a statement. “Understanding this new mechanism of cardiovascular disease could lead to the development of new therapies to treat individuals who suffer from heart and blood vessel ailments due to these mutations.”

Prior research shows that the accumulation of somatic DNA mutations is associated with aging, but there is little data on how it affects disorder beyond cancer.

However, more recent studies suggest that aging can cause an increase in somatic mutations in the hematopoietic system, which increases the number of blood cells—a process associated with atherosclerosis.

But in the BUSM study, researcher explored whether there is a clear and direct relationship between somatic mutations and atherosclerosis by testing how TET2, a gene found in mutated blood cells of elderly individuals, affected plaque development.

Results showed that plaque formed more quickly in cells transplanted with the TET2 because of an increasing macrophage-driven inflammation of the artery wall, supporting a hypothesis that hematopoietic mutations do in fact play a role in the development of atherosclerosis.

“Because these mutations become prevalent starting at middle age, these studies suggest that genetic analyses of blood samples could add to the predictive value of traditional risk factors—high cholesterol, hypertension, diabetes and smoking—that are currently monitored,” Walsh said.