But an unexpected contributor to that risk has emerged in the past decade. Nothing can be done to specifically tackle this risk factor yet, but the discovery offers a new angle to understanding cardiovascular disease. And it might partly explain why some people develop the disease even when they don’t check the familiar boxes on the modifiable risk list. A 2021The newly found risk arises from specialized cells, called stem cells, that live in the bone marrow.
As scientists develop a better understanding of its impact on inflammation and atherosclerosis, it’s possible that CHIP could be a target for treatment. “We‘ve got 10 15 years of really new science to do,” says cardiologist and physician-scientist Peter Libby of Brigham and Women’s Hospital and Harvard Medical School in Boston. Studying clonal hematopoiesis and how it influences the development of cardiovascular disease, Libby says, “is going to open up many many doors.
compared with people without it, over a period of roughly eight years. In a twist, “it wasn’t cancer-related deaths that people were dying of most often when they had CHIP,” says physician-scientist Siddhartha Jaiswal of the Stanford School of Medicine. “It was actually cardiovascular causes.” After five weeks on a high-cholesterol diet, plaques in the aortas of mice with CHIP were roughly twice as large as in those without CHIP .Molecular biologist Ken Walsh of the University of Virginia School of Medicine in Charlottesville and his colleagues reported similar findings in their 2017study on the impact of CHIP in atherosclerosis-prone mice. Walsh’s team’s work also nodded toward the possibility that something could be done about the increased risk of cardiovascular disease from CHIP.
But when the clinical trial team learned of the effect of CHIP on cardiovascular disease, the group, which included Peter Libby, wondered: “If CHIP is involved in inflammation and we’ve got an anti-inflammatory, could we get a bigger bang in people who had CHIP?” Libby says.
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