Abstract
At least 10% of the elderly population above the age of 70 carry a condition termed clonal hematopoiesis indeterminate potential (CHIP) due to oligoclonal expansion of mutated hematopoietic stem cells. Although CHIP is known to predispose patients to a higher risk of malignant blood disorders, the recent revelation of its association with higher morbidity and mortality of atherosclerotic cardiovascular disease and ischemic stroke is rather surprising. Two independent research groups published studies indicating that Tet2 mutated monocytes from mice modeling CHIP had a causal role in accelerating the growth of atherosclerotic lesions due to their pro-inflammation activities. This important discovery points to CHIP as a risk factor and raises the prospect of novel treatment to minimize the adverse cardio/cerebro-vascular events.