Klonale hematopoëse: kans om de hartfalenepidemie aan te pakken

Clonal hematopoiesis driven by somatic mutations, often termed clonal hematopoiesis of indeterminate potential (CHIP), has emerged as an important and independent cardiovascular risk factor. This condition arises when somatic mutations acquired in certain genes, most frequently the epigenetic regulators DNMT3A and TET2, confer a competitive advantage to hematopoietic cells, enabling their clonal expansion and the propagation of the mutation to a substantial proportion of immune cells, which can influence inflammatory responses central to cardiovascular pathophysiology. A growing body of evidence has associated CHIP with atherosclerotic disease, heart failure (HF), arrhythmias, and myocarditis/pericarditis. Among these conditions, HF stands out for its high prevalence in the aging population, socioeconomic impact, and complex pathophysiology. Now, in this issue of JAMA Cardiology, Flynn and colleagues provide new insight into the relationship between CHIP and HF, reporting the results o