Unidirectional association of clonal hematopoiesis with atherosclerosis development.

The magnitude of this effect was dependent on mutant clone size, with smaller clones (VAF 0.2–2%) conferring a 1.4-fold higher risk of developing de novo femoral atherosclerosis, which did not reach statistical significance ( P = 0.072), and larger clones leading to a 2.1-fold higher risk, an effect comparable to that of traditional modifiable risk factors such as dyslipidemia or smoking (Extended Data Fig. 3a ).

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