In recent years, the potential involvement of clonal cell populations in atherosclerosis has gained renewed interest. Evidence from independent research groups unambiguously showed that smooth muscle cells clonally expand in experimental atherosclerosis, and clonal hematopoiesis of indeterminate potential (CHIP) was identified as a novel independent risk factor for atherosclerotic cardiovascular disease. However, the extend of clonal population partaking in human atherosclerosis remains elusive. In this study, whole-exome sequencing of 14 carotid plaques unveiled a landscape of somatic mutations. Based on variant allele frequencies, we found that individual locally expanded clones contributed with up to 15% of the plaque cell population, and in seven patients carrying CHIP, haemopoietic clones were represented in plaques in some cases comprising over 30% of plaque cells. Taken together, we provide evidence that somatic mutations and clonal cell populations (expanded locally or invading from the circulation) are inherent features of atherosclerosis.