Clonal hematopoiesis (CH), defined by the age-related expansion of hematopoietic stem cells harboring somatic driver mutations, has emerged as a novel and clinically relevant contributor to atherosclerotic cardiovascular disease (ASCVD). Once considered primarily a precursor to hematologic malignancy, CH is now recognized as a systemic pro-inflammatory state linking somatic evolution to cardiovascular pathology. Epidemiological studies consistently demonstrate that CH is independently associated with increased risks of coronary artery disease, heart failure, aortic stenosis, and cardiovascular mortality. Mechanistically, CH-associated mutations-most commonly in DNMT3A, TET2, and ASXL1-reprogram immune cells toward a pro-inflammatory phenotype, characterized by activation of the NLRP3 inflammasome and increased cytokine production, thereby promoting endothelial dysfunction, atherogenesis, and adverse cardiac remodeling. These insights have catalyzed the development of targeted therapeutic strategies, particularly anti-inflammatory interventions, as well as approaches aimed at modulating clonal expansion and leveraging cardiometabolic agents. Clinically, incorporation of CH genotype and clonal burden into risk assessment may refine cardiovascular risk stratification and guide personalized prevention strategies. In this review, we summarize current evidence on the biological mechanisms linking CH to ASCVD, its clinical implications across cardiovascular phenotypes, and emerging therapeutic approaches. Collectively, CH represents a paradigm shift toward inflammation-driven precision cardiology.