Clonal hematopoiesis and thromboembolic diseases: a review

Clonal hematopoiesis of indeterminate potential (CHIP) has been identified as a novel risk factor for cardiovascular diseases, primarily mediated by CHIP-induced systemic inflammation. Emerging evidence suggests that CHIP may also contribute to the risk of thromboembolic diseases. This review highlights recent findings on the impact of CHIP on various thromboembolic conditions, such as deep vein thrombosis, pulmonary embolism, chronic thromboembolic pulmonary hypertension, and ischemic stroke. Studies have demonstrated an association between CHIP and an increased risk of deep vein thrombosis, pulmonary embolism, chronic thromboembolic pulmonary hypertension and ischemic stroke. CHIP-induced systemic inflammation may amplify vascular endothelial damage and complement cascade activation, which in turn promote platelet activation, fibrin deposition, and the release of neutrophil extracellular traps. These processes collectively may drive thromboembolic events. Further mechanistic studies are warranted to elucidate the biological pathways through which CHIP influences the risk of thromboembolic diseases and to identify potential therapeutic targets.