Researchers reveal that clonal hematopoiesis (CH) significantly increases the risk of developing femoral atherosclerosis, suggesting a unidirectional relationship independent of traditional cardiovascular risk factors.
By Vijay Kumar MalesuReviewed by Susha Cheriyedath, M.Sc.Sep 2 2024 Study: Unidirectional association of clonal hematopoiesis with atherosclerosis development. Image Credit: Explode / Shutterstock
Some studies suggest that CH could directly contribute to atherosclerosis by exacerbating inflammatory responses. In contrast, others propose that atherosclerosis or related traits may accelerate the expansion of mutant hematopoietic clones, indicating reverse causality. Further research is essential to clarify this relationship, which could inform the development of targeted strategies for preventing CVD in individuals with CH.
High-sensitivity targeted DNA sequencing was conducted on blood samples to identify CH-related somatic mutations. A custom gene panel was used to detect mutations in 54 CH-related genes. Statistical analysis was performed using RStudio, with adjustments for relevant covariates. The most frequently observed mutations were in the DNA -Methyltransferase 3 Alpha gene, present in 14.8% of individuals, followed by Ten-Eleven Translocation Methylcytosine Dioxygenase 2
When examining the pathophysiological effects of CH, mutation carriers showed higher absolute blood cell counts across all hematopoietic lineages, though the effect was mild. There was also a trend toward higher blood pressure and glycated hemoglobin levels among CH carriers, but these associations were not statistically significant after adjusting for age and sex. However, the study’s longitudinal analysis revealed a more nuanced relationship between CH and atherosclerosis.
Hematopoiesis Blood Blood Vessels Cancer Cardiovascular Disease Cell DNA DNMT3A Gene Genes Genetic Heart Heart Disease Imaging Medicine Mutation Research Stem Cells Vascular
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