The Predictive Value of Hemoglobin Glycation Index and Clonal Hematopoiesis of Indeterminate Potential Among AMI Patients-A Prospective Registry Study.
The objective of this research is to explore the combined effect of hemoglobin glycation index (HGI) and clonal hematopoiesis of indeterminate potential (CHIP) on all-cause mortality among patients diagnosed with acute myocardial infarction (AMI).
The presence of CHIP in peripheral blood cells was detected using deep targeted sequencing. AMI patients were divided into groups based on the median value of HGI and assessed for the effect of CHIP on all-cause mortality using multivariable Cox regression and Kaplan-Meier analysis.
Multivariable Cox regression indicated that among patients with HGI above the median value, CHIP carriers exhibited a significantly higher all-cause mortality (any CHIP, adjusted HR: 2.06 95% CI: 1.10-3.85; p = 0.023), with analysis of specific mutations identifying particularly high risks for TET2 (adjusted HR: 3.72, 95% CI: 1.37-10.09; p = 0.010) and TET2/ASXL1 co-mutations (adjusted HR: 2.61, 95% CI: 1.08-6.30; p = 0.033). Kaplan-Meier analysis in the high-HGI group confirmed that carriers of any CHIP (p < 0.001) and common CHIP (p = 0.019) had a higher risk of mortality than noncarriers.
Our study reveals that HGI significantly modifies CHIP-related all-cause mortality risk, which provides a way for refined risk stratification in patients with AMI.
The presence of CHIP in peripheral blood cells was detected using deep targeted sequencing. AMI patients were divided into groups based on the median value of HGI and assessed for the effect of CHIP on all-cause mortality using multivariable Cox regression and Kaplan-Meier analysis.
Multivariable Cox regression indicated that among patients with HGI above the median value, CHIP carriers exhibited a significantly higher all-cause mortality (any CHIP, adjusted HR: 2.06 95% CI: 1.10-3.85; p = 0.023), with analysis of specific mutations identifying particularly high risks for TET2 (adjusted HR: 3.72, 95% CI: 1.37-10.09; p = 0.010) and TET2/ASXL1 co-mutations (adjusted HR: 2.61, 95% CI: 1.08-6.30; p = 0.033). Kaplan-Meier analysis in the high-HGI group confirmed that carriers of any CHIP (p < 0.001) and common CHIP (p = 0.019) had a higher risk of mortality than noncarriers.
Our study reveals that HGI significantly modifies CHIP-related all-cause mortality risk, which provides a way for refined risk stratification in patients with AMI.
Authors
Xue Xue, Dong Dong, Li Li, Chen Chen, Li Li, Liu Liu, Zhou Zhou, Chen Chen, Song Song, Zhao Zhao, Yan Yan, Zhao Zhao
View on Pubmed