Why the study?
To explore the combined effect of hemoglobin glycation index and clonal hematopoiesis of indeterminate potential on all-cause mortality among patients diagnosed with AMI.
Does the combination of high hemoglobin glycation index and clonal hematopoiesis of indeterminate potential increase the risk of all-cause mortality in patients with acute myocardial infarction?
Does the combination of high hemoglobin glycation index and clonal hematopoiesis of indeterminate potential increase the risk of all-cause mortality in patients with acute myocardial infarction?
Answers are grounded in this paper and cite their sources.
Elevated hemoglobin glycation index synergistically amplifies the all-cause mortality risk associated with CHIP mutations (especially TET2 and ASXL1) in patients with acute myocardial infarction, suggesting a novel multidimensional approach for risk stratification.
Aims 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). Methods 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. Results 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. Conclusions 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.
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Xue et al. (2026) studied this question.
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