Key result
Concurrent CHIP and elevated hs-CRP linked to ~6.5-fold higher STEMI mortality.
Cohort (n=1,403)
Hazard Ratio: 6.54
p-value: p=<0.05
Investigates how CHIP mutations and inflammation biomarkers affect outcomes in STEMI patients, suggesting new risk stratification methods.
Background and aims Epidemiological studies reveal an age-dependent penetrance of clonal hematopoiesis of indeterminate potential (CHIP), with carriers exhibiting excess mortality not fully explained by cancer progression. This study investigates the prognostic interplay between CHIP mutations, systemic inflammation quantified by high-sensitivity C-reactive protein (hs-CRP), and Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) clinical outcomes in ST-segment elevation myocardial infarction (STEMI). Methods In a prospective cohort of 1,403 consecutive STEMI patients (March 2017–January 2020), deep targeted sequencing with unique molecular identifiers (UMIs) identified 42 CHIP-associated mutations. Result (i) Patients harboring CHIP variants (variant allele frequency [VAF] >2%) with elevated hs-CRP exhibited distinct high-risk features: advanced age, impaired left ventricular function (LVEF 52.4% ± 8.8 vs 54.4% ± 7.5), elevated cardiac biomarkers (peak troponin T (31.7 vs 20.2 mmol/L; NT-proBNP 1,658 vs 630 mmol/L), and heightened diabetes prevalence (50.0% vs 31.1%; all P<0.05). Age stratification revealed a biological gradient, with mortality rates escalating from 0% in CHIP+/hs-CRP>median patients aged <60 years to 23.5% in those ≥75 years. (ii) Multivariable Cox regression demonstrated synergistic mortality risk in diabetic patients with dual CHIP/hs-CRP elevation or dual CHIP/PCSK9 elevation, persisting after adjustment （p＜0.05）. Patients with concurrent CHIP and hs-CRP above median exhibit a 6.54-fold increased mortality risk, amplified in diabetic subgroups (adjusted HR 7.39); (iii) Stratification by CHIP status and hs-CRP levels (above/below median) or PCSK9 levels (above/below median)revealed a stepwise mortality gradient (p＜0.05). Conclusion These findings align with emerging paradigms of somatic mutation-driven inflammation while providing novel insights into risk stratification and therapeutic targeting in post-MI populationsKM curve of CHIP and PCSK9 KM curve of CHIP and CRP
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Zhao et al. (2025) conducted a cohort in ST-segment elevation myocardial infarction (STEMI) (n=1,403). Concurrent CHIP mutations and elevated hs-CRP vs. Absence of concurrent CHIP mutations and elevated hs-CRP was evaluated on Mortality (HR 6.54, p=<0.05). Concurrent CHIP mutations and elevated hs-CRP above the median were associated with a 6.54-fold increased mortality risk in patients with STEMI (P<0.05).
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