Background <p>Heart failure (HF) has high morbidity and mortality, worsened by aging and metabolic diseases. The triglyceride–glucose (TyG) index and its obesity-related derivatives are markers of metabolic dysfunction, but large-scale prospective data linking them with cardiac structure, biventricular function, and HF risk are scarce.</p> Methods <p>In UK Biobank participants free of HF at baseline, we examined associations of the TyG, TyG–BMI, TyG–WC and TyG–WHtR with cardiac structure and function by cardiovascular magnetic resonance and with incident HF. Multivariable linear and Cox models with restricted cubic splines assessed associations; mediation analyses evaluated the roles of left ventricular volumes and ejection fraction.</p> Results <p>Higher TyG and its derivatives were associated with larger Left ventricular(LV) and Right Ventricular(RV) end-diastolic volumes and lower LV and RV ejection fractions after adjustment; TyG–WC and TyG–BMI showed the strongest associations. Compared with the lowest TyG quartile, the highest quartile had a 1.51-fold higher risk of HF, with a clear dose–response. LV end-diastolic and end-systolic volumes and LV ejection fraction partially mediated the TyG–HF association; for TyG–WC, 57.7% of the effect operated via LV-EDV. Findings were robust in sensitivity analyses.</p> Conclusions <p>TyG related metabolic burden, particularly when integrated with central adiposity, is linked to biventricular remodeling and increased HF risk. These results extend TyG evidence to right-ventricular function and support its use for HF risk stratification.</p>

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Triglyceride–glucose index and its derivatives, biventricular remodeling, and risk of incident heart failure: a large-scale prospective CMR study

  • Rui Fan,
  • Xingyun He,
  • Zhixing Fan

摘要

Background

Heart failure (HF) has high morbidity and mortality, worsened by aging and metabolic diseases. The triglyceride–glucose (TyG) index and its obesity-related derivatives are markers of metabolic dysfunction, but large-scale prospective data linking them with cardiac structure, biventricular function, and HF risk are scarce.

Methods

In UK Biobank participants free of HF at baseline, we examined associations of the TyG, TyG–BMI, TyG–WC and TyG–WHtR with cardiac structure and function by cardiovascular magnetic resonance and with incident HF. Multivariable linear and Cox models with restricted cubic splines assessed associations; mediation analyses evaluated the roles of left ventricular volumes and ejection fraction.

Results

Higher TyG and its derivatives were associated with larger Left ventricular(LV) and Right Ventricular(RV) end-diastolic volumes and lower LV and RV ejection fractions after adjustment; TyG–WC and TyG–BMI showed the strongest associations. Compared with the lowest TyG quartile, the highest quartile had a 1.51-fold higher risk of HF, with a clear dose–response. LV end-diastolic and end-systolic volumes and LV ejection fraction partially mediated the TyG–HF association; for TyG–WC, 57.7% of the effect operated via LV-EDV. Findings were robust in sensitivity analyses.

Conclusions

TyG related metabolic burden, particularly when integrated with central adiposity, is linked to biventricular remodeling and increased HF risk. These results extend TyG evidence to right-ventricular function and support its use for HF risk stratification.