Background <p>Estimated glucose disposal rate (eGDR), a validated surrogate for insulin resistance, is associated with cardiovascular disease, but its relationship with chest pain, which is a common presenting symptom of cardiovascular events, remains unclear. This study investigated the associations of eGDR with chest pain prevalence and all-cause mortality.</p> Methods <p>Using cross-sectional and cohort study designs, we analyzed data from 1999 to 2018 National Health and Nutrition Examination Survey (NHANES). Survey-weighted logistic regression was used to examine the association between eGDR and chest pain prevalence, while weighted Cox model was used to evaluate the relationship between eGDR and all-cause mortality in participants with and without chest pain. Restricted cubic splines (RCS) examined potential nonlinearity, and Kaplan–Meier curves visualized survival differences by eGDR category. Mediation analysis examined whether white blood cells (WBC) count mediated the eGDR–mortality association.</p> Results <p>The study included 13,161 participants, with the sample being weighted to reflect a population of 54,616,985 individuals. After full adjustment, each standard deviation (SD) increase in eGDR correlated with an 11% lower odds of chest pain (<i>P</i> &lt; 0.001). Cox regression revealed each SD rise in eGDR was associated with a 7% lower risk of all-cause mortality among participants with chest pain (<i>P</i> = 0.004). RCS confirmed linear relationships for eGDR with both chest pain prevalence and mortality risk, irrespective of chest pain status. When eGDR was dichotomized at the population median (7.34&#xa0;mg/kg/min), participants with high eGDR was significantly associated with reduced odds of chest pain (OR = 0.67, 95% CI: 0.59–0.77, <i>P</i> &lt; 0.001) and lower all-cause mortality (HR = 0.85, 95% CI: 0.75–0.95, <i>P</i> = 0.006) compared to those with low eGDR. Kaplan–Meier curves demonstrated a clear survival advantage for participants with higher eGDR. WBC mediated 20.04% of the association between eGDR and all-cause mortality (<i>P</i><sub>indirect</sub> &lt; 0.001).</p> Conclusion <p>Higher eGDR is robustly associated with lower chest pain prevalence and reduced all-cause mortality risk, irrespective of chest pain status. The partial mediation by WBC suggests a potential inflammatory pathway. These findings support the potential value of eGDR in non-invasive cardiometabolic risk stratification.</p>

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Associations of estimated glucose disposal rate with chest pain prevalence and mortality risks: a population-based study

  • Jieke Wang,
  • Manli Ye

摘要

Background

Estimated glucose disposal rate (eGDR), a validated surrogate for insulin resistance, is associated with cardiovascular disease, but its relationship with chest pain, which is a common presenting symptom of cardiovascular events, remains unclear. This study investigated the associations of eGDR with chest pain prevalence and all-cause mortality.

Methods

Using cross-sectional and cohort study designs, we analyzed data from 1999 to 2018 National Health and Nutrition Examination Survey (NHANES). Survey-weighted logistic regression was used to examine the association between eGDR and chest pain prevalence, while weighted Cox model was used to evaluate the relationship between eGDR and all-cause mortality in participants with and without chest pain. Restricted cubic splines (RCS) examined potential nonlinearity, and Kaplan–Meier curves visualized survival differences by eGDR category. Mediation analysis examined whether white blood cells (WBC) count mediated the eGDR–mortality association.

Results

The study included 13,161 participants, with the sample being weighted to reflect a population of 54,616,985 individuals. After full adjustment, each standard deviation (SD) increase in eGDR correlated with an 11% lower odds of chest pain (P < 0.001). Cox regression revealed each SD rise in eGDR was associated with a 7% lower risk of all-cause mortality among participants with chest pain (P = 0.004). RCS confirmed linear relationships for eGDR with both chest pain prevalence and mortality risk, irrespective of chest pain status. When eGDR was dichotomized at the population median (7.34 mg/kg/min), participants with high eGDR was significantly associated with reduced odds of chest pain (OR = 0.67, 95% CI: 0.59–0.77, P < 0.001) and lower all-cause mortality (HR = 0.85, 95% CI: 0.75–0.95, P = 0.006) compared to those with low eGDR. Kaplan–Meier curves demonstrated a clear survival advantage for participants with higher eGDR. WBC mediated 20.04% of the association between eGDR and all-cause mortality (Pindirect < 0.001).

Conclusion

Higher eGDR is robustly associated with lower chest pain prevalence and reduced all-cause mortality risk, irrespective of chest pain status. The partial mediation by WBC suggests a potential inflammatory pathway. These findings support the potential value of eGDR in non-invasive cardiometabolic risk stratification.