1,753 patients with were followed for a median of 6.25 years, during which 624 deaths occurred.
A positive association was observed between the (GLR) and both all-cause and cardiovascular disease (CVD) mortality.
A J-shaped nonlinear relationship between GLR and all-cause mortality was identified, with an inflection point at 3.13.
When GLR was less than 3.13, it was significantly associated with a lower risk of all-cause mortality (HR 0.65).
When GLR was 3.13 or greater, it correlated positively with all-cause mortality (HR 1.13).
The correlation between GLR and CVD mortality was generally positive but weaker than that of all-cause mortality.
GLR demonstrated superior predictive performance for mortality risk compared to glucose or lymphocyte levels.
Simplified
(ASCVD) is a leading cause of mortality worldwide. Dysregulation of glucose metabolism and inflammation are key factors in the development of atherosclerosis. The (GLR) is a comprehensive marker for assessing glucose metabolism and inflammation. This study aims to evaluate the association between GLR and all-cause as well as cardiovascular disease (CVD) mortality in patients with ASCVD within the U.S. population. This retrospective cohort study recruited 1,753 ASCVD patients from the 2003-2018 National Health and Nutrition Examination Survey (NHANES) with a median follow-up of 6.25 years. Mortality outcomes were determined by linkage to the National Death Index (NDI) records up to December 31, 2019. Weighted Cox proportional hazard models were used to assess the independent association between GLR and mortality risk. Restricted cubic spline (RCS) curves were used to display the relationship between GLR and all-cause mortality visually, and two-segment Cox proportional hazards models were constructed on either side of the inflection points. Kaplan-Meier survival curves were further used to assess the relationship between GLR and mortality, and further subgroup analyses were performed. Receiver operating characteristic curve (ROC) analysis was conducted to assess the predictive ability of GLR for survival. During a median follow-up of 6.25 years, 624 deaths from various causes were observed, with 254 deaths from CVD. Cox regression analysis revealed a positive association between GLR and both all-cause and CVD mortality. Based on RCS, a J-shaped nonlinear relationship was observed between GLR and all-cause mortality in ASCVD patients, with an inflection point at 3.13. When the GLR < 3.13, it showed a significant negative association with all-cause mortality (HR 0.65, 95% CI 0.47-0.89). When GLR ≥ 3.13 for all-cause mortality, there was a significant positive correlation with all-cause mortality (HR 1.13, 95% CI 1.09-1.17). Subgroup analysis revealed a positive association between GLR and CVD mortality across most subgroups, but the correlation between GLR and CVD mortality was weaker compared to its association with all-cause mortality. In addition, an interaction was detected between GLR and age in relation to all-cause mortality. Moreover, the predictive performance of GLR on all-cause and CVD mortality seemed superior to that of glucose or lymphocytes. Our findings indicate that elevated GLR was closely associated with an increased risk of all-cause mortality and CVD mortality in ASCVD patients. Notably, the relationship between GLR and all-cause mortality exhibited a J-shaped nonlinear pattern, with an inflection point at 3.13.
Key numbers
1.13
Increase in All-Cause Mortality Risk
Hazard Ratio for all-cause mortality with ≥ 3.13
0.65
Decrease in All-Cause Mortality Risk
Hazard Ratio for all-cause mortality with < 3.13
0.58
Predictive Value of
Area under the curve for in predicting all-cause mortality
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Declarations. Competing interests: The authors declare no competing interests. Ethics approval and consent to participate: The studies involving human participants were reviewed and approved by the NCHS Research Ethics Review Board (ERB). All participants provided written informed consent.
