What is the clinical evidence from this study?

Study design: Cohort. Population: Cardiovascular disease (n=2714). Intervention: Stress hyperglycemia ratio (SHR) vs. Quartile 2 of stress hyperglycemia ratio. Primary outcome: All-cause mortality (HR 1.57, 95% CI 1.12-2.19, p=0.009).

What does this research mean for the field?

The stress hyperglycemia ratio (SHR) exhibits a U-shaped association with all-cause mortality and premature death in patients with cardiovascular disease, with both lower and higher SHR values correlating with elevated risk. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

October 8, 2025Diabetology & Metabolic Syndrome1 citationsOpen Access

U-shaped association of the stress hyperglycemia ratio with all-cause mortality and premature death in patients with cardiovascular disease: a cohort study

NWNa WangHubei University of Medicine YSYa ShaoHubei University of Medicine YZYan ZhanHubei University of Medicine

Key Result

The stress hyperglycemia ratio exhibited a U-shaped association with all-cause mortality in patients with cardiovascular disease, with higher continuous levels increasing mortality risk (HR 1.57).

Study Design

Type

Cohort (n=2,714)

Structured PICO

Is the stress hyperglycemia ratio (SHR) associated with all-cause mortality and premature death in patients with cardiovascular disease?

Population

2,714 adults aged 20 years or older with cardiovascular disease from the NHANES cohort, followed for an average of 88.38 months.

Exposure

Stress hyperglycemia ratio (SHR) levels (analyzed as continuous and in quartiles)

Comparator

Second quartile of SHR (reference group with highest survival probability)

Outcome

All-cause mortality and premature deathhard clinical

There is a U-shaped association between the stress hyperglycemia ratio and both all-cause mortality and premature death in patients with cardiovascular disease, suggesting moderate SHR levels are optimal.

Main Result

Hazard Ratio: 1.57 (95% CI 1.12–2.19)

p-value: p=0.009

Limitations

Self-reported data for lifestyle choices and medical history may introduce recall bias or misreporting.
Single baseline measurement of SHR may not capture dynamic changes in blood glucose response over time.
Potential unmeasured confounding factors such as dietary patterns, medication adherence, and psychological stress.
Observational design limits causal inference.

Abstract

BACKGROUND: The stress hyperglycemia ratio (SHR) is recognized as a significant indicator of relative hyperglycemia that has demonstrated to correlate with poor outcomes, including elevated mortality rates in individuals facing severe acute conditions. However, the connection between SHR and all-cause mortality and premature death in individuals with cardiovascular disease (CVD) remains insufficiently investigated. This research intended to investigate the relationship between SHR and all-cause mortality and premature death among individuals with CVD. METHODS: This cohort study involved data extracted from 2,714 follow-up cohorts sourced from the National Health and Nutrition Examination Survey (NHANES). Participants were categorized based on SHR quartiles. The relationship between SHR and all-cause mortality and premature death in CVD patients was analyzed using Kaplan-Meier survival curves, restricted cubic splines (RCS), Cox proportional hazards models, threshold effect analysis, and subgroup analyses. RESULTS: Over an average follow-up duration of 88.38 months, 1,201 deaths were documented, of which 351 were classified as premature. The Kaplan-Meier curves illustrated that individuals in quartile 2 of SHR exhibited highest survival probability compared to other quartiles. Cox proportional hazards regression revealed a positive association between SHR (for continuous) and all-cause mortality (HR 1.57, 95% CI 1.12-2.19) as well as premature death (HR 1.96, 95% CI 1.10-3.49). Compared with the second quartile, both lower and higher SHR values were significantly correlated with elevated risk of all-cause mortality and premature death (HR > 1, P-value < 0.05). The RCS analysis elucidated a U-shaped association of SHR with risk of all-cause mortality and premature death. Furthermore, the threshold effect analysis pinpointed the inflection points for SHR relative to all-cause mortality and premature death at 0.86 and 0.87, respectively. E-value indicated that the model demonstrated robust stability concerning potential unknown confounding variables. CONCLUSION: An independent association of SHR with all-cause mortality and premature death was observed among individuals with CVD. Maintaining SHR within a moderate range might improve their prognosis.

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