# Fasting stress hyperglycemia ratio as a predictor of intramyocardial hemorrhage and adverse outcomes in ST-segment elevation myocardial infarction

**Authors:** Hang Zhao, Zhengyu Tao, Xu Wang, Xinli Li, Hao Chang, Ding-Kun Ji, Weiliang Xia, Meng Jiang, Jun Pu

PMC · DOI: 10.3389/fendo.2026.1761471 · Frontiers in Endocrinology · 2026-02-11

## TL;DR

A new blood sugar metric called fasting stress hyperglycemia ratio (SHR) predicts heart muscle bleeding and poor outcomes in heart attack patients.

## Contribution

The fasting stress hyperglycemia ratio (SHR) is introduced as a novel predictor of intramyocardial hemorrhage and adverse outcomes in STEMI patients.

## Key findings

- Fasting SHR was the strongest independent predictor of intramyocardial hemorrhage (IMH) in STEMI patients.
- Elevated fasting SHR was significantly associated with increased risk of major adverse cardiac events (MACE).
- The relationship between SHR and IMH risk was nonlinear, with rapid risk escalation at lower SHR levels.

## Abstract

Intramyocardial hemorrhage (IMH) represents the most severe form of microvascular injury and is associated with poor prognosis in patients with ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PPCI). However, the associations of glycemic parameters with the occurrence of IMH remain unclear. We aimed to evaluate the association of fasting stress hyperglycemia ratio (SHR)—a novel metric that adjusts acute glucose for chronic glycemia—with the presence of IMH and to explore its relationship with clinical outcomes in patients with STEMI.

This study utilized data from the prospective, multicenter EARLY-MYO-CMR registry (NCT03768453). We enrolled consecutive STEMI patients undergoing PPCI who had cardiac magnetic resonance (CMR) imaging within a week after the index infarction. The primary endpoint was the presence of IMH defined by CMR T2* mapping. A secondary clinical endpoint was the composite of major adverse cardiac events (MACE) during follow-up.

Among the 496 patients included in this study, 205 (41.3%) exhibited IMH. Multivariable analysis identified fasting SHR as the strongest independent predictor of IMH (adjusted odds ratio [aOR] per 0.1-unit increase: 1.21; 95% CI: 1.10–1.33, P<0.001), outperforming fasting blood glucose and HbA1c. This association was consistent in both non-diabetic (aOR: 1.27; P=0.001) and diabetic patients (aOR: 1.21; P=0.015). Restricted cubic spline analysis revealed a significant nonlinear relationship (P for nonlinearity=0.004), characterized by a rapid increase in IMH risk at lower SHR levels, where the study population was primarily concentrated, and remained consistently high thereafter. During a median follow-up of 25 months, elevated fasting SHR was significantly associated with an increased risk of MACE (Unadjusted hazard ratio per 0.1-unit increase: 1.20; 95% CI: 1.11–1.31; P<0.001; adjusted hazard ratio per 0.1-unit increase:1.20; 95% CI: 1.09–1.31; P<0.001), with Kaplan-Meier analysis confirming a significantly higher cumulative incidence of MACE in the high SHR group (log-rank P<0.001).

Fasting SHR was a potent, independent predictor of IMH in reperfused STEMI. Notably, the IMH risk escalates rapidly even at lower SHR levels, underscoring the critical need for early management of stress hyperglycemia. Elevated SHR was significantly associated with increased risk of MACE. These findings establish fasting SHR not only as a biomarker for microvascular injury but also as a pivotal tool for early risk stratification in STEMI.

CMR, cardiac magnetic resonance; FBG, fasting blood glucose; IMH, intramyocardial hemorrhage; MACE, major adverse cardiac events; PPCI, percutaneous coronary intervention; SHR, stress hyperglycemia ratio; STEMI, ST-segment elevation myocardial infarction.Infographic titled “Fasting Stress Hyperglycemia Ratio as a Predictor of Intramyocardial Hemorrhage and Adverse Outcomes in ST-Segment Elevation Myocardial Infarction.” It displays study details: 496 STEMI patients treated with PPCI. Method involves calculation of Fasting SHR using FBG and HbA1c. CMR T2* mapping used for defining IMH. Key findings: Primary endpoint shows 25.0% IMH incidence at Q1 vs. 56.2% at Q4; Fasting SHR is an independent IMH predictor. Secondary endpoint shows high SHR linked to increased MACE risk, with graphs illustrating non-linear relationship and clinical outcomes.

CMR, cardiac magnetic resonance; FBG, fasting blood glucose; IMH, intramyocardial hemorrhage; MACE, major adverse cardiac events; PPCI, percutaneous coronary intervention; SHR, stress hyperglycemia ratio; STEMI, ST-segment elevation myocardial infarction.

## Linked entities

- **Diseases:** ST-segment elevation myocardial infarction (MONDO:0041656)

## Full-text entities

- **Genes:** CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, MMP9 (matrix metallopeptidase 9) [NCBI Gene 4318] {aka CLG4B, GELB, MANDP2, MMP-9}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, AP2B1 (adaptor related protein complex 2 subunit beta 1) [NCBI Gene 163] {aka ADTB2, AP105B, AP2-BETA, CLAPB1}, ACE (angiotensin I converting enzyme) [NCBI Gene 1636] {aka ACE1, CD143, DCP, DCP1}, RNF130 (ring finger protein 130) [NCBI Gene 55819] {aka G1RP, G1RZFP, GOLIATH, GP}, TNNI3 (troponin I3, cardiac type) [NCBI Gene 7137] {aka CMD1FF, CMD2A, CMH7, RCM1, TNNC1, cTnI}
- **Diseases:** acute coronary syndromes (MESH:D054058), death (MESH:D003643), hypertension (MESH:D006973), hyperglycemic (MESH:D006944), Hyperglycemia (MESH:D006943), dysmetabolism (MESH:D024821), reperfusion injury (MESH:D015427), thrombotic (MESH:D013927), hyperlipidemia (MESH:D006949), MVO (MESH:D017566), inflammation (MESH:D007249), shock (MESH:D012769), insulin resistance (MESH:D007333), myocardial edema (MESH:D004487), congenital heart disease (MESH:D006330), hemorrhagic stroke (MESH:D000083302), valvular disease (MESH:D006349), ischemic (MESH:D002545), endothelial dysfunction (MESH:D014652), Diabetes (MESH:D003920), HR (MESH:D002303), MACE (MESH:D002318), TIMI (MESH:D009203), CMR (MESH:D006331), Stroke (MESH:D020521), chest pain (MESH:D002637), cardiomyopathy (MESH:D009202), anterior infarction (MESH:D056988), IMH (MESH:D006470), hypercholesterolemia (MESH:D006937), ST-segment elevation (MESH:D000072657), Infarct (MESH:D007238), Heart failure (MESH:D006333), arrhythmia (MESH:D001145), left ventricular dysfunction (MESH:D018487), acute pain (MESH:D059787), PPCI (MESH:D003323), metabolic derangement (MESH:D008659), neurologic deficit (MESH:D009461), ischemia (MESH:D007511)
- **Chemicals:** ticagrelor (MESH:D000077486), clopidogrel (MESH:D000077144), GP IIb/IIIa inhibitor (-), carbohydrate (MESH:D002241), cortisol (MESH:D006854), catecholamines (MESH:D002395), lipid (MESH:D008055), gadolinium (MESH:D005682), aspirin (MESH:D001241), reactive oxygen species (MESH:D017382), blood glucose (MESH:D001786), glucose (MESH:D005947), heparin (MESH:D006493)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

27 references — full list in the complete paper: https://tomesphere.com/paper/PMC12932205/full.md

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Source: https://tomesphere.com/paper/PMC12932205