Stress hyperglycemia and early mortality in non-ST elevation myocardial infarction

BACKGROUND Acute hyperglycemia is frequently observed in patients presenting with acute coronary syndromes and is considered a marker of metabolic and neurohormonal stress. However, its prognostic significance relative to chronic glycemic status remains incompletely understood, particularly in patients with non-ST-segment elevation myocardial infarction (NSTEMI). Glycated hemoglobin (HbA1c) reflects long-term glycemic control but may not adequately capture acute metabolic derangements occurring during myocardial ischemia. Stress hyperglycemia reflects a transient metabolic response to acute illness mediated by counter-regulatory hormones, systemic inflammation, and increased hepatic gluconeogenesis, and does not necessarily indicate pre-existing insulin resistance or chronic dysglycemia. Recent studies suggest that stress-related hyperglycemia indices may better reflect short-term risk, yet comparative data in NSTEMI populations remain limited. AIM To determine whether admission stress hyperglycemia indices are associated with early mortality in patients with non-ST elevation myocardial infarction. METHODS This prospective, single-center observational study consecutively enrolled 171 patients admitted with confirmed NSTEMI. Stress hyperglycemia was assessed using the stress hyperglycemia ratio (SHR) and the admission glucose-to-chronic glycemia ratio (ACGR), calculated from admission plasma glucose and HbA1c values obtained at hospital presentation. Patients were categorized according to established HbA1c thresholds. Clinical, laboratory, and echocardiographic data were systematically collected. All patients were followed for three months after discharge. The primary endpoint was the occurrence of major adverse cardiovascular events (MACE), defined as a composite of cardiovascular death, non-fatal myocardial infarction, or urgent coronary revascularization. The secondary endpoint was all-cause mortality. Discriminatory performance was evaluated using receiver operating characteristic (ROC) curve analysis. Multivariable logistic regression models were constructed to assess the independent and incremental prognostic value of stress hyperglycemia indices before and after adjustment for established clinical and echocardiographic predictors. RESULTS During the three-month follow-up period, 88 MACE and 25 deaths were recorded. HbA1c categories were not significantly associated with all-cause mortality or MACE. In contrast, admission glucose levels, SHR, and ACGR were significantly higher in non-survivors than in survivors. No significant differences in HbA1c were observed between outcome groups. Stress hyperglycemia indices demonstrated modest discriminatory ability for predicting mortality and showed greater discrimination than HbA1c in ROC analyses. In multivariable models, both SHR and ACGR remained independently associated with early mortality after adjustment for demographic, clinical, and echocardiographic variables, whereas no independent association with the composite MACE endpoint was observed. ROC-derived thresholds used for survival analyses were exploratory and have not been externally validated. CONCLUSION In patients with NSTEMI, stress hyperglycemia indices assessed at hospital admission are independently associated with early mortality, whereas chronic glycemic status shows limited prognostic relevance. These indices appear to reflect acute systemic stress and metabolic instability and may provide clinically useful information for early risk stratification during the initial phase of hospitalization, particularly when comprehensive echocardiographic assessment is not yet available.