Glycemia as a predictor of acute myocardial infarction severity in non diabetics

Introduction Hyperglycaemia is frequently observed in acute illness and is associated with increased disease severity. In acute myocardial infarction, previous studies suggest that elevated glucose levels may contribute to additional myocardial injury. Objective To evaluate whether admission glycaemia is related to the severity of acute coronary syndrome (ACS) in non-diabetic patients. Methods This observational, retrospective study included patients admitted with ACS to our center between October 2010 and July 2025, all registered in a nationwide registry. Patients with previously known diabetes were excluded. Participants were stratified according to their Killip classification at admission. Comparisons between groups were performed using the chi-square test for categorical variables and mean or median comparison tests for continuous variables. Differences in glycaemia between Killip classes were assessed using one-way ANOVA followed by Bonferroni post hoc tests. Results A total of 985 patients were included, of whom 765 (76.6%) were male. Significant differences between Killip groups were observed for gender, height, age, arterial hypertension, smoking history, previous heart failure, chronic obstructive pulmonary disease, and ACS type at admission (Table 1). The mean admission glycaemia was 131 ± 42 mg/dL. One-way ANOVA revealed significant differences in glycaemic values among Killip classes (F (3, 981) = 37.389, p < 0.001), and Bonferroni post hoc analysis showed significant differences between all classes except Killip III and IV (Tables 2 and 3). Discussion Admission hyperglycaemia was progressively and significantly associated with higher Killip class at admission, indicating that elevated glucose levels correlate with increased ACS severity. This finding suggests that early recognition and management of hyperglycaemia may represent an opportunity to improve outcomes in these patients. The lack of significant differences between Killip III and IV may be explained by the small number of patients in these groups.