Abstract
BackgroundLeft ventricular systolic dysfunction (LVSD) occurs frequently after acute ST-segment elevation myocardial infarction (STEMI). The predisposing factors and underlying mechanism of post-infarct LVSD are not fully understood. The present study mainly investigated the correlation between glycaemic gap, a novel index of stress-induced hyperglycaemia (SIH), and post-infarct LVSD.MethodsA total of 274 first STEMI patients were enrolled in this cross-sectional study. Transthoracic echocardiography was performed within 48 h after admission and at 6 months after discharge to obtain left ventricular ejection fraction (LVEF). The change in LVEF was calculated as LVEF at 6 months after discharge minus baseline LVEF. Additionally, post-infarct LVSD was defined as LVEF ≤ 50%. Most importantly, glycaemic gap was calculated as admission blood glucose (ABG) minus the estimated average glucose over the previous 3 months.ResultsIn patients without diabetes mellitus (DM), multivariate linear regression analysis revealed that both glycaemic gap (Beta = − 1.214, 95% CI − 1.886 to − 0.541, p < 0.001) and ABG (Beta = − 1.124, 95% CI − 1.795 to − 0.453, p = 0.001) were associated with change in LVEF. In DM patients, only glycaemic gap was still associated with change in LVEF, although this association was not observed in univariate linear regression analysis. Regarding the association between SIH and post-infarct LVSD, multivariate logistic regression analysis revealed that both glycaemic gap (OR = 1.490, 95% CI 1.043 to 2.129, p = 0.028) and ABG (OR = 1.600, 95% CI 1.148 to 2.229, p = 0.005) were associated with an increased risk of having post-infarct LVSD in non-DM patients. However, after multivariate adjustment in DM patients, only glycaemic gap (OR = 1.399, 95% CI 1.021 to 1.919, p = 0.037) remained associated with an increased risk of having post-infarct LVSD. Furthermore, the predictive value of glycaemic gap for post-infarct LVSD was not inferior to ABG in non-DM patients (p = 0.499), and only glycaemic gap, instead of ABG, could significantly predict post-infarct LVSD in DM patients (AUC = 0.688, 95% CI 0.591 to 0.774, p = 0.002).ConclusionsGlycaemic gap was strongly associated with a change in LVEF and an increased risk of having post-infarct LVSD in patients following STEMI. In STEMI patients with DM, glycaemic gap could provide more valuable information than ABG in identifying patients at high risk of developing post-infarct LVSD.
Highlights
Left ventricular systolic dysfunction (LVSD) occurs frequently after acute ST-segment elevation myocardial infarction (STEMI)
Predictive value of glycaemic gap compared to Admission blood glucose (ABG) for post‐infarct LVSD at the 6‐month follow‐up After receiver operating characteristic (ROC) analysis (Table 4), we demonstrated that both glycaemic gap (AUC = 0.697, 95% CI 0.622 to 0.766, p = 0.001) and ABG (AUC = 0.713, 95% CI 0.638 to 0.781, p = 0.002) could provide a moderate predictive value for post-infarct LVSD at the 6-month follow-up, and the predictive value of glycaemic gap was not inferior to ABG (p = 0.499) in non-diabetes mellitus (DM) patients
Teraguchi et al further demonstrated that myocardial salvage index (MSI) assessed cardiac magnetic resonance (CMR) in patients with stressinduced hyperglycaemia (SIH) (ABG ≥ 10 mmol/L) was lower than that in patients without SIH among non-DM patients; no significant difference was observed in MSI between patients with or without SIH in DM patients [33]. In line with these studies, our present study revealed that ABG was associated with changes in left ventricular ejection fraction (LVEF) and the risk of having post-infarct LVSD in non-DM patients, but the association was not observed in DM patients
Summary
Left ventricular systolic dysfunction (LVSD) occurs frequently after acute ST-segment elevation myocardial infarction (STEMI). The present study mainly investigated the correlation between glycaemic gap, a novel index of stressinduced hyperglycaemia (SIH), and post-infarct LVSD. Recent studies further indicated that stress-induced hyperglycaemia (SIH) and concomitant metabolic perturbations play an extremely important role in the initiation and progression of post-infarct LVSD [10,11,12]. Critical illness such as acute myocardial infarction (AMI), sepsis, and major surgeries could lead to transient hyperglycaemia, termed SIH, through multiple potential mechanisms in patients with or without diabetes mellitus (DM) [13]. We mainly investigated the correlation between glycaemic gap and post-infarct LVSD in the present study
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