Augmented glycaemic gap is a marker for an increased risk of post-infarct left ventricular systolic dysfunction

Abstract

Background: Left 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 stressinduced hyperglycaemia (SIH), and post-infarct LVSD. Methods: A 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. Results: In 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 postinfarct 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). Conclusions: Glycaemic gap was strongly associated with a change in LVEF and an increased risk of having postinfarct 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.

Hyperglycemia, inflammatory response and infarct size in obstructive acute myocardial infarction and MINOCA

“…The link between hyperglycemia and large infarct size in the context of obs-AMI is well established, and our results are in line with previously published studies [ 40 , 41 ]. In fact, several strategies have been adopted to assess the impact of admission hyperglycemia on the extent of myocardial damage, all leading toward the same conclusion [ 42 , 43 ].…”

Hyperglycemia, Inflammatory Response and Infarct Size in Obstructive Acute Myocardial Infarction and MINOCA

“…The link between hyperglycemia and large infarct size in the context of obs-AMI is well established, and our results are in line with previously published studies 41,42 . In fact, several strategies have been adopted to assess the impact of admission hyperglycemia on the extent of myocardial damage, all leading toward the same conclusion 43,44 .…”

Sex-specific differences in left ventricular mass and myocardial energetic efficiency in non-diabetic, pre-diabetic and newly diagnosed type 2 diabetic subjects

“…It has been reported that visit‑to‑visit fasting plasma glucose variability is associated subclinical left cardiac remodeling and systolic dysfunction, independently of conventional risk factors [ 54 ]. Additionally, evidence has been provided that glycemic gap, a marker of glycemic excursion that measures the magnitude of a relative glycemic rise from chronic glycaemia, was associated with a change in left ventricular ejection fraction, and a high risk of postinfarct left ventricular systolic dysfunction [ 55 ].…”