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Myocardial Infarction and Functional Outcome Assessment in Pigs
Published on: April 25, 2014
Augmented glycaemic gap is a marker for an increased risk of post-infarct left ventricular systolic dysfunction
Yong Zhu1, Kesen Liu1, Shuai Meng2
1Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, 100029, China.
Insights
The glycaemic gap, a measure of stress-induced hyperglycemia, is linked to reduced left ventricular ejection fraction after ST-segment elevation myocardial infarction (STEMI). This index is particularly valuable for identifying high-risk patients with diabetes.
Area of Science:
- Cardiology
- Endocrinology
- Metabolic Syndrome
Background:
- Left ventricular systolic dysfunction (LVSD) is a common complication following acute ST-segment elevation myocardial infarction (STEMI).
- The factors contributing to and mechanisms behind post-infarct LVSD are not fully elucidated.
- This study explores the relationship between the glycaemic gap and post-infarct LVSD.
Purpose of the Study:
- To investigate the correlation between the glycaemic gap, an indicator of stress-induced hyperglycemia, and left ventricular systolic dysfunction (LVSD) after STEMI.
- To assess the predictive value of the glycaemic gap for post-infarct LVSD in patients with and without diabetes mellitus (DM).
Main Methods:
- A cross-sectional study of 274 STEMI patients.
- Transthoracic echocardiography was used to measure left ventricular ejection fraction (LVEF) at baseline and 6 months post-discharge.
- Glycaemic gap was calculated as admission blood glucose (ABG) minus estimated average glucose over the preceding 3 months.
Main Results:
- In non-diabetic patients, both glycaemic gap and ABG were associated with changes in LVEF and increased risk of post-infarct LVSD.
- In diabetic patients, only the glycaemic gap remained associated with changes in LVEF and predicted an increased risk of post-infarct LVSD.
- The glycaemic gap demonstrated comparable or superior predictive value for post-infarct LVSD compared to ABG, especially in diabetic patients.
Conclusions:
- The glycaemic gap is strongly associated with changes in LVEF and the risk of post-infarct LVSD in STEMI patients.
- In STEMI patients with diabetes, the glycaemic gap offers more valuable predictive information for post-infarct LVSD than admission blood glucose alone.
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 stress-induced 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 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).
Conclusions:
Glycaemic 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.
