Impact of Hyperglycemia on Long-Term Outcome in Patients With ST-Segment Elevation Myocardial Infarction

Kojima, Takayuki; Hikoso, Shungo; Nakatani, Daisaku; Suna, Shinichiro; Dohi, Tomoharu; Mizuno, Hiroya; Okada, Katsuki; Kitamura, Tetsuhisa; Kida, Hirota; Oeun, Bolrathanak; Sunaga, Akihiro; Kurakami, Hiroyuki; Yamada, Tomomi; Sakata, Yasuhiko; Sato, Hiroshi; Hori, Masatsugu; Komuro, Issei; Sakata, Yasushi

doi:10.1016/j.amjcard.2019.12.034

Cited by 47 publications

(57 citation statements)

References 25 publications

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“…Many observational studies have documented that hyperglycemia occurs frequently among patients hospitalized with ACS, even those without diabetes mellitus ( 1 – 3 ). It has been well-established that elevated glucose is associated with increased in-hospital and long-term mortality in ACS patients, especially in non-diabetic patients ( 4 – 10 ). Yet, hyperglycemia is not identified as an independent risk factor of ACS to date.…”

Section: Introductionmentioning

confidence: 99%

Stress Induced Hyperglycemia in the Context of Acute Coronary Syndrome: Definitions, Interventions, and Underlying Mechanisms

Guo

Feng

et al. 2021

Front. Cardiovasc. Med.

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Elevation of glucose level in response to acute coronary syndrome (ACS) has been recognized as stress induced hyperglycemia (SIH). Plenty of clinical studies have documented that SIH occurs very common in patients hospitalized with ACS, even in those without previously known diabetes mellitus. The association between elevated blood glucose levels with adverse outcome in the ACS setting is well-established. Yet, the precise definition of SIH in the context of ACS remains controversial, bringing confusions about clinical management strategy. Several randomized trials aimed to evaluate the effect of insulin-based therapy on outcomes of ACS patients failed to demonstrate a consistent benefit of intensive glucose control. Mechanisms underlying detrimental effects of SIH on patients with ACS are undetermined, oxidative stress might play an important role in the upstream pathways leading to subsequent harmful effects on cardiovascular system. This review aims to discuss various definitions of SIH and their values in predicting adverse outcome in the context of ACS, as well as the effect of intensive glucose control on clinical outcome. Finally, a glimpse of the underlying mechanisms is briefly discussed.

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Section: Introductionmentioning

confidence: 99%

Stress Induced Hyperglycemia in the Context of Acute Coronary Syndrome: Definitions, Interventions, and Underlying Mechanisms

Guo

Feng

et al. 2021

Front. Cardiovasc. Med.

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“…To assess the effect of SIH more accurately, glycaemic gap and stress hyperglycaemia ratio (SHR), which eliminates the interference of chronic baseline glycaemic levels, were proposed as a novel index of SIH [18][19][20]. Considerable evidence have confirmed both glycaemic gap and SHR were strongly correlated with adverse cardiovascular outcome in AMI patients [15,21,22], but we knew little about the association between these indexes and post-infarct LVSD. Therefore, we mainly investigated the correlation between glycaemic gap and post-infarct LVSD in the present study.…”

mentioning

confidence: 99%

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

Zhu

Liu

Meng

et al. 2020

Cardiovasc Diabetol

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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.

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“…[2,3] The fi ve-year follow-up for a cohort of STEMI patients who were not diagnosed with diabetes mellitus showed that stress hyperglycemia implied a greater risk of death (relative risk, RR = 1.45; 95% CI 1.06-1.98; p = 0.021) and of readmission for heart failure (RR = 1.48; CI al 95% = 1.04-2.10; p = 0,031); however, in diabetic patients it did not imply a worse prognosis (mortality RR = 1.0; 95% CI 0.68-1.48; p = 0.996 or readmissions due to heart failure RR = 1.31; 95% CI 0.90-1.89; p = 0.154). [42] These fi ndings may suggest a greater tolerance to hyperglycemia in diabetic patients.…”

Section: Discussionmentioning

confidence: 98%

“…In both scenarios, the infl ammatory infi ltrate appears substantially reduced. [42] Therefore, EGF positively impacts the local microenvironment of both pathogenic classifi cations of DFU.…”

Section: Gene Transcriptional Response In Granulation Cellsmentioning

confidence: 99%

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2020

MEDICC Review

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MEDICC Review is a unique open-access platform for Latin American and Caribbean praxis addressing today's critical interactions between human health, development of sustainable societies, and the health of our planet. Drawing upon the contributions of the region in social medicine, social movements, rich diversity and scientifi c prowess, Latin America and Caribbean authors published in the journal can help fi ll gaps in thinking and evidence sorely needed to build a sustainable future and a hopeful legacy for future generations.We look forward to contributing to increased visibility for their work and to its positive impact on both regional integration and worldwide solutions.MEDICC Review is published by MEDICC, a US nonprofi t organization founded in 1997, based in Oakland, California, USA, and dedicated to US, Cuban and global health cooperation and equity.

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Impact of Hyperglycemia on Long-Term Outcome in Patients With ST-Segment Elevation Myocardial Infarction

Cited by 47 publications

References 25 publications

Stress Induced Hyperglycemia in the Context of Acute Coronary Syndrome: Definitions, Interventions, and Underlying Mechanisms

Stress Induced Hyperglycemia in the Context of Acute Coronary Syndrome: Definitions, Interventions, and Underlying Mechanisms

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

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