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      Association of stress induced hyperglycemia with angiographic findings and clinical outcomes in patients with ST-elevation myocardial infarction

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          Abstract

          Background

          Stress induced hyperglycemia (SIH) is common among patients with ST-elevation myocardial infarction (STEMI), even in patients without diabetes mellitus. However, evidence regarding its role on the angiographic outcomes and the prognosis of patients presenting with STEMI is scarce.

          Methods

          This study included 309 consecutively enrolled STEMI patients undergoing primary percutaneous coronary intervention (pPCI). Patients were diagnosed with SIH if blood glucose on admission was > 140 mg/dl. Also, patients had to fast for at least 8 hours before blood sampling. The objective was to assess whether SIH was associated with major adverse cardiovascular and cerebrovascular (MACCE) events and explore its relationship with angiographic predictors of worse prognosis such as poor initial TIMI flow, intracoronary thrombus burden, distal embolization, and presence of residual thrombus after pPCI.

          Results

          SIH in diabetic and non-diabetic patients was associated with a higher incidence of LTB (aOR = 2.171, 95% CI 1.27–3.71), distal embolization (aOR = 2.71, 95% CI 1.51–4.86), and pre-procedural TIMI flow grade = 0 (aOR = 2.69, 95% CI 1.43–5.04) after adjusting for relevant clinical variables. Importantly, during a median follow-up of 1.7 years STEMI patients with SIH with or without diabetes experienced increased occurrence of MACCE both in univariate (HR = 1.92, 95% CI 1.19–3.01) and multivariate analysis (aHR = 1.802, 95% CI 1.01–3.21).

          Conclusions

          SIH in STEMI patients with or without diabetes was independently associated with increased MACCE. This could be attributed to the fact that SIH was strongly correlated with poor pre-procedural TIMI flow, LTB, and distal embolization. Large clinical trials need to validate SIH as an independent predictor of adverse angiographic and clinical outcomes to provide optimal individualized care for patients with STEMI.

          Supplementary Information

          The online version contains supplementary material available at 10.1186/s12933-022-01578-6.

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          Most cited references34

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          Fourth Universal Definition of Myocardial Infarction (2018).

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            Stress hyperglycaemia and increased risk of death after myocardial infarction in patients with and without diabetes: a systematic overview.

            High blood glucose concentration may increase risk of death and poor outcome after acute myocardial infarction. We did a systematic review and meta-analysis to assess the risk of in-hospital mortality or congestive heart failure after myocardial infarction in patients with and without diabetes who had stress hyperglycaemia on admission. We did two searches of MEDLINE for English-language articles published from 1966 to October, 1998, a computerised search of Science Citation Index from 1980 to September, 1998, and manual searches of bibliographies. Two searchers identified all cohort studies or clinical trials reporting in-hospital mortality or rates of congestive heart failure after myocardial infarction in relation to glucose concentration on admission. We compared the relative risks of in-hospital mortality and congestive heart failure in hyperglycaemic and normoglycaemic patients with and without diabetes. 14 articles describing 15 studies were identified. Patients without diabetes who had glucose concentrations more than or equal to range 6.1-8.0 mmol/L had a 3.9-fold (95% CI 2.9-5.4) higher risk of death than patients without diabetes who had lower glucose concentrations. Glucose concentrations higher than values in the range of 8.0-10.0 mmol/L on admission were associated with increased risk of congestive heart failure or cardiogenic shock in patients without diabetes. In patients with diabetes who had glucose concentrations more than or equal to range 10.0-11.0 mmol/L the risk of death was moderately increased (relative risk 1.7 [1.2-2.4]). Stress hyperglycaemia with myocardial infarction is associated with an increased risk of in-hospital mortality in patients with and without diabetes; the risk of congestive heart failure or cardiogenic shock is also increased in patients without diabetes.
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              Oxidative stress and inflammatory markers in prediabetes and diabetes.

              Prediabetes is a state of elevated plasma glucose in which the threshold for diabetes has not yet been reached and can predispose to the development of type 2 diabetes and cardiovascular diseases. Insulin resistance and impaired beta-cell function are often already present in prediabetes. Hyperglycemia can upregulate markers of chronic inflammation and contribute to increased reactive oxygen species (ROS) generation, which ultimately cause vascular dysfunction. Conversely, increased oxidative stress and inflammation can lead to insulin resistance and impaired insulin secretion. Proper treatment of hyperglycemia and inhibition of ROS overproduction is crucial for delaying onset of diabetes and for prevention of cardiovascular complications. Thus, it is imperative to determine the mechanisms involved in the progression from prediabetes to diabetes including a clarification of how old and new medications affect oxidative and immune mechanisms of diabetes. In this review, we discuss the relationship between oxidative stress and hyperglycemia along with links between inflammation and prediabetes. Additionally, the effects of hyperglycemic memory, microvesicles, micro-RNA, and epigenetic regulation on inflammation, oxidative state, and glycemic control are highlighted. Adipose tissue and their influence on chronic inflammation are also briefly reviewed. Finally, the role of immune-targeted therapies and anti-diabetic medication on glycemic control and oxidative stress are discussed.
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                Author and article information

                Contributors
                ggiannakoulas@auth.gr
                Journal
                Cardiovasc Diabetol
                Cardiovasc Diabetol
                Cardiovascular Diabetology
                BioMed Central (London )
                1475-2840
                26 July 2022
                26 July 2022
                2022
                : 21
                : 140
                Affiliations
                [1 ]First Department of Cardiology, AHEPA University Hospital, Aristotle University of Thessaloniki, St. Kiriakidi 1, 54636 Thessaloniki, Greece
                [2 ]GRID grid.4793.9, ISNI 0000000109457005, Laboratory of Forensic Medicine and Toxicology, School of Medicine, , Aristotle University of Thessaloniki, ; 54124 Thessaloniki, Greece
                [3 ]GRID grid.4793.9, ISNI 0000000109457005, Biomic_Auth, Bioanalysis and Omics Lab, , Centre for Interdisciplinary Research of Aristotle University of Thessaloniki, Innovation Area of Thessaloniki, ; 57001 Thermi, Greece
                [4 ]GRID grid.4793.9, ISNI 0000000109457005, Pathology Department, Faculty of Medicine, , Aristotle University of Thessaloniki, ; Thessaloniki, Greece
                Article
                1578
                10.1186/s12933-022-01578-6
                9327277
                35883091
                4ce78e0f-431c-4531-b6b0-84efde076acd
                © The Author(s) 2022

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                : 2 June 2022
                : 21 July 2022
                Categories
                Research
                Custom metadata
                © The Author(s) 2022

                Endocrinology & Diabetes
                stemi,stress induced hyperglycemia,diabetes,thrombus,distal embolization
                Endocrinology & Diabetes
                stemi, stress induced hyperglycemia, diabetes, thrombus, distal embolization

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